Medical education and learning never ends, especially amongst academics. These do not stop after graduation from the medical school, as all the knowledge and skills required by the doctor cannot be taught in the medical school. Medical knowledge is dynamic as it changes with the evolution of new technologies and advances in biomedical science. Education and training during undergraduate study period do not adequately equip students with required skills to cope with these changes and the changing environment concerning communication skills, ethical and human rights issues, management skills, basic research skills, information technology, etc. The demand for keeping abreast of these changes is particularly important for university teaching staff as they are responsible to transmit the most updated knowledge and skills to their students. Advances in health care and scientific discoveries are reported every day. Internet access to this information is almost immediate. Drugs are recalled; significant findings are reported regarding diagnostic procedures, treatment options, and other issues such as genetics; and lifestyle links are reported on a daily basis. keeping up with this information can prove to be quite a challenge for anyone, but it is important to stay abreast of the most important changes and know where to access more information as this impacts the practice and profession. Continuing medical education (CME) can be defined as educational activities which serve to maintain, develop, and increase the knowledge, skills and professional. It involves in-service training necessary to update knowledge and skills and maintain an effective and relevant delivery of health task under changing conditions. Continuing medical education has long been recognized as the key to updating and maintaining the knowledge and skills of health professionals and academics. CME activities are well advocated, accepted and regulated in the developed world with sanctions for non-participation. In Europe and America, a national board is usually responsible for the quality of CME in their countries and decides on reward or sanction for participation and non-participation. In most developing countries, including Iraq, CME activities are less effective and there is usually no practical enforcement to compel individual’s participation. Lack of accreditation and licensing systems constitute a major problem to ensure the quality of health care in Iraq. Once a doctor or a nurse graduate, they continue to practice without requirements for continuing education. Thus, the outdated theories and practice prevail since there have been few opportunities to upgrade health workers’ skills and knowledge. One of the main goals of establishment of Hawler Medical University was to improve medical education in Kurdistan and Iraq. Since its establishment, the university is not saving efforts to achieve this goal. Hawler Medical University played a major role in initiating CME activities in Iraq through its collaboration with the Medical Alliance for Iraq (MAI), a volunteer group of western doctors, and International Medical Crops (IMC), a nonprofit group that has been working to improve medical care in Iraq. Several training and educational courses were conducted for academic staff and doctors from different parts of Kurdistan and Iraq. These CME activities were later handed over to the Ministry of Health. The university continued to play. An active role in all CME activities in collaboration with the Royal College of Pediatrics and Child Health, by conducting three annual courses for advanced pediatrics life support for pediatricians from both Kurdistan and Iraq. Reactivation of quality assurance process and continuing academic development program by the ministry of higher education and scientific research in Kurdistan region assisted in establishing a solid foundation for CME activities in the region and encouraging teaching staff to participate in these activities. Under this program, each academic regardless of their degree are required to allocate at least 25-50 credits (depending on academic title) through Seeking knowledge and participating in various academic activities. Hawler Medical University and its colleges, work hard to support the teaching staff to achieve this requirement by creating numerous CME activities under close monitoring by the university to ensure participants active contribution to the educational process. In order to scale-up CME activities in Kurdistan, all relevant academic, professional and regulating bodies of medical practice should rise up to the challenge of enforcing CME and have the political will to impose sanction if deemed necessary.
Background and objective: Leukemia is a significant public health and life-threatening problem for pediatric cancer patients. Adolescents leukemic may face long periods of treatment; may describe the irritability, fatigue, bone pain, mouth ulcer, alopecia, and loss of appetite. The aim of the study was to assess the common physical problems among leukemic adolescent patients undergoing chemotherapy, and identify the association between their socio-demographic characteristics with physical problem.
Methods: A descriptive study was carried out in Nanakali Hospital for Blood Diseases / Erbil city from the period of /1st Nov. /2010 to/ 1st of Feb. /2011/. Eighty adolescent who are receiving chemotherapy in face to face interview, were selected regarding the study.
Results: The study shows that there were highly significant associations between socio-demographic characteristics with some of physical problems such as pain, fatigue, loss of appetite, and oral ulcer (mucositis).
Conclusion: The study shows that there were significant association between adolescent patient and some physical problems. The study recommends giving more support and attention by medical and nursing staff manage to reduce their physical problems.
Keywords: Physical Problems, Leukemic Adolescent, Chemotherapy.
1. Babgi AA. Pain Coping Behaviors of Saudi Patients Suffering from Advanced Cancer: A Revisited Experience. Asian Pacific Journal of Cancer Prevention; 2010. 11:103-106.
2. Lanzkowsky P, Leukemias. In Lanzkowsky P. Pediatric Hematology and Oncology. 4th ed. San Diego: Academic Press; 2005. pp. 415- 450.
3. Iraqi Cancer Board. Iraqi cancer registery 2005, Ministry of health, Iraqi cancer registry center, Iraqi_cancerboard@yahoo.com. Baghdad; 2008. Table 2. p 20.
4. Tubingen DG, and Bleyer A. The leukemia. In Behrman RE, Kingman RM, and Jenson HB. Nelson text book of pediatric. 17th edit. Tokyo. Sanders, printed in China; 2004. PP. 1694-1697.
5. Huckleberry MJ, and Wilson D. Wong’s nursing care of infant and children, 8th edit, Mosby, printed in Canada; 2007. pp. 1583-1588.
6. Suwatthi W. Childhood cancer. In: Intrakhumtronchai T. Hematology. Bangkok: B-Yorn Enterprice Company; 1999. p. 334-351.
7. Fallat ME, and Hutter J. Preservation of Fertility in Pediatric and Adolescent Patients with Cancer, pediatric 2008.121(5) May. pp. e1461-e1469. (doi:10.1542/peds.2008-0593).
8. Hutheerat P. Treatment of Childhood cancer. In: Huttheerat P, Juansumlit A, and Isarangkul P. Hematology in Childhood. 3th edit. Bangkok: Chaijalearn Company; 1995.p. 421-434.
9. Atlanta GA, Grunberg SM, Deuson RR, Mavros P, Geling O, Hansen, and et al. Incidence of chemotherapy-induced nausea and emesis after modern antiemetics. Cancer j 2004. 100(10), 2261–2268.
10. Maunsell E, Pogany L, Barrera M, Shaw AK, and Speechley KN. Quality of Life Among Long-Term Adolescent and Adult Survivors of Childhood. Cancer, J Clin Oncol; 2006. 24 (24):2527-2535. www.jco.ascopubs.org. on September 17, 2009.
11. Leukemia Foundation.Young Adults with a Blood Cancer A guide for young adult patients, their families and friends; (2007). pp 1-50.
12. Langhorne ME, Fulton JS, and Otto Sh E. Oncology nursing, 5th edit, Mosby Elesivier, printed in UAS; 2007. pp 232-242.
13. Stiff PJ. The Challenges of Oral Mucositis and Its Therapy, J Support Oncol 2004;2 (suppl 2):70–72. www.SupportiveOncology.net.
14. Fadda G, Campus G and Lugliè P. Risk factors for oral mucositis in paediatric oncology patients receiving alkylant chemotherapy, BMC Oral Health J; 2006. 6:13. doi:10.1186/1472-6831-6-13.http://www.biomedcentral.com/1472-6831/6/13
15.Mieszkowski MR, Bruce A, Cooper BA, Paul SM, Dodd M, Kathryn F, and et al. Subgroups of Patients With Cancer With Different Symptom Experiences and Quality-of-Life Outcomes: A Cluster Analysis, oncology nursing forum; 2006. 33( 5). PP. e79-e89.
16. Hokkanen H, Eriksson E, Ahonen Q, and Salantera S. Adolescents With Cancer: Experience of Life and How it Could be Made Easier, Cancer Nurs J; 2004.27.
17. Barakat LP, Marmer PL, and Schwartz LA. Quality of life of adolescents with cancer: family risks and resources, Health and Quality of Life Outcomes; 2010. 8:63, http:// www.hqlo.com/content/8/1/63.
18. Scarpelli AC, Paiva S M, Pordeus I A, Ramos-Jorge M L, Varni J W, and Allison P J. Measurement properties of the Brazilian version of the Pediatric Quality of Life Inventory PedsQL™) cancer module scale, Health and Quality of Life Outcomes; 2008. 6:7 (doi:10.1186/1477-7525-6-7, Available from: http://www.hqlo.com/content/6/1/7.
19. Till T. Coping with cancer: the adolescent experience. Published theses submitted Australian Catholic University College of nursing in total fulfillment of the requirements of the degree of Master of nursing research. 2004. p6.
20. Al-Jauissy MS. Health care needs of Jordanian caregivers of patients with cancer receiving on an outpatient basis, Eastern Mediterranean Health Journal; 2010.16 (10). PP 1-8.
21. Schumacher A, Kessler T, Chner T Bu, Wewers D, and Van de Loo J. Quality of life in adult patients with acute myeloid leukemia receiving intensive and prolonged chemotherapy – a longitudinal study, Leukemia Medicine Hematology/Oncology J;1998. 12, 586–592. 0887-6924/98 http://www.stockton-press.co.uk/leu.
22. Imbach P, Kühne T, and Arceci R. Pediatric Oncology, A Comprehensive Guide, Springer-Verlag Berlin Heidelberg, Printed in Germany; 2006. pp 1-39.
23. Sung L, Yanofsky R, Klaassen RJ, Dix D, Pritchard S, Winick N, et al. Quality of life during active treatment for pediatric acute lymphoblastic leukemia ; 2011.1;128(5):1213-20. doi: 10.1002/ijc.25433.
24 .Saeui W, Chintanadilo N, Sriussadaporn P, and Sanasuttipun W. The Effects of an Empowerment Program on the Competence of Caregivers in Caring for Preschool Children with Acute Leukemia Undergoing Chemotherapy* J Nurs Sci; 2009. 27 (2). P.1.
25. Erickson JM, Beck SL, Christian BR, Dudley W, Hollen P J, Albritton K A, and et al. Fatigue, Sleep-wake Disturbances, and Quality of Life in Adolescents Receiving Chemotherapy, J Pediatric Hematol Oncol Jan; 2011.33 (1). PP. e17-e25. Available at www.jpho-online.com .
26. Viva MB, Ferreir RA, Olivera BM, Paes CA,Duarte AA. Nutritional and socio-economic status in the prognosis of childhood acute lymphoblastic leukemia, haematologica J; 2001.86:113-120, http://www.haematologica.it/2001_02/0113.htm.
27. Gates RA, and Fink RM. Oncology nursing secrets, 3rd edit, Mosbey. Eleveser, NewJersy; 2008. PP. 398, 410, and 483.
28. Wood LM, Rachet B, and Coleman MP. Origins of socio-economic inequalities in cancer survival: A review. Annals of Oncology 17; 2006. (1) 5–19, Available at www.annonc. oxfordjournals.org.
29. Langhorne ME, Fulton JS, and Otto Sh E. Oncology Nursing, 5th edit, Mosby Elesever, printed in USA; 2007. P. 505-607
Background and objective: Tonsillectomy is defined as the surgical excision of the palatine tonsils. This single blind prospective study of (200) patients underwent tonsillectomy in Al- Rizgary Teaching Hospital-Erbil- Iraq from February 2006 through June 2006.The main aim of this study is to evaluate the effect of post-tonsillectomy amoxicillin in preventing infection and secondary haemorrhage.
Methods: Our patient’s ages ranged from 2.5 years-55 years and were randomly divided postoperatively into two equal groups. The first group received amoxicillin antibiotic with analgesic paracetamol up to one week postoperatively. The second group received only paracetamol for one week. All tonsillectomy surgeries were done by cold knife dissection method.
Results: In the first group no one developed complications neither postoperative infection nor secondary hemorrhage , whereas in the second group who received only paracetamol, 4 patients (4%) had features of infections post operatively with another 2 patients (2%) developed secondary hemorrhage controlled conservatively.
Conclusion: The above results showed no significant effect of post-tonsillectomy antibiotic to prevent infection or delayed bleeding.
Keywords: Tonsillectomy, post tonsillectomy bleeding, complications of tonsillectomy, antibiotics in tonsillectomy
1. Kenna MA, Amin A. Anatomy and physiology of the oral cavity. In: Snow JB, Wackym PA. Anatomyand physiology of the oral cavity in Ballinger's
otorhinolaryngology. 17th edition. Shelton: BC decker Inc; 2009:769-774.
2. Baugh RF, Archer SM,, Mitchell RB. Clinical Practice Guide: Tonsillectomy in Children. Otolaryngology-Head Neck Surg. 2011;144(1 suppl):S1-S30.
3. Paradise JL, Bluestone CD, Bachman RZ. Efficacy of tonsillectomy for recurrent throat infection in severely affected children: results of parallel randomized and nonrandomized clinical trials.N Engl J Med.1984;310:674-683.
4. Bull P.D. Tonsillectomy. Lecture Notes on Diseases of the Ear, Nose and Throat. Ninth edition. Blackwell Publishing .2002; 29:116-118
5. Paradise JL, Bluestone CD, Colborn DK. Tonsillectomy and adenotonsillectomy for recurrent throat infection in moderately affected children. Pediatrics. 2002;110:7-15.
6. Goldstein NA, Stewart MG, Witsell DL. Quality of life after tonsillectomy in children with recurrent tonsillitis. Otolaryngol Head Neck Surg. 2008;138:S9-S16.
7. William S Mckerrow and Ray Clarke. Tonsillectomy. In: Gleeson M. Scott-Brown's otorhinolaryngology, head and neck surgery. Volume 1. 7th edition. London: Hodder Arnold publications; 2008:1229-1239
8. Flanary VA. Long-term effect of adenotonsillectomy on quality of life in pediatric patients. Laryngoscope. 2003 Oct;113(10):1639-44.
9. Mitchell RB, Kelly J. Adenotonsillectomy for obstructive sleep apnea in obese children . Otolaryngol Head Neck Surg. 2004 Jul;131(1):104-8.
10. Hall MD and Brodsky L: The effect of post-operative diet on recovery in the first twelve hours after tonsillectomy and adenoidectomy, Int J Pediatr Otorhinolaryngol. 1995; 31:215,
11. Herzon FS. Harris P. Mosher Award thesis. Peritonsillar abscess: Incidence, current management practices, and a proposal for treatment guidelines, Laryngoscope 1995;105:1-17.
12. Tucker A. Peritonsillar abscess-A retrospective study of medical treatment. J Laryngol Otol 1982;96:639-43.
13. Dempster JH. Post-tonsillectomy analgesia: the use of benzocaine lozenges. J Laryngol Otol. 1988;102:813-814.
14. Cowan D.L and John Hibbert. Acute and chronic infection of the pharynx and tonsils In: John Hibbert. Scott-Brown's Otorhinolaryngology. volume1. 6th edition. London: Butterworth-Heinemann publications; 1997:5/4/17 to 5/4/22.
15. Lee WC, Duignan MC, Walsh RM , McCrae-Moore J R. An audit of prophylactic antibiotics treatment following tonsillectomy in children . Journal of Laryngology and Otology. 1996; 110 : 357-9.
16. O,Reilly B.J: Is the routine use of Antibiotics j
ustified in adult tonsillectomy? Journal of Laryngology and Otology 2003 May; 117:382-385.
17. Kramer SP, Pasha R. Otolaryngology: Head and Neck Surgery-A Clinical&Reference Guide, Second Edition. Plural Publishing. 2005; (ISBN 1-59756-023-5.)
18. Cullen KA, Hall MJ, Golosinskiy A. Ambulatory Surgery in the United States, 2006. National Health Statistics reports no. 11, revised. Hyattsville, MD: National Center for Health Statistics; 2009.
19. Maw AR .Tonsillectomy today. Arch Dis Child1986; 61:421–3.
20. Rosenfeld RM, Green RP. Tonsillectomy and adenoidectomy: changing trends. Ann Otol Rhinol Laryngol. 1990;99:187-191
21.Yardley M.P. Tonsillectomy, adenoidectomy and Adeno-tonsillectomy: are they safe day case procedures? J. aryngol. Otol.1992 April; 106:299-300.
22.Bennett AM, Clark AB, Bath AP, Montgomery PQ. Meta-analysis of the timing of haemorrhage after tonsillectomy: an important factor in determining the safety of performing tonsillectomy as a day case procedure. Clin Otolaryngol. 2005 Oct;30(5):418-23.
23. Walsh R. M: The Use of Antibiotics in the Hot Dissection Tonsillectomy. Arch Otolaryngology Head and Neck Surg, Jul 2000; 126: 837-841.
24. Colreavy MP, Nanan D, Benamer M, Dinnelly M, Blney AW, O’Dwyer TP et al. Antibiotic prophylaxis post tonsillectomy: Is it of benefit? International Journal of Pediatric Otorhinolaryngology.1999; 50: 15-22.
25. Iqbal Husain Udaipurwala: Use of Antibiotics in Tonsillectomy: is it really beneficial? Med channel September 2004; 10(3):17-20.
26. Stephen F. Conley, MD; Matthew D. Ellison, MD Avoidance of Primary Post-tonsillectomy Hemorrhage in a Teaching Program. Arch Otolaryngol Head Neck Surg. 1999;125:330-333.
27. Bhattacharyya, Neil: Evaluation of Post-tonsillectomy Bleeding in Adult population. Ear, Nose and Throat Journal date 8/1/2001.
28. Windfuhr JP, Chen YS, Remmert S. Hemorrhage following tonsillectomy and adenoidectomy in 15,218 patients. Otolaryngol Head Neck Surg. 2006;132:281-286.
29. Alasdair Robertson: Four Year Prospective Audit of Tonsillectomy Practice; SMJ 2004; 49(3):70.
30. Steven A. Telian, MD; Steven D. Handler, MD; Gary R. Fleisher, MD; et al. The Effect of Antibiotic Therapy on Recovery After Tonsillectomy in Children. A Controlled Study Arch Otolaryngol Head Neck Surg. 1986;112(6):610-615.
31. Alexander RJ, Kukreja R, Ford GR. Secondary post-tonsillectomy haemorrhage and informed consent. J Laryngol Otol. 2004 Dec;118(12):937-40.
32. Jochen P. Windfuhr, Yue-Shih Chen. Incidence of post-tonsillectomy hemorrhage in children and adults: a study of 4,848 patients. Ear, Nose & Throat Journal ,Sept, 2002.
Background and objective: Cervical cancer is the second most common female cancer in the world. It is the commonest cause of female cancer deaths in South-East Asia and Africa and accounts for 15% of all female cancers in developing countries. the aims of this study was to determine the frequency of abnormal cervical cytology among women underwent Pap smear and assess for the presence of risk factors related to abnormal Pap smear results.
Methods: A hospital-based cross sectional study, using a questionnaire and involved 2,146 women at the Maternity Teaching Hospital in Erbil city from January to December 2009. All Pap smears cytological examinations were conducted using Bethesda classification system.
Results: Histological reports were found to be normal in 88.4% of women; meanwhile, 248 (11.6%) women had abnormal cytological findings with a mean age of 36.84 years, significantly older than those with normal results (p <0.05). The duration of marriage was also found to be significantly longer among those with abnormal Pap smear (18.34 years versus 15.72 years, (p < 0.05).
Conclusion: This study was able to indicate that during reproductive life, the older ages of women and longer duration of marriage were associated with an increased risk of abnormal Pap smear results.
Keywords: : Cervical Dysplasia, Pap smear
1. Arbyn M, Sankaranarayanan R, Muwonge R, Keita N, Dolo A, Mbalawa CG et al. Pooled analysis of the accuracy of five cervical cancer screening tests assessed in eleven studies in Africa and India. Int J Cancer 2008;123(1):153-60.
2. Parkin MD, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin 2005; 55:74-108.
3. World Health Organization [homepage on the Internet]. Catala d’ Oncologia. Human Papiloma Virus Information Center Report-Iraq. [Updated 2010 Sept 15; cited 2011 Feb 15]. Available from: http://apps.who.int/hpvcentre.
4. Rosai J. Rosai and Ackermani surgical pathology. 9th ed. St.Louis:CV Mosby;2004.
5. Scott JR, Gibbs RS, Karlan BY, Haney AF, editors. Danforth’s obstetrics and gynecology. 9th ed. Philadilphia,: Lippincott Williams and Wilkins; 2003.
6. Patro BK, Nongkynrih B. Review of screening and preventive strategies for cervical cancer in India. Indian J Public Health 2007;51:216-21.
7. Al-Mashadani JS. Hepatitis B virus markers in diabetic.[MSc Thesis]. Baghdad: Baghdad University; 1988.
8. Flores YN, Bishai DM, Shah KV, Lazcano-Ponce E, Lörincz A, Hernández M, et al. Risk factors for cervical cancer among HPV positive women in Mexico. Salud Publica Mex. 2008;50:49-58.
9. Muñoz N, Bosch FX, De Sanjosé S, Herrero R, Castellsagué X, Shah KV Snijders PJF and Meijer CJLM. Epidemiologic classification of human papillomavirus types associated with cervical cancer. N Engl J Med. 2003;348: 518-27.
10. Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S. Human papillomavirus and cervical Cancer. Asian Pac J Cancer Prev. 2010;11:537-8.
11. Winkelstein W. Smoking and cervical cancer: current status — a review. Am J Epidemiol 1990;131:945-57.
12. Castellsague X and Muñoz N. Cofactors in human papillomavirus carcinogenesis-role of parity, oral contraceptives, and tobacco smoking. J Natl Cancer Inst Monogr.2003;31: 20-28
13. Tay SK and Tay KJ. Passive cigarette smoking is a risk factor in cervical neoplasia. Gynecol Oncol. 2004;93: 116–20.
14. Franco EL, Duarte-Franco E, Ferenczy A. Cervical cancer: epidemiology, prevention and the role of human papillomavirus infection. CMAJ 2001;164(7):1017-25.
15. Ghaffari SR, Sabokbar T, Mollahajian H, Dastan J, Ramezanzadeh F Ensani F, Yarandi F, Mousavi-Jarrahi A, Mohagheghi MA, Moradi A Prevalence of Human Papillomavirus Genotype in Women with Normal and Abnormal Cervical Cytology in Iran. Asian Pacific J Cancer Prev. 2006,7:529-32.
Background and objective: Alopecia areata, is an organ-specific autoimmune disease with genetic predisposition and an environmental trigger, characterized by discrete, well - demarcated area of non scaring terminal hair loss. It affects sex, children and young adults. This study aims at assessing different aspects of alopecia areata and its clinical characteristics.
Methods: A descriptive study conducted during October 2006 and April 2007 on 100 patients with alopecia areata using a structured questionnaire, at the outpatient clinic of Dermatology and Venereology at Rizgary Teaching Hospital.
Results: Male-to-female ratio was 2.3:1, 42% of cases had a single patchy lesion while 52% had multiple patchy lesions, 5% had Alopecia Universalis and one case had Alopecia Totalis. The scalp was involved in 82% while mustache area in only 7% of the cases. Itching and burning were positive in 8%, exclamation marks in 23% and nail involvement in 22% of cases. Ophiasis found in 13% while past history of atopy was positive only in 11% of the cases. Family history was positive in 20% of all cases while past personal history in 31% of the cases. The age of first attack in most of cases was during the first three decades of life.
Conclusion: There is a significant relationship between the age of first attack and negative prognostic signs. Scalp with multiple patchy lesions was the common type of alopecia areata among our patients.
1. Xiao F- L, Yang S, Lin G-S, Gao M, Yong C, Yin X –Y et al. HLA haplotypic association with different phenotype of AA in Chinese Hans. J of Dermatological sciences, 2006; 45(3): 206-209
2. Green J, and Sinclair RD. Genetics of Alopecia areata. Australas J Dermatol, 2000;41(4): 213-218
3. Safavi K. Prevelence of AA in the first national health and nutrition Examination survey. Arch Dermatol, 1992; 128: 702.
4. Hordinsky MK. Clinical presentation of Alopecia Areata. dermatol Ther, 2001; 14(4):291-96.
5. Bertolino AP. Alopecia areata, A clinical overview. Cited in Post graduate medicine, 2000; 107: 7.
6. Olsen EA, Hordinsky M, and McDonald-Hull, Alopecia areata investigational assessment guidelines. J Am Acad Dermatol, 1999; 40: 242– 246.
7. Wasserman D, Guzman-Sanchez DA, Scott K, and McMichael A. Alopecia areata. Int J Dermatol, 2007; 46(2):121–131.
8. Sperling LC and Lupton GP. Histopathology of non-scarring alopecia. J Cutan Pathol,1995; 22: 97-114.
9. McDonagh JG and Messenger AG. Alopecia areata. Clin Dermatol, 2001; 19: 141–147
10. Oslen EA. Disorder of epidermal appendages and related doisorder. In: freedberg IM, EisenAZ, Wolff K, Austen KF, Goldsmith LA, katzs SI, Editors. Fitzpatrick's Dermatology in General Medicine, 6th Edition. Mcgrow-hill, New York, 2003; pp 633-655..
11. de Berker DAR Mesenger AG and Sinclair RD. Disorder of hair. In Burns T, Breathnach S, Cox N and Christopher G, Editors. Rook's text book of dermatology, 7th Edition. Boston: Blackwell Scientific Publication, 2004; pp 63.1- 63.120.
12. Manolache L and Benea V. Stress in Alopecia areata and Vitiligo. J Eur Acad Dermatol Venerol, 2007; 21(7):921-928
13. Seiter S, Ugurel S, and Tilgen W.High-dose pulse corticosteroid therapy in the treatment of severe alopecia areata. Dermatol Online J, 2001; 202:230-4.
14. Bloduc Ch, Lui H, and Shapiro J. Alopecia areata last updated. Cited in e-Medicine 2006.
15. Yang S, Yang J, Liu J B, Wang HY, Yang Y, and Gao M. The genetic epidemiology of alopecia areata in China. Br Dermatol, 2004; 151(1):16–23.
16. Shamsadini S, Eshkavary Sh and Sepehr V. Determination prevalence of clinical pattern of AA in Relation to some varieties In Kerman Iran. Int. J. Dermatol, 2006; 3: 2.
17. Valikhani M, Bazegari M and Aghaeii nia N. Epidemiological compare study on alopecia areata varieties Skin disease seasonal. Journal of Iranian dermatological association, 2001; pp 11-14.
18. Qadir NO. Treatment of Patchy Alopecia Areata Using Topical 15% Lactic Acid Solution. ICMS thesis, Dermatology and Venereology, Iraqi Board for medical specialization, 2005; pp 1-3
19. Nanda A, AL- Fouzan A, and AL- Hasawi F. Alopecia Areata in Children: A clinical profile. Pediatr Dermatol, 2002; 19(6):482-485.
20. Tan E, Tay Y-K, and Giam Y-Ch. A Clinical Study of Childhood Alopecia Areata in Singapore. Pediatr Dermatol, 2002; 19(4):298-301.
21. Habif TP. Clinical dermatology /A color guide to diagnosis and therapy, 4th Edition, Philadelphia. The mosby company, 2004; pp 843-63.
22. Green J, and Sinclair RD. Genetics of Alopecia areata. Australas J Dermatol, 2000;41(4):213-218
23. Al-Rubaiy LQ, and Al-Rubaiy KK. Stress: A Risk Factor for Psoriasis, Vitiligo and Alopecia Areata. Int. J Dermatol, 2006; 4: 2.
Background and objective: Facial soft-tissue injuries are the most common injuries presenting to surgical causality reception. The present study aimed to provide a preliminary data base about the distribution, type, pattern and etiology of facial soft tissue injuries.
Methods: In a prospective clinical study all patients with facial injury were enrolled in this study, over a ten months period (from 1st October 2010- 1st July 2011), who attended Surgical Casualty Reception in Rojh-halat Emergency Hospital. A questionnaire was used to collect patients’ database and relevant information. The wound configuration was divided as laceration, abrasion and contusion as well as the site of facial soft tissue injuries were recorded using the modified MCFONTZL system.
Results: A total of 168 patients with facial soft tissue injuries were received and managed at Surgical Casualty Reception in Rojh-halat Emergency Hospital. The age of the patients were ranged from 1-80 years old. Most of the patients were within the age range of 1-10. Male patients constitute 62.5% of the cases. The most common etiology of facial soft tissue injury was falls. Regarding type of the injury, laceration was the most common type. The lips and chin region were mostly involved.
Conclusion: Fall is the most common cause of facial injury. Lower third of the face is mostly involved. road traffic legislations have a role in decreasing road traffic accidents.
Keywords: face, soft tissue, injury
1. Hussaini H. M., Rahman N. A., Rahman R. A., Nor G. M., Al Idrus S. M., Ramli R. Maxillofacial trauma with emphasis on soft-tissue injuries in Malaysia. Int. J. Oral Maxillofac. Surg. 2007; 36: 797–801
2. Krishna G. Patel, Jonathan M. Sykes. Management of soft-tissue trauma to the face. Operative techniques in Otolaryngology, 2008 June, Volume 19, Issue 2, Pages 90-97
3. Perry M, Dancey A, Mireskandari K, et al: Emergency care in facial trauma—a maxillofacial and ophthalmic perspective. Injury 2005; 36:875- 896
4. Hussain K, Wijetunge DB, Grubnic S, Jackson IT. A compre- hensive analysis of craniofacial trauma. J Trauma 1994;36:34-47.
5. Scherer M, Sullivan WG, Smith DJ, Phillips LG, Robson MC. An analysis of 1423 facial fractures in 788 patients at an urban trauma center. J Trauma 1989;29:388±90.
6. Telfer MR, Jones GM, Shepherd JP. Trends in the aetiology of maxillofac fractures in the United Kingdom (1977±1987). Br J Oral Maxillofac Surg 1991;29:250±5.
7. Dimitroulis G, Eyre J. A 7-year review of maxillofacial trauma in a central London hospital. Br Dent J 1991;170:300±2.
8. Lee RH, Gamble WB, Bradley R, Manson PN. The MCFONTZL Classification system for soft tissue injuries to the face. Plast Reconstruct Surg 1999; 103: 1150–1157.
9. Haug RH, Prather J, Indressano T. An epidemiologic survey of facial fractures and concomitant injuries. J Oral Maxillofac Surg. 1990; 48: 926–932.
10. Telfer MR, Jones GM, Shepherd JP. Trends in the aetiology of maxillofacial fractures in the United Kingdom (1977–1987). Br J Oral Maxillofac Surg. 1991; 29: 250–255.
11. Zarina S. Shaikh, Stephen F. Worrall. Epidemiology of facial trauma in a sample of patients aged 1–18 years. Injury, Int. J. Care Injured 2002; 33: 669–671
12. Hogg, Nicholas J. V., Stewart, Tanya Charyk; Armstrong, Jerrold E. A., Girotti, Murray J. Epidemiology of Maxillofacial Injuries at Trauma Hospitals in Ontario, Canada, Between 1992 and 1997. The Journal of Trauma: Injury, Infection, and Critical Care. 2000 September ; 49 (3): 425-432.
13. Chrcanovic BR, Freire-Maia B, Souza LN, Araújo VO, Abreu MHNG. Facial fractures: a 1-year retrospective study in a hospital in Belo Horizonte. Braz Oral Res. 2004;18:322-8.
14. Rajendra PB, Mathew TP, Agrawal A, Sabharawal G. Characteristics of associated craniofacial with head injuries: An experience with 100 cases. J Emerg Trauma Shock. 2009;2:89-94.
15. Carvalho T.B.O.; Cancian L.R.L; Marques C.G.; Piatto V.B.; Maniglia J.V.; Molina F.D. Six years of facial trauma care: an epidemiological analysis of 355 cases. Braz. j. otorhinolaryngol. 2010; vol.76 (5): 565-574.
16. Zerfowski M, Bremerich A. Facial trauma in children and adolescents. Clin Oral Invest 1998;2:120–4.
17. Telfer MR, Jones GM, Shepherd JP. Trends in the aetiology of maxillofacial fractures in the United Kingdom (1977–1987). Br J Oral Maxillofac Surg. 1991; 29: 250–255.
18. Ong TK, Dudley M. Craniofacial trauma presenting at an adult accident and emergency department with emphasis on soft tissue injuries. Injury 1999: 30: 357–363.
19. Bataineh AB. Etiology and incidence of maxillofacial fractures in the north of Jordan. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998; 86: 31–35.
Background and objective: The goal of this study was to determine the association of complete left bundle branch block (LBBB), site , severity & risk factors of coronary artery disease (CAD). Complete Left bundle branch block increases the risk of cardiac mortality, and prognosis is primarily determined by the underlying CAD. Because the presence of complete LBBB makes the noninvasive identification of CAD less informative, patients with complete LBBB often are referred for coronary angiography to assess the presence and severity of CAD.
Methods: A total of 150 consecutive patients with complete LBBB admitted to the coronary care unit were enrolled from the age of 27 to 81 years with the mean age of 59.32 ± 10.5. Male 84 (56%), Female (44%). History, basal investigations echocardiography and virology screen were performed. Coronary angiography has been done for all patients for different reasons of presentation.
Results: Critical CAD 70 (46.7%), Left ventricular systolic dysfunction (LVSD) 50 (33.3%). Hypertension found in 83 (55.3%), diabetes mellitus (DM) in 44 (30%), DM& left ventricular systolic dysfunction(LVSD) were more associated with critical CAD.
Conclusion: In our study complete LBBB was more common among hypertensive patients. In DM patients was associated with severe CAD. With Left anterior descending artery being the most common artery involved.
Keywords: left bundle branch block, coronary artery disease.
1. Josephson, ME. Clinical Cardiac Electrophysiol ogy: Techniques and Interpretations. 2d ed, Lea&Febiger,Philadelphia,1993.
2. Francia P. Left bundle-branch block — Pathophysiology, prognosis and clinical management. Clinical Cardiology. 2007;30:110.
3. Schwartz PJ, Zipes DP: Autonomic modulation of cardiacarrhytmia.In: Zipes DP, Jalife J, ed. Cardiac Electrophysiology: From Cell to Bedside, 3rd ed. Philadelphia: WB Saunders; 1999:300-314.
4. riksson P. Hansson PO. Eriksson H. Dellborg M. Bundle-branch block in a general male population: the study of men born 1913. Circulation 1998; 98:2494.
5. Imanishi R. Seto S. Ichimaru. Prognostic significance of incident complete left bundle branch block observed over a 40-year period. Am J Cardiol 2006; 98:644.
6. Bavelaar-Croon CD. Wahba FF. van Hecke MV. Perfusion and functional abnormalities outside the septal region in patients with left bundle branch block assessed with gated SPECT. Q J Nucl Med 2001; 45:108–114.
7. McAnulty JH. Rahimtoola SH. Murphy E. Natural history of “high-risk” bundle-branch block: final report of a prospective study. N Engl J Med 1982;307:137– 43.
8. DePuey EG. Guertler-Krawczynska E. Robbins WL. Thallium-201 SPECT in coronary artery disease patients with left bundle branch block. J Nucl Med 1988;29:1479–85.
9. Iskandrian AE, Verani MS, editors. Nuclear Cardiac Imaging: Principles and Applications. 3rd ed. New York, NY: Oxford University Press, 2003:164–89.
10. Gibbons RJ, Balady JT, Chaitman BR. ACC/AHA 2002 Guidelines Update for Exercise Testing. Available at: www.acc.org. Accessed July 6, 2006.
11. Duncan AM, Francis DP, Gibson DG, Henein MY. Differentiation of ischemic from nonischemic cardiomyopathy during dobutamine stress by left ventricular long-axis function: additional effect of left bundle-branch block. Circulation 2003;108:1214 –20.
12. Geleijnse ML, Vigna C, Kasprzak JD. Usefulness and limitations of dobutamine-atropine stress echocardiography for the diagnosis of coronary artery disease in patients with left bundle branch block. A multicentre study. Eur Heart J 2000; 21:1666 –73.
13. Lev M, Kinare SG, Pick A. The pathogenesis of atrioventricular block in coronary disease. Circulation 1970; 42:409 –25.
14. Hesse, B, Diaz, L, Snader, CE. Complete bundle branch block as an independent predictor of all-cause mortality: Report of 7,073 patients referred for nuclear exercise testing. Am J Med 2001; 110:253.
15. Baldasseroni, S, Opasich, C, Gorini, M. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure. Am Heart J 2002; 143:398.
16. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 1997;20:1183-97.
17. Eoin O’Brien. Practice guidelines of the European Society of Hypertension for clinic, ambulatory and self-blood pressure measurement. Journal of Hypertension 2005; 23:697–701.
18. Swedberg K, Cleland J, Dargie H: Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary. Eur Heart J. 2005, 26: 1115-1140.
19. Tomas B. Garcia, Geoffrey T. Miller. Arrhythmia recognition. Sudbury, Mass.: Jones and Bartlett Publishers, 2004. isbn:0763722464.
20. Scolon P, Faxon D, Audei A.et al.ACC/AHA guideline for coronary angiography . J Am Coll Cardiol 1999; 33:1765
21. Schneider JF, Thomas HE, McNamara PM, Kannel WB. Clinical-electrocardiographic correlates of newly acquired left bundle branch block: the Framingham Study. Am J Cardiol 1985; 55: 1332-8.
22. Rajjit Abrol; Jeffrey C Trost; Keith Nguyen; Joaquin E Cigarroa; Sabina AMurphy: Predictors of Coronary Artery Disease in Patients with Left Bundle Branch Block Undergoing Coronary Angiography: Am J Cardiol. 2006; 10:1307-10.
23. Schneider JF. Thomas HE Jr, Kreger BE. Newly acquired left bundle branch block. The Framingham study. Ann Intern Med 1979; 90:303
24. Ozeke, O, Aras, D, Deveci, B. Comparison of presence and extent of coronary narrowing in patients with left bundle branch block without diabetes mellitus to patients with and without left bundle branch block but with diabetes mellitus. Am J Cardiol 2006; 97:857.
25. Tameem H. M. Alshami, Ou Mao, Yang Kan, et al. Complete left bundle branch block in patients with clinical and coronary angiographic analysis. H Complete left bundle branch block in patients with clinical and coronary angiographic analysis. Hunan Normal University (Medical Sciences), 2007; 4: 4748.
Background and objective: Consuming of opium is a new phenomenon that could be significantly observed in some regions of Iraqi Kurdistan region, especially in districts near to Iran borders. Long term consumption of opioids affects body homeostasis. This study is designed to determine the effects of opium on reproductive histological and hormonal parameters in addition to the study of qualitative sperm abnormalities in experimental rats. Methods: The rats of the experiment were divided into three groups: Control group and the two experimental groups which were treated with two different concentrations of opium (25 and 50 mg/kg/day) for 7 days. After the decided period, the rats were dissected. Serum testosterone and sperm quality was determined and histological sections were prepared from the testis.
Results: Testosterone significantly reduced in opium treated rats in both low and high doses. The histological sections of testis showed testicular degeneration in the seminiferous tubules, while higher dose showed loss of normal architecture of seminiferous tubules, in addition to present of giant cell in lumen of tubules. Several types of sperm abnormalities were observed, but the head-neck connection abnormality was the dominant.
Conclusion: This finding suggests that opium addiction can cause significant decrease in the male sexual hormone secretion and it also leads to the alteration in the sperms and testis structure. This may lead to sexual suppression and infertility which needs further investigations.
Keywords: Opium-Sperm- Testosterone-Histology- Testis
1. International narcotics control strategy report (INCSR), issued March 1, 2004.
2. Mendelson JH, Meyar RF, Ellingboe J, Mirin SM, McDougle M. Effects of Heroin and Methadone of plasma cortisol and testostrone. J Pharmacol Exp ther. 1975, 195: 296-302.
3. Celani MF, Carani C, Montanini V, Baraghini GF, Zini D,Simoni M. Further studies on the effects of heroin addiction on the hypothalamic-pituitary-gonadal function in man. Pharmacol. Res. Commun. 1984,16: 1193.
4. Festa ED, Jenab S, Chin J, Gazi FM, Wu HB, Russo SJ, Quinones-Jenab V. Frequency of cocaine administration affects behavioral and endocrine responses in male and femalefischerrats. Cell Mol Biol (Noisy–le- grand) 2003, 49:1275-1280.
5. Serturner F.W.A.F. Darstellung der reinen Mohns¨aure (Opiums¨aure) nebst einer chemischen Untersuchung des Opiums mit vorz¨uglicher Hinsicht auf einen darin neu entdeckten Stoff und die dahin geh¨origen Bemerckungen . Pharm. Chem. 1806,14:47–93.
6. Costa AM. World Drug Report: United Nations Office on Drugs and Crime. 2007, 37–61.
7. Aksenov VS, Numanov IU, Pogosov AV, Degtyarev VA. Chromatographic investigation of the alkaloids of the opium poppy and their acetyl derivatives. Chemistry of Natural Compounds. 1993, 29:92–94.
8. Mahani SE, Motamedi F, Ahmadiani A. Involvement of hypothalamic pituitary adrenal axis on the nifedipine-induced antinociception and tolerance in rats. Pharmacol. Biochem. Behav. 2006, 85:422–427.
9. Ipp E, Schusdziarra V, Harris V, Unger RH. Morphine-induced hyperglycemia: role of insulin and glucagon. Endocrinology.1980, 107:461–463.
10. Ipp E, Dobbs R, Unger RH. Morphine and beta-endorphin influence the secretion of the endocrine pancreas. Nature, 1978, 276:190–191.
11. Molina PE, Hashiguchi Y, Ajmal M, Mazza M, Abumrad NN. Differential homodynamic, metabolic and hormonal effects of morphine and morphine-glucoronide. Brain Research, 1994, 664: 126–132.
12. Bossone CA, Hannon JP. Metabolic actions of morphine in conscious chronically instrumented pigs. Am. J. Physiol.1991, 260: 1051–1057.
13. Gupta K, Weber ML. Renal effects of opioid exposure: Considerations for therapeutic use. J Opioid Manag, 2006, 2: 236–240.
14. Wyrobek, A.J. Changes in Mammalian Sperm Morphology After X-ray and Chemical Exposures, Genetics, 1979, (Suppl) 91: 105-119.
15. Bancroft, J .D.; Steven, A. and Dawson, I. Theory and Practice of Histological Techniques. Edinburgh, London, New York. Churchill-Livinstone, 1977.
16. Karbakhsh, M., Salehian Zandi, N. Acute opiate overdose in Tehran: the forgotten role of opium. Addictive Behaviors, 2007, 32:1835–1842.
17. Razzaghi, E. M., Rahimi Movaghar, A., Hosseini, M., Madani, S., Chatterjee, A. Rapid situation assessment of drug abuse in Iran. IranianWelfare Organization and UNDCP, 1999.
18. Ziaaddini, H., Ziaaddini,M. R. The household survey of drug abuse in Kerman, Iran. Journal of Applied Science, 2005, 5:380–382.
19. Conti G, Teboul JL, Gasparetto A. Acute heroin intoxication. In: Vincent JL. Update in intensive care and emergency medicine,10th ed, Berlin, Springer-Verlag, 1990: 478-481
20. D'Agostino RS & Ernest NA. Acute myoglobinuria and heroin snorting. JAMA, 1990, 241: 277
21. Seyed Hassan, H. and Mohamad, H. D. The effect of opium on serum LH, FSH and testosterone concentration in addicted men.Iranian Journal of Reproductive Medicine, 2007, 5(1):35-38.
22. Ganong WF. Review of medical physiology. 21th ed. Stamford: Appleton & Lange, 2003: 393-414.
23. Antony, S.F. Hormone’s principles of internal medicine. 16th ed. , 2005; 1: 1648-1812.
Background and objective: Nausea and vomiting are among the most common distressing complications encountered by patients postoperatively. The aim of this study is to evaluate the prophylactic effect of small dose of dexamethasone (5 mg) on postoperative nausea and vomiting (PONV) after laparoscopic cholecystectomy (LC).
Methods: A prospective double blind placebo controlled study of 160 patients who underwent elective LC at Rizgary Teaching and Hawler Private Hospitals in Erbil, Kurdistan in a period between Jan 2009 and Dec 2009. Preoperatively the patients were allocated randomly to one of the four groups (n = 40 each).
1. The dexamethasone group received dexamethasone 5mg.
2. The metoclopramide group received metoclopramide 10mg.
3. The tropisetron group received tropisetron 2mg.
4. The placebo group received normal saline 2ml.
Results: Both the dexamethasone and tropisetron groups were significantly different from the placebo group in the incidence of nausea and vomiting. The differences between the dexamethasone and tropisetron groups were not significant (P = 0.799).
Conclusion: : prophylactic IV dexamethasone 5 mg significantly reduces the incidence of PONV in patients undergoing LC.
Keywords: Postoperative, nausea , vomiting, laparoscopy
1. Gupta P, Khanna J, Mitramustafi A, Bhartia V. Role of preoperative Dexamethasone as prophylaxis for postoperative nausea and vomiting in laparoscopic surgery, Journal of Minimal Access Surgery 2006;3(2): 12-15.
2. Begos DG, Modlin IM. Laparoscopic cholecystectomy: from gimmick to gold standard. J clin Gastroenterol 1994;19:325-30.
3. Sandor J, Sandor A, Zaborszky A. Why laparoscopic cholecystectomy today? Surg Today 1996; 26:556-60.
4. Naguib M, Bakry AKEI, Khoshim MHB. Prophylactic antiemetic therapy with ondansetron, Tropisetron, granisetron and Metoclopramide in patients undergoing laparoscopic cholecystectomy: a randomized, double-blind comparison with placebo. Can J Anaesth 1996; 43: 226-31.
5. Jokela R, Koivuranta M. Tropisetron or droperidol in the prevention of postoperative nausea and vomiting. Acta Anaesthesiol Scand 1999; 43: 645-50.
6. Wang JJ, Ho St, Liu YH. Dexamethasone reduces nausea and vomiting after laparoscopic cholecystectomy. Br J Anaesth 1999; 83: 772-5.
7. Fujii Y, Saitoh Y, Tanaka. Ramosetron vs granisetron for the prevention of postoperative nausea and vomiting after laparoscopic cholecystectomy. Can J Anaesth 1999; 46: 991-3.
8. Kapur PA. The big, little problem. Anaesth Analg 1991; 72:243-5.
9. Leksowski K, Peryga P, Szyca R. Ondansetron, Metoclopramide, Dexamethasone, and their combinations compared for the prevention of postoperative nausea and vomiting in patients undergoing laparoscopic cholecystectomy: A prospective randomized study, Surg Endosc 2006;20:878-882.
10. Sapolsky RM, Romero LM, Munck AU. How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions. Endocr Rev. 2000;21:55-89.
11. Holte K, Kehlet H. Perioperative single dose glucocorticoid administration—Pathophysiological effects and clinical implications. J Am Coll Surg. 2000;195:186-712.
12. Henzi I, Walder B, Tramer MR. Dexamethasone for the prevention of postoperative nausea and vomiting: a quantitative systematic review. Anesth Analg. 2000;90:186-194.
13. Fujii Y, Saitoh Y, Tanaka H. Granisetron/dexamethasone combination for the prevention of postoperative nausea and vomiting after laparoscopic cholecystectomy. Eur J Anaesthesiol. 2000;17:64-68.
14. The Italian Group for Antiemetic Research. Dexamethasone, granisetron, or both for the prevention of nausea and vomiting during chemotherapy for cancer: N Engl J Med 1995; 332: 1–5.
15. The Italian Group for Antiemetic Research. Ondansetron versus metoclopramide, both combined with dexamethasone, in the prevention of cisplatin-induced delayed emesis: the Italian Group for Antiemetic Research. J Clin Oncol 1997; 15: 124–30.
16. Sehine I, Nishiwaki Y, Kakinuma R. Phase II study of high-dose dexamethasone-based association in acute and delayed high-dose cisplatin-induced emesis: study 9413. Br J Cancer 1997; 76: 90–2.
17. Jeng-Chai, Ja-Ping Shieh, Chao-Shun Tang, Jann-Inn Tzeng, Koung-Shing Chu and Jhi-Joung Wang. Low dose Dexamethasone effectively prevents postoperative nausea and vomiting after ambulatory laparoscopic surgery, Canadian Journal of Anesthesia 2001; 48(10):973-977.
18. Henzi I, Walder B, Tramer M. Dexamethasone for the prevention of postoperative nausea and vomiting: a quantitative systemic review. Anaesth Analg 2000; 90: 186-94.
19. Wang JJ, Ho ST, Lee SC. The use of Dexamethasone for preventing postoperative nausea and vomiting in females undergoing thyroidectomy: a dose-ranging study. Anaesth Analg 2000;91:1404-7.
21. Simpson K, Spencer CM, McClellan KJ. Tropisetron: an update of its use in the prevention of chemotherapy-induced nausea and vomiting. Drugs 2000; 59:1297-315.
22. Gregory RE, Ettinger DS. 5-HT3 receptor antagonists for the prevention of chemotherapy-induced nausea and vomiting. Drugs 1998; 55: 173-89.
23. Alon E, Buchser E, Herrera E. Tropisetron for treating established postoperative nausea and vomiting: a randomized, double-blind, placebo-controlled study. Anaesth analg 1998; 86:617-23.
24. Cunningham RS. 5-HT3 receptor antagonists: a review of pharmacology and clinical efficacy.
25. Purhonen S, Kauko M, Koski E. Comparison of Tropisetron, droperidol, and saline in the prevention of postoperative nausea and vomiting after gynecological surgery. Anesth Analg 1997; 84: 662-7.
26. Capouet V, De Pauw C, Vernet B. Single dose i.v. Tropisetron in the prevention of postoperative nausea and vomiting after gynecological surgery. Br J Anaesth 1996; 76: 54-60.
27. Henzi I, Walder B, and Tramer M. Metoclopramide in the prevention of postoperative nausea and vomiting: a quantitative systemic review of randomized, placebo-controlled studies, BJA 1999; 83(5): 761-71.
28. Wilson E, Bass C. S, Abrameit W. Metoclopramide versus ondansetron in prophylaxis of nausea and vomiting for laparoscopic cholecystectomy, The American Journal of Surgery 2001; 181: 138-141.
29. Quaynor H and reader J. Incidence and severity of postoperative nausea and vomiting are similar after Metoclopramide 20 mg and ondansetron 25.8 mg given by the end of laparoscopic cholecystectomies, Acta Anaesthesiol Scand 2002; 46: 109-113.
30. Nesek-Adam V, Grizelj-Stojcic E, Rasic Z, Comparison of Dexamethasone, Metoclopramide, and their combination in the prevention of postoperative nausea and vomiting after laparoscopic cholecystectomy, Surg Endosc 2007; 21: 607-612.
31. Nesek V, Grizelj E, Mrsic V. Prophylactic antiemetics for laparoscopic cholecystectomy: droperidol, Metoclopramide, and droperidol plus Metoclopramide, J of the laparoendoscopic & advanced surgical techniques 2004; 14(4): 212-18.
32. Piper S, Suttner S, Rohm K. Dolasetron, but not Metoclopramide prevents nausea and vomiting in patients undergoing laparoscopic cholecystectomy, Can J anesth 2002; 49(10): 1021-1018.
33. Dabbagh A. Ali. A Comparative Study Between Dexamethasone, Meoclopramide, and Esmoprazole in the prevention of Postoperative Nausea and Vomiting after Laparoscopic Cholecystectomy, Zanco Journal of Medical Sciences 2008;12:55-62.
34. Wang J, Tai Ho Sh, Tzeng J, and Tang Ch, The effect of timing of Dexamethasone administration on its efficacy as a prophylactic antiemetic for postoperative nausea and vomiting, Anaesth Analg 2000; 91: 136-9.
35. Feo C, Sortini D, Ragazzi R. Randomized clinical trial of the effect of preoperative Dexamethasone on nausea and vomiting after laparoscopic cholecystectomy, British Journal of Surgery 2006; 93: 295-299.
Background and objective: Infertility remains a global health challenge with devastating psycho-social consequences in many communities and an underlying long-term risk for separation of the couple, also remains a major clinical and social problem. Infertility is defined as inability of a couple to conceive naturally after one year of intercourse. An understanding of the medical causes of infertility is crucial in order to reduce incidences of infertility and for improving the clinical management of infertility. The aim of the study was to determine the causes of infertility in couples.
Methods: A retrospective study was done in IVF Unit at Maternity Teaching Hospital in Erbil. Data of infertile couples were collected from already prepared patient’s files.
Results: The frequency of primary and secondary infertility among women was 62.97% and 37.03%, respectively. Among 370 couples, 35.68% had female factor, 29.46% had both male and female factors, and 19.73% had male factor, while 15.14% of the couples had unexplained infertility.
Keywords: Infertility, Etiology, Hormones, Semen.
1. Hassa H, Ayranci U, Unluoglu I, Metintas S, Unsal A. Attitudes to and management of fertility among primary health care physicians in Turkey: An epidemiological study. BMC Public Health 2005; 5(33).
2. Frey KA, Patel KS. Initial Evaluation and Management of Infertility by the Primary Care Physician. Mayo Clin Proc 2004; 79(11): 1439–1443.
3. Meacham RB, Joyce GF, Wise M, Kparker A, Niederberger C. Male Infertility. J Urol 2007; 177: 2058–66.
4. Ombelet W, Cooke I, Dyer S, Serour G, Devroey P. Infertility and the provision of infertility medical services in developing countries. Hum Reprod Update 2008; 14(6): 605–621.
5. Lashen H. Investigations for infertility. obstetrics, gynaecology and reproductive medicine 2007;17: 211–216.
6. Kamel RM. Management of the infertile couple: an evidence-based protocol. Reprod Biol Endocrinol 2010; 8(21): 1–7.
7. Moldenhauer JS, Ostermeier GC, Johnson A, Diamond MP, Krawetz SA. Diagnosing Male Factor Infertility Review Using Microarrays. J Androl 2003: 24(6); 783–789.
8. Randolph JF, Ginsburg KA, Leach RE, Blacker CM, Moghissi KS, Diamond MP et al. Elevated early follicular gonadotropin levels in women with unexplained infertility do not provide evidence for disordered gonadotropin-releasing hormone secretion as assessed by luteinizing hormone pulse characteristics. Fertil Steril 2003; 80(2): 320– 327.
9. O’Flynn O’Brien KL, Varghese AC, Agarwal A. The genetic causes of male factor infertility: A review. Fertil Steril 2010; 93(1): 1–12.
10. Irvine DS. Epidemiology and aetiology of male infertility. Hum Reprod 1998: 13; 33–44.
11. Saleh RA, Agarwal A, Nada EA, El-Tonsy MH, Sharma RK, Meyer A et al. Negative effects of increased sperm DNA damage in relation to seminal oxidative stress in men with idiopathic and male factor infertility. Fertil Steril 2003; 79(3): 1597–1605.
12. Johansson M, Hellström A, Berg M. Severe male infertility after failed ICSI treatment-a phenomenological study of men’s experiences. Reprod Health 2011; 8(4): 1–7.
13. Yu SL, Yap C. Investigating the Infertile Couple. Ann Acad Med Singapore 2003; 32: 611–614.
14. Miller JH, Weinberg RK, Canino NL, Klein NA, Soules MR., The pattern of infertility diagnoses in women of advanced reproductive age. Am J Obstet Gynecol 1999;181: 952–957.
15. Al Khsrajy LA, Al Abayechi. Knowledge and Attitudes of infertile Male Patients Attending kamal Alsamaraee Fertility Center about Assisted Reproductive Technique in Practice. Am J Applied Sci 2009; 6(9): 1725–1730.
16. La Rochebrochard E, Thonneau P. Paternal age ≥40 years: An important risk factor for infertility. Am J Obstet Gynecol 2003; 189: 901–905.
17. Rutstein SO, Shah IH. Infecundity, Infertility, and Childlessness in Developing Countries, DHS Comparative Reports, No. 9. Maryland: USA; 2004.
18. Ceballo R, Abbey A, Schooler D. Perceptions of women’s infertility: what do physicians see?. Fertil Steril 2010; 93: 1066–1073.
19. Künzle R, Mueller MD, Hänggi W, Birkhäuser MH, Drescher H, Bersinger NA. Semen quality of male smokers and nonsmokers in infertile couples. Fertil Steril 2003; 9: 287–91.
20. Ashiru AO, Odusanya OO. Fertility and Occupational hazards. Afr J Reprod Health 2009:13(1); 159–165.
21. Macaluso M, Wright-Schnapp TJ, Chandra A, Johnson R, Satterwhite CL, Pulver A et al. A public health focus on infertility prevention, detection, and management. Fertil Steril 2010; 93(6): 1–10.
22. Lunenfeld B, Steirteghem AV. Infertility in the third millennium: implications for the individual, family and society: Condensed Meeting Report from the Bertarelli Foundation’s Second Global Conference. Hum Reprod Update 2004: 10 (4); 317–326.
23. World Health Organization. WHO laboratory manual for the examination of human semen and sperm-cervical mucus interaction, 5th ed. Avenue Appia: Switzerland WHO Library Cataloguing; 2010.
24. Sbaragli C, Morgante G, Goracci A, Hofkens T, DeLeo V, Castrogiovanni P. Infertility and psychiatric morbidity. Fertil Steril 2008; 90 (6): 2107–2111.
25. Oladokun A, Arulogun O, Oladokun R, Morhason-Bello IO, Bamgboye EA, Adewole IF et al. Acceptability of Child Adoption as Management Option for Infertility in Nigeria: Evidence from Focus Group Discussions. Afr J Reprod Health 2009; 13(1): 79–91.
26. Razzak AH, Wais SA. The infertile couple: A cohort study in Duhok, Iraq. Est Mediterr Health J. 2002; 8(2-3): 234–238.
27. Oskay UY, Beji NK, Serdaroglu H. The Issue of Infertility and Sexual Function in Turkish Women. Sex Disabil 2010; 28: 71–79.
28. Aflatoonian A, Seyedhassani SM.,Tabibnejad N. The epidemiological and etiological aspects of infertility in Yazd province of Iran. Iranian Journal of Reproductive Medicine 2009; 7(3): 117–122.
29. Tayebi N, Ardakani SM. The prevalence of sexual dysfunctions in infertile women. Middle MEFSJ 2007; 12(3): 184–187.
30. Abdalla NM. Epidemiology of Infertility in Gezira Region, Central of Sudan. Research journal of Medical Science 2011; 5(1); 56–60.
32. Ugwuja EI, Ugwu NC, Ejikeme BN. Prevalence of Low sperm Count and Abnormal Semen Parameters in Male Partners of Women Consulting at Infertility Clinic in Abakaliki, Nigeria. Rev Afr Santé Reprod 2008; 12(1): 67–73.
Background and objective: This study aims to determine the role of breast ultrasound in assessing patients with localized or diffuse pain in the breast.
Methods: This cross-sectional study involved 170 women with the mean age of 31 years presenting with breast pain who were referred to the Radiology Department of the Maternity and Rizgari Teaching Hospitals from October 2008 to September 2009. The breasts of each woman were examined by ultrasound scan with special attention was focused on the milk ducts. The presence and the width of the ducts were documented. Each woman was asked for pain intensity and breast pain intensity evaluated as mild, moderate and severe.
Results: The ultrasonic assessment of the affected breast classified the participants into 4 categories; normal (29.9%), tubular (18.6%), ductasia (18.6%) and mass (32.8%). Among the 58 participants having mass in the breast, 48.3% had cystic mass and 51.7% had solid mass. The ultrasonic features of the mass showed that 86.2% of cases were benign and 13.8% were intermediate. The histopathological assessment of the masses shown that 46.4% were fibrocystic changes, 20.7% were fibroadenoma, 24.1% were benign cysts, 3.4% were malignancies and 5.2% were breast infections.
Conclusion: The study results show that duct ectasia is a major factor in determining the severity of mastalgia with no significance difference between cyclical and non-cyclical mastalgia.
Keywords: Mastalgia, ultrasound, breast mass.
1. Naz N, Sohail S, Memon MA. Utility of breast imaging in mastalgia. JLUMHS 2010; 9(1): 12-6.
2. Marrow M. The evaluation of common breast problems. Am Fam Physician 2000;61:2371-8.
3. Yakut ZI, Kafali H, Karaoglanoglu M, Koktener A, Duvan CI. A new radiological approach to cyclic mastalgia: Venous Doppler ultrasound. The Breast 2009;18:123-5.
4. Smith RL, Pruthi S, Fitzpatrick LA. Evaluation and management of breast pain. Mayo Clin Proc 2004;79:353–72.
5. Gumm R. Evidence for the management of mastalgia. Cur Med Res Opin 2004;20:681-4.
6. Hanif AM, Rasool S. Presentation, management and outcome of mastalgia. J Surg Pak 2005;10:15-7.
7. Plu-Bureau G, Lê MG, Sitruk-Ware R, Thalabard JC. Cyclical Mastalgia and Breast Cancer Risk: Results of A French Cohort Study. Cancer Epidemiol Biomarkers Prev 2006; 15:12-29.
8. Smith RL, Pruthi S, Fitzpatrick LA. Evaluation and management of breast pain. Mayo Clin Proc 2004;79(3):353-72.
9. Preece PE, Mansel RE, Bolten PM, Hughes LE, Baum M, Gravelle IH. Clinical syndromes of mastalgia. Lancet 1976;2:670-3.
10. Kiguli-Malwadde E, Mubuuke AG, Businge F, Kawooya GM, Nakatudde R, Byanyima KR, Muyinda Z. Current knowledge, attitudes and practices of women on breast cancer and mammography at Mulago Hospital. Pan African Medical Journal. 2010; 5:9.
11. Kailash S, Tariq A, Ghanshyam DG. The accuracy of ultrasound in diagnosis of palpable breast lumps. JK Science. 2008; 10:4
12. Morrow M. The Evaluation of Common Breast Problems. Am Fam Physician 2000; 61(8):2371-8.
13. Khanna S, Arya NC, Khanna NN. Spectrum of benign breast diseases. Ind J surgery. 1988;3:169-75
14. Smallwood JA, Guyer P, Dewbury K. The accuracy of ultrasound in the diagnosis of breast disease. Ann R Coll surg Engl. 1986;68:19-22.
15. Gonzaga MA. How accurate is ultrasound in evaluating palpable breast masses? Pan Afr Med J. 2010; 7: 1.
16. Kopans DB, Meyer JE, Lindfors KK. Whole breast ultrasound imaging: four year follow up. Radiology. 1985;157:505-7.
17. Mansoor T, Ahmed A, Syed HH. Role of ultrasonography in the differential diagnosis of palpable breast lumps. Ind J Surgery. 2002;64(6):499-501
18. Stavros AT, Thickman D, Rapp CL, Dennis MA, Parker SH, Sisney GA. Solid breast nodules: use of sonography to distinguish between benign and malignant lesions. Radiology. 1995; 196: 123-34.
19. Fleischer AC, Muhletaler CA, Reynolds VH. Palpable breast masses: evaluation by high frequency hand held real-time sonography and xero-mammography. Radiology. 1983;148:813-17.
20. Harvey JA. Sonography of palpable breast masses. Semin Ultrasound CT MR. 2006;27(4):284-97.
Background and objective: Fatigue, is a common presenting symptom in primary care which negatively impacts work performance, family life, and social relationships. The aim of this study is to determine the causes of fatigue and to explore the relationship between fatigue and physical, mental, social and demographic factors among patients with special reference to gender.
Methods: A cross sectional study was carried out at the Brayati Family Medicine Center in Erbil city from 1st of July to the 31st of October 2011. We studied 320 patients of both genders attending the center for various reason complaining from fatigue. Formal consent was obtained. Demographic data in addition to two questionnaires were completed, Lowa fatigue scale and Hospital Anxiety and Depression Scale.
Results: 86 males (26.88%) and 234 females (73.12%). The age of the subjects varied from 16-74 years .The mean age was 29.2 years, 39.69% were in the age range 30-44 years. 58.12% were illiterate or read and write only; 65.63% were married and 57.19% reported their economic level as medium. 38.44% were fatigued according to lowa fatigue scale. Higher level was detected among older age group, singles, and low economic and minimum educational status (51.16%, 45.31%, 41.80%, 41.18 and 42.57% respectively). Depression was significantly associated with fatigue, 70% of patients who were depressed complained from fatigue. Findings indicated that, in addition to increasing anxiety among the study sample, higher levels of fatigue were detected in 61.36% of them.
Conclusion: Fatigue as a symptom is very common both in community and health care settings but remains medically unexplained. The most important confounders in our studied population were depression and anxiety.
Keywords: fatigue, anxiety, depression, family medicine
1. Thomas C. Rosenthal, MD; Barbara A. Majeroni, MD; Richard Pretorius, MD, MPH; and Khalid Malik, MD, MBA, Fatigue overview, Am Fam Physician. 2008 Nov 15;78(10):1173-1179.
2. Deale A, Wessely S: Patients' perceptions of medical care in CFS. Social Science and Medicine 2001, 52:1859-1864.
3. Kisely S: Treatment for CFS and in the internet: a systematic survey of what your patients are reading. Austraia and New Zealand Journal of Psychiatry 2002, 36:240-245.
4. Steven S: General Practitioners' beliefs, attitudes and reported actions towards CFS. Australian Family Physician 2000, 29:80-85.
5. Bowen J, Pheby D, Charlett A, McNulty C: Chronic Fatigue Syndrome: a survey of GPs' attitudes and knowledge. Family Practice 2005, 389-393.
6. Cullen W, Kearney Y, Bury G. Prevalence of fatigue in general practice. Ir J Med Sci 2002;171:10-2.
7. Nelson E, Kirk J, McHugo G. Chief complaint fatigue: a longitudinal study from the patient’s perspective. Fam Pract Res J 1987;6:175–88.
8. Sharpe M, Wilks D. ABC of psychological medicine: fatigue. BMJ 2002;325:480–3.
9. Chaudhuri A, Behan PO. Fatigue in neurological disorders. Lancet 2004;363:978–88.
10. Cornuz J, Guessous I, Favrat B. Fatigue: a practical approach to diagnosis in primary care. CMAJ 2006;174:765–7.
11. Dick ML, Sundin J. Psychological and psychiatric causes of fatigue. Assessment and management. Aust Fam Physician 2003;32:877–81.
12. Lewis G, Wessely S. The epidemiology of fatigue: more questions than answers. J Epidemiol Community Health 1992;46:92–7.
13. Kenter EG, Okkes IM. Patients with fatigue in family practice: prevalence and treatment [article in Dutch]. Ned Tijdschr Geneeskd 1999;143:796–801.
14. Zautra AJ, Fasman R, Parish BP, et al. Daily fatigue in women with osteoarthritis, rheumatoid arthritis, and fibromyalgia. Pain 2007;128:128–35.
15. Hwang SS, Chang VT, Rue M, et al. Multidimensional independent predictors of cancer-related fatigue. J Pain Symptom Manage 2003;26:604–14.
16. Nijrolder I, van der Windt D, de Vries H, van der Horst H: Diagnoses during follow-up of patients presenting with fatigue in primary care. CMAJ 2009.DOI:10.1503/cmaj.090647.
17. Wockenfuss R, Frese T, Herrmann K, Claussnitzer M, Sandholzer H: Three- and four-digit ICD-10 is not a reliable classification system in primary care. Scand J Prim Health Care 2009;27:131-136.
18. Hartz A, Bentler S, Watson D. Measuring fatigue severity in primary care patients. J Psychosom 2003; 54(6):515-21.
19. Snaith RP. The Hospital Anxiety and Depression Scale. Health and Quality of Life Outcomes 2003;1:29 http://www.hqlo.com/content/1/1/29 cited 15th may 2011
20. Mclivenny S, DeGlume AM, Elewa M, Fernandez DT, and Dormer P, Factors associated with fatigue in a family Medicine clinic in the United Arab Emirates. Family Practice 2000; 17: 408-413.
21. David A. Pelosi A, McDonald E. Tired, weak or in need of rest; fatigue among general practice attainders. Br Med J 1990: 301: 1190-1202.
22. Kroenke K, Price R. Symptoms in the community: prevalence, classification and psychiatric comorbidity. Arch Intern Med 1993;153:2474–2480.
23. Wessely S, Hotopf M, Sharpe M. Chronic Fatigue and its Syndromes. Oxford: Oxford University Press, 1998.
24. OPCS. Morbidity Statistics from General Practice: Third National Morbidity Survey, 3rd edn. London: HMSO, 1985.
25. Pawlikowska T, Chalder T, Hirsch SR, Wallace P, Wright DJM, Wessely SC. Population-based study of fatigue and psychological distress. Br Med J 1994;308:763–766.
26. Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RK, et al. A community based study of chronic fatigue syndrome. Arch Intern Med 1999;159: 2129–2137.
27. Cox B, Blaxter M, Buckle A. The Health and Lifestyle Survey. London: Health Promotion Research Trust, 1997.
28. Fuhrer R, Wessely S. Fatigue in French primary care. Psychol Med 2005;25:895–905.
29. Henningsen P, Zimmermann T, Sattel H. Medically unexplained physical symptoms, anxiety, and depression: a meta-analytic review. Psychosom Med 2003;65:528–533.
30. Skapinakis P, Lewis G, Mavoreas V. Unexplained fatigue syndromes in a multinational primary care sample: specificity of definition and prevalence and distinctiveness from depression and generalised anxiety. Am J Psychiatry 2003;160:785–787.
31. Sullivan PF, Kovalenko P, York TP, Prescott CA, Kendler KS. Fatigue in a community sample of twins. Psychol Med 2003;33:263–281.
Background and objective: As the etiology of mastalgia is poorly understood this study applied ultrasonography to mastalgia patients with the aim of analyzing the significance of milk duct dilatation in patients with mastalgia.
Results: The mean±SD diameter of duct was 3.99±1.37 mm. The mean diameter of the duct was higher among the younger age group of <25 years than older age groups (4.28 vs 3.95 and 3.87), among married than singles (3.99 vs 3.90) and among those having cyclic pain compared to those having non-cyclic pain (4.0 vs 3.95). However, these differences were not statistically significant. The mean diameter of the duct was significantly higher among those having bilateral pain than those having unilateral pain (4.47 for bilateral vs 4.02 for left side and 3.61 for right side) and among those having severe pain compared to those having moderate or mild pain (4.91 vs 3.40 and 3.28).
Keywords: Mastalgia, duct ectasia, ultrasound, Erbil.
1. Lamarque JL. The commonest complaints in the radiology clinic. In: An Atlas of the Breast: Clinical Radiodiagnosis. London, England: Wolfe Medical Publi.; 1984. P210.
2. BRIDGE Study Group. The presentation and management of breast symptoms in general practice in South Wales. Br J Gen Pract 1999;49:811-812.
3. Mansel RE. ABC of breast disease: breast pain. BMJ. 1994;309:866-868.
4. Roberts MM, Elton RA, Robinson SE, French K. Consultations for breast disease in general practice and hospital referral patterns. Br J Surg 1987;74:1020-1022.
5. Marrow M. The evaluation of common breast problems. Am Fam Physician 2000;61:2371-8.
6. Preece PE, Mansel RE, Bolten PM, Hughes LE, Baum M, Gravelle IH. Clinical syndromes of mastalgia. Lancet 1976;2:670-3.
7. Davies EL, Gateley CA, Miers M, Mansel RE. The long-term course of mastalgia. J R Soc Med. 1998;91:462-464.
8. Hanif AM, Rasool S. Presentation, management and out come of mastalgia. J Surg Pak
9. Watt-Boolsen S, Emus H, Junge J. Fibrocystic disease and mastalgia. Dan Med Bull 1982;29:252-4.
10. Jorgensen J, Watt-Boolsen S. Cyclical mastalgia and breast pathology. Acta Chir Scand 1985;151:319-21.
11. BeLieu RM. Mastodynia. Obstet Gynecol Clin North Am. 1994; 21:461-477.
12. Klimberg VS. Etiology and management of breast pain. In: Harris JR, Lippman ME, Morrow M, Hellman S, eds. Diseases of the Breast. Philadelphia, Pa: Lippincott-Raven; 1996:99-106.
13. Smith RL, Pruthi S, Fitzpatrick LA. Evaluation and management of breast pain. Mayo Clin Proc 004;79(3):353-72.
14. Peters F, Diemer P, Mecks O, Behnken LJ. Se verity of mastalgia in relation to milk duct dilatation. Obstetrics and Gynecology 2003; 101(1): 56-60.
15. Smith RL, Pruthi S, Fitzpatrick LA. Evaluation and management of breast pain. Mayo Clin Proc 2004; 79:353-72.
16. Carmichael AR. Can Vitex Agnus Castus be used for the treatment of mastalgia? What is the current evidence? Evid Based Complement Alternat Med 2008; 5(3):247–50.
17. Snowden HM, Renfrew MJ, Woolridge MW. Treatments for breast engorgement during lactation. Cochrane Database Syst Rev 2001; (2):CD000046.
Background and objective: Inflammation is a physiological response to injury and infection. However, chronic inflammation causes tissue damage and is a feature of most chronic diseases. Despite significant progress in developing therapies to target chronic inflammation over the years, almost all current therapies have serious side effects. The current investigation is to identify naturally-existing anti-inflammatory therapies with fewer side effects.
Methods: The anti-inflammatory effects and mechanisms of action of extracts and fractions obtained using vacuum liquid chromatography (VLC) from ginger (Zingiber officinale) on the production of nitric oxide (NO) and prostaglandin E2 (PGE2) were investigated. NO and PGE2 production were induced by stimulating the mouse RAW264.7 monocyte/macrophage cell line with lipopolysaccharide (LPS). Levels of NO and PGE2 were determined using the Griess method and enzyme linked sorbent assay (ELISA), respectively.
Results: Extracts of two Zingiber officinale species obtained with chloroform showed potent inhibitory effects on NO and PGE2 production. The extracts had a higher potency than N(G)-nitro-L-arginine methyl ester (L-NAME), a known specific inducible nitric oxide synthase (iNOS) inhibitor and were comparable in their effects on PGE2 with Indomethacin, a specific PGE2 inhibitor. Further, we identified a fraction (F6) that had most potent inhibitory effects.
Conclusion: The study shows that extract of Zingiber officinale have strong inhibitory effects on key pro-inflammatory mediators involved in chronic inflammation. Both the extracts and F6 had better inhibitory effects than established pharmaceutical inhibitors of NO and PGE2.
Keywords: Zingiber officinale roscoe, inflammation, nitric oxide, prostaglandin E2
1. Tracey KJ. The inflammatory reflex. Nature 2002;420: 853-9.
2. McGettigan P, Henry D. Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Med 2011; 8: e1001098.
3. Murakami A, Takahashi D, Kinoshita T, Koshimizu K, Kim HW, Yoshihiro A, Nakamura Y, Jiwajinda S, Terao J, Ohigashi H. Zerumbone, a Southeast Asian ginger sesquiterpene, markedly suppresses free radical generation, proinflammatory protein production, and cancer cell proliferation accompanied by apoptosis: the alpha,beta-unsaturated carbonyl group is a prerequisite. Carcinogenesis 2002; 23: 795-802.
4. Coleman JW. Nitric oxide in immunity and inflammation. Int Immunopharmacol 2001; 1: 1397-1406.
5. Rocca B, FitzGerald GA. Cyclooxygenases and prostaglandins: shaping up the immune response. Int Immunopharm 2002; 2: 603-630.
6. Vernin G, Párkányi C: Chemistry of Ginger, p. 87, in: P. N. Ravindran and K. Nirmal Babu (Eds.), Ginger - the Genus Zingiber. CRC Press, Boca Raton, FL (2005).
7. Kizhakkayil J, Sasikumar B. Diversity, characterization and utilization of ginger: a review. Plant Gen Resources 2011; 9: 464-477.
8. Ibrahim HN, Hussin K. Cultivated Gingers of Peninsular Malaysia: Utilization, profiles and micropropagation. Gardens' Bulletin Singapore 2007; 59: 71-88.
9. Fouda A-MM, Berika MY. Evaluation of the effect of hydroalcoholic extract of Zingiber officinale rhizomes in rat collagen-induced arthritis. Basic Clin Pharmacol Toxicol 2009; 104: 262-271.
10. Ramadan G, Al-Kahtani M, El-Sayed W. Anti-inflammatory and anti-oxidant properties of curcuma longa (Turmeric) versus Zingiber officinale (Ginger) rhizomes in rat adjuvant-induced arthritis. Inflammation 2011; 34: 291-301.
11. Landers JP. Handbook of capillary electrophoresis. J. P. Landers (Ed.), CRC Press Inc., Boca Raton, FL, USA 1996, pp. 1–912.
12. Handy RLC, Moore PK. A comparison of the effects of L-NAME, 7-NI and L-NIL on carrageenan-induced hindpaw oedema and NOS activity. Br J Pharmacol 1998; 123: 1119-1126.
13. Salvemini D, Misko TP, Masferrer JL, Seibert K, Currie MG, Needleman P. Nitric oxide activates cyclooxygenase enzymes. Proc Nat Acad Sci 1993; 90: 7240-7244.
14. Pan M-H, Hsieh M-C, Hsu P-C, Ho S-Y, Lai C-S, Wu H, Sang S, Ho C-T. 6-Shogaol suppressed lipopolysaccharide-induced up-expression of iNOS and COX-2 in murine macrophages. Mol Nutr Food Res 2008; 52: 1467-1477.
Background and objective: Thalassaemia is a heredity blood diseases characterised by decreased synthesis of one of the two types of polypeptide chains (β or α) which form the normal adult human hemoglobin molecule (HbA, α2‚β2), resulting in decreased filling of the red cells with haemoglobin, and cause anaemia. The study aimed to improve mothers’ knowledge and practices of Thalassaemic children who are using Desferal therapy.
Methods: A quasi-experimental study was carried out at Hawler Thalassemia Center in Erbil City from the 1st of March to the end of May 2010. One hundred mothers were selected and divided into two groups, 50 mothers exposed to the educational programme (study group) and a second group of (50) mothers were served as control. Pre and post test of subject of interest were done during the two occasions.
Results: The results revealed that mothers’ knowledge and practices in the study group were improved. There is no significant association between mothers’ knowledge and practices with socio-demographic characteristics at pre-test which became significant at post-test .
Conclusion: Yet, most of the mothers in the study group have gained benefit from implementation of this educational programme.
1. Rund D. and Rachmilewitz E., Medical progress β -Thalassemia. N Engl J Med [on online]. 2005. 353(11):1135-46. Available from: www.nejm.org. [Accessed on 21/1/2010].
2. Goljan E., Pathology, 2nd ed. Mosby Elsevier, Rapid Review Series 2009. Available from: www.ask.com. [Accessed on 1/4/2010].
3. Birgens H., Haemoglobinopathies. Available from: Available from: www.orebroll.se. 2007. [Accessed on 27/1/2010].
4. Gardi L., MIH foundation Mediterranean Institute of hematology. Dubai.16-18 MAY 200 [on online]. Available from: www.araburban.org. 2005. [Accessed on 21/1/2010].
5. Abolghasemi H., Amid A, Zeinali S, Radfar M. H., Eshghi P., Rahiminejad M S., Ehsani M A., et al., Thalassemia in Iran Epidemiology, Prevention, and Management. J Pediatr Hematol Oncol [on online]. 2007. 29 (4):233–238. Available from: www.journals.lww.com. [Accessed on 23/2/2010].
6. Rasheed N. Ezzaddin and Ahmed S. Adnan, Effect of ß- Thalassemia on Some Biochemical Parameters. Middle East Journal of Family medicine [on online]. 2005. 7(2). Available from: www.mejfm.com. [Accessed on 21/1/2010].
7. Sufferers' organizations (2009), Plans to improve specialists medical treatment in Kurdistan. Available from: www.KRG.org. [Accessed on 22/2/2010].
8. Franchini M., and Veneri D., Iron-chelation therapy: an update. The Hematology Journal [on online]. 2004. 5: 287–288. Available from: www.online.haematologica.org. [Accessed on 1/4/2010].
9. Al-Mosowi H. Salim Essa, Effect of health Educational Programme on Mother’s knowledge and Practices toward Thalassaemia in children. M.Sc. thesis: University of Baghdad, College of Nursing 2000, PP (47-48, 64-65, 75).
10. Dehkordi A. Hassanpour, and Heydarnejad M. Saeed, Enhancement of parents’ awareness about β-thalassemia major disorder through two educational programs. Pak J Med Sci [on online]. 24 (2): 283-284. Available from: www.pjms.com.pk. 2006. [Accessed on 21/1/2010].
11. Al-attar M. Sabir and Shekha M. Sabir. The prevalence of Thalassemia in Erbil province. Zanko [on online]. 2006. 18 (2).
12. Mahanil W., Effects of a Teaching Program on Knowledge and Self-Care Behavior Regarding Decreasing Iron Accumulation in the Body of Children with Thalassemia at Nan Hospital, Thailand. M.Sc. Thesis, Thailand: Mahidol University. College of Nursing 2009.
13. Dhamcharee V., Romyanan O. and Ninlagarn T., Genetic Counseling FOR Thalassemia in Thailand: Problems and Solutions. Southeast Asian J Trop MED Public Health [on online]. 2001. 32 No. 2:414-417. Available from: www.tm.mahidol.ac.th. [Accessed on 21/1/2010].
Background and objective: Urinary tract infection (UTI) is a condition in which the urinary tract is infected with a pathogen causing inflammation. One of the predisposing factors for UTIs is diabetes mellitus (DM), spillage of glucose into the urine provide a good culture medium for bacteria. The objectives of this study were to evaluate the distribution of UTIs among diabetic patients of both genders with studying the effect of some relative factors, and identifying types of the causal microorganisms.
Methods: Diabetic patients (type1 and 2), from both genders were included in this study. All patients were interviewed. Uncontaminated urine samples were collected for microscopic and macroscopic analysis. Isolations and identifications of bacteria were done by standard methods.
Results: Out of 150 diabetic patients, 53 (35.33%) have UTI. Gender, middle age and high level of proteinuria were risk factors, while type and duration of DM with its type of treatment, body mass index (BMI), and hypertension were non significant. The isolated types of pathogens were Escherichia coli (45.3%), Klebsiella pneumoniae (15.1%), Staphylococcus saprophyticus (15.1%), Citrobacter diversus (11.3%), Candida albicans (7.5%) and Staphylococcus aureus (5.7%).
Conclusion: This study revealed that diabetic females were most susceptible to get UTIs than diabetic males. In both genders the most reliable age for UTI were between 31-40 years. The results showed that the level of proteinuria was higher in patients suffering from UTIs associated with DM, which considered as a risk factor. Certain types of microorganisms were isolated; the most common types were Escherichia coli, Klebsiella pneumoniae and Staphylococcus saprophyticus.
Keywords: Diabetes mellitus; Urinary tract infections; Bacteria.
1. Hooton TM, Stamm WE. Diagnosis and treatment of uncomplicated urinary tract infection. Infect Dis Clin North AM 1997: 11(3):551-81.
2. Barnett BJ, Stephens DS. Urinary tract infection: an overview. Am J Med Sci 1997; 314(4):245-9.
3. Johnson JR, Roberts PL, Stamm WE. P fimbriae and other virulence factors in Escherichia coli urosepsis: association with patients’ characteristics. J Infect Dis 1987; 156(1):225-9.
4. Nicolle LE, Fries D, Harding GK, Roos LL. Hospitalization for acute pyelonephritis in Manitoba, Canada, during the period from 1989 to 1992, impact of diabetes, pregnancy, and aboriginal origin. Clin Infect Dis 1996; 22(6):1051-6.
5. Yass MA, Ali SS, Ahmed AA. ABO-Rh blood groups and type of food are amongst urinary tract infection causatives. Zanco J Med Sci 2012: 16(1):71-77.
6. Zhanel GG, Harding GK, Nicolle LE. Asymptomatic bacteriuria in patients with diabetes mellitus. Rev Infect Dis 1991; 13(1):150-4.
7. Forland M, Thomas V, Shelokov A. Urinary tract infections in patients with diabetes mellitus. Studies on antibody coating of bacteria. JAMA 1977; 238(18): 1924- 6.
8. Paterson JE, Andrriole VT. Bacterial urinary tract infection in diabetes. Infect Dis Clin North Am 1997; 11(3):735-50.
9. United States Renal Data System. USRDS 2007 Annual Data Report. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Department of Health and Human Services; 2007.
10. Simerville JA, Maxted WC, Pahira JJ. Urinalysis: a comprehensive review. Am Fam Physician 2005; 71:1153-62.
11. Stamm WE, Hooton TM. Management of urinary tract infections in adults. N Engl J Med 1993; 329:1328-34.
12. Tomson C. Urinary tract infection. In: Warrell DA, Cox TM, Firth JD, Benz EJ Jr, editors. Oxford Textbook of Medicine. 4th ed. Oxford, UK: Oxford University Press; 2003:420-33.
13. Pacurari A, Serban C, Narita A, Romosan I. Is urinary tract infection a risk factor for hypertension in elderly? J Hypertens, 2010; 28: P e512.
14. Geerlings SE, Stolk RP, Camps MJL, et al. Asymptomatic bacteriuria may be considered a complication in women with diabetes. Diabetes Care, 2000; 23(6): 744-9.
15. Wheat LG. Infection and diabetes mellitus. Diabetes Care.1980; 3(1):187-97.
16. Hoepelman IM, Meiland R, Geerling SE. Pathogenesis and management of bacterial urinary tract infections in adult patients with diabetes mellitus. Int J Antmicrob Agents, 2003; 22: S35-S43.
Background and objective: Viral Hepatitis Type B&C is serious public health challenge throughout the world.Hepatitis B and C viruses still remain to be the major causes of chronic hepatitis.It is estimated that around 350-400 million people in the world are chronic carriers of HBV, which represents approximately 7% of the total populationwhereas infection with HCV is found in approximately 3% of the world population, which represents 160 million people. Hepatitis B infection has a wide range of seroprevalence in the Mediterranean countries ranging from intermediate (=>2% ) to high prevalence ( =>7%). World Health Organization estimated a prevalence rate for HCV infection of about 4.6% in Eastern Mediterranean in 1999. During the eightieths years of the last century, Iraq was considered to be of intermediate endemicity with hepatitis B as reflected by 3% seroprevalence of HBsAg in normal population. Hepatitis C was found to be of low endemicity among blood donors 0.5%. There were no national wide epidemiological studies regarding the prevalence of hepatitis B&C accordingly we conduct this study to determine the prevalence of both types all over the Iraq.
Methods: From the 1st of January 2005 to 31st of December 2006, a community based cross-sectional study was conducted all over Iraqi governorates. A total of 9610 persons, recruited by surveying a nationally representative random sample of households were analyzed. A stratified random sample proportional to size of each of the 18 Iraqi governorates, both urban and rural areas were included. Prevalence estimates were therefore weighted and age-adjusted. Five (5ml) of blood samples were taken from the study subjects, and tested for hepatitis B surface antigen, antibody to hepatitis B core antigen antibody to hepatitis B surface antigen and hepatitis C antibodies .
Results: The national prevalence rate of HBs Ag was 1.6% and correlated positively with age. The prevalence rate of anti-HBs antibodies was 17%. The prevalence of anti-HBc was 9.7%. The prevalence of anti-HCV was low (0.4%). The prevalence rate of anti-HBs antibodies in <10 years children is only 32.2%, which raise the issue of incomplete coverage of hepatitis B vaccine during the years preceding the study years.
Conclusion: The findings revealed that Iraq is of low prevalence with HBsAg.On the other hand,hepatitis C was found to be of very low prevalence. As a marker of exposure to hepatitis B, Anti HBcIgG was found to increase with age.
Keywords: hepatitis B, hepatitis C, Iraq.
1. Walsh K., Alexander G.J. Update on chronic viral hepatitis. Postgrad Med J 2001;77:498-505
2. Holmes-Mc Nary M. Impact factors on development of cirrhosis and subsequent hepatocellular carcinoma.CompendContinEduc ent2001;22,19-33.
3. Goh K.,Doraisingham S., Tan K. The hepatitis B immunization programme in Singapore.Bulletin of the World Health Organization1989;67:65-70
4. Benvegnu L., Fattovich G., Noventa F. Concurrent hepatitis B and C virus infection and risk of hepatocellular carcinoma in cirrhosis. A prospective study.Cancer1994;74(9):2442-8.
5. Simonetti R.G., Camma C., Fiorello F. Hepatitis C virus infection as a risk factor for hepatocellular carcinoma in patients with cirrhosis. A case-control study.Ann Intern Med1992;116(2):97-102.
6. Kao J.H., Chen P.J., Lai M.Y., Chen D.S. Occult hepatitis B virus infection and clinical outcomes of patients with chronic hepatitis C. J ClinMicrobiol2002;40(11):4068-71
7. Sánches N.M., González H.B., Gómez R.H.S. Prevalência de hepatitis B y C em donadores de sangre em um hospital de tercer ´veç de Ciudad de México. SaludPublica de México. 1999;41(6):475-8.
8. Zou S., Tepper M., Giulivi A. Current status of hepatitis C in Canada.Can J Public Health2000;91 Suppl 1:S10-5, S10-6.
9. Tandon BN, Acharya SK, Tandon A. Epidemiology of hepatitis B virus infection in India. Gut 1996; 38 (Suppl 2): S56-S59.
10. Wittet S: Hepatitis B vaccine introduction. Lessons learned in advocacy, communication and training.Bill &Malindea Gates Children's Vaccine Program at PATH. 2001.
11. Awan Z, Idrees M, Amin I, Butt S, Afzal S, Akbar H, Rehman I, Younas S, Shahid M, Lal A, Saleem S, Rauff B: Pattern and molecular epidemiology of Hepatitis B virus genotypes circulating in Pakistan. Infect Genet Evol 2010, 10(8):1242-6.
12. Komas NP, Baï-Sepou S, Manirakiza A, Léal J, Béré A, Faou AL: The prevalence of hepatitis B virus markers in a cohort of students in Bangui, Central African Republic. BMC Infect Dis 2010, 10:226.
13. Michielsen PP, Francque SM, Van Dongen JL: Viral hepatitis and hepatocellular carcinoma. World J SurgOncol 2005, 3:1-18.
14. WijdanA.Hussein,AbdulRhida Al – Abassy : Hepatitis Profile In Baghdad 2002, dissertation for board degree in community medicine.2002.AlmustansiryaUniversity.
15. Bond WW, Petersen NJ, Favero MS: Viral hepatitis B: aspects of environmental control. Health Lab Sci 1977, 14:235-52.
16. Workowski KA, Berman SM: CDC sexually transmitted diseases treatment guidelines. Clin Infect Dis 2002, 35(Suppl 2):S135-7Publisher Full Text
17. Workowski KA, Berman SM: Sexually transmitted diseases treatment guidelines. Centers for Disease Control and Prevention.MMWR Recomm Rep 2006, 55(RR-11):1-94. PubMed Abstract |
18. J.F. Perz, G.L. Armstrong, L.A. Farrington, Y.J. Hutin and B.P. Bell, The contributions of hepatitis B virus and hepatitis C virus infections to cirrhosis and primary liver cancer worldwide. J Hepatol2006, 45 , pp. 529–538.
19. N. Previsani and D. Lavanchy, Hepatitis B. WHO/CDS/CSR/LYO/2002 :Hepatitis B, World Health Organization, Geneva 2002.
20. Awan Z, Idrees M, Rafique S, Rehman I, Akbar H, Butt S, Manzoor S, Khan LA, Munir S, Afzal S, Fatima Z, Rauff B, Naudhani M, Ali M, Saleem S, Badar S: Hepatitis B virus YMDD-motif mutations with emergence of lamivudine-resistant mutants: a threat to recovery. GastroenterolHepatol Bed to Bench 2010, 3(3):108-114.
21. Akbar N, Basuki B, Mulyanto M, Garabrant DH, Sulaiman A, Noer HM: Ethnicity, Socioeconomic status, Transfusions and risk of Hepatitis B and Hepatitis C infection. J GastroenterolHepatol 1997, 12:752-757
22. Alam MM, Zaidi SZ, Malik SA, Naeem A, Shaukat S, Sharif S, Angez M, Khan A, Butt JA: Serology based disease status of Pakistani population infected with Hepatitis B virus.
23. Cavalletto L, Chemello L, Donada C. The pattern of response to interferon alpha (alpha-IFN) predicts sustained response to a 6-month alpha-IFN and ribavirin retreatment for chronic hepatitisC. BMC Infect Dis 2007, 7:64.
24. World Journal of Gastroente WHO: Hepatitis B surface Ag assays; operational characteristics. Phase 1.Report, World Health Organization, 2004, (WHO/BCT/BTS/01.4).
25. Seo H.S., Park J.S., Han K.Y., Bae K.D., Ahn S.J., Kang H.A. et al. Analysis and characterization of hepatitis B vaccine particles synthesized from Hansenulapolymorpha. Vaccine2008, 26(33), 4138-4144
26. World Health Organization fact sheets, Hepatitis C, World Health Organization, Geneva (2000), Available at: http://www.who.int/mediacentre/factsheets/fs164/en/ (accessed August 2008).
27.Tahan V, Ozdogan O, Tozun N. Epidemiol ogy of viral hepatitisin the Mediterranean Bain· Annales AcademiaeMedicaeBialostocensis 2003.Vol. 48.
28. Kleinbaum D.G., Sullivan K.M., & Barker N.D. A pocket guide to Epidemiology. (1st ed.).New York, USA: Springer Science and Business media. 2007.
29. Sebastion M, Ichhpujani RL, Kumari S. Incidence of different types of viral hepatitis in Delhi, Uttar Pradesh and Rajasthan areas. J Commun Dis 1990; 22: 729-733.
30. Damle AS, Deshmukh AB, Kanyakarte RB, Patwardhan NS, Anvikan AR, Bajaj JK, et al. HBV carriage rate in resident doctors.Ind J Med Microbiol 1999; 17(3): 135-136.
31. Dasarthy S, Mishra SC, Acharya SK. Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India. Liver 1992; 12: 116-120.
32. Ameen R, Sanad N, Al-Shemmari S, Siddique I, Chowdhury RI, Al-Hamdan S, et al. Prevalence of viral markers among first-time Arab blood donors in Kuwait. Transfusion2005 ,45(12):1973–1980.
33. Usman HR, Akhtar S, Rahbaqr MH, Hamid S, Moattar T, Luby SP: Injection in health care settings: a risk factor for acute hepatitis B virus infection in Karachi, Pakistan. J Epidemol Infect 2003, 130:293-300.
34. Mahtab M, Rahman S, Karim , Khan M, Foster G, Solaiman S, Afroz S: Epidemiology of hepatitis B virus in Bangladeshi general population. HepatobiliaryPancreat Dis Int2008, 7:595-600.
35. Annemarie Wasley, Deanna Kruszon-Moran, Wendi Kuhnert, Edgar P. Simard, Lyn Finelli, Geraldine McQuillan. Beth Bell: The Prevalence of Hepatitis B Virus Infection in the United States in the Era of Vaccination. J Infect Dis. 2010; 202 (2): 192-201. doi: 10.1086/653622.
36. CDC Epidemiology & prevention of Vaccine preventable diseases – 10 th edition
37. National Center for Health Statistics. NHANES 1999–2004. http://www.cdc.gov/nchs/about/major/nhanes/datalink.htm. Accessed 12 May 2008.
38. Centers for Disease Control and Preven tion. National Center for Health Statistics
(NCHS).NHANES 1999–2000 addendum to the NHANES III analytic guidelines.46-7.
39. EPI/General directorate of preventive medicine /Iraqi MoH,1993.
40. Mohamed MK. Epidemiology of HCV in Egypt 2004.The Afro-Arab Liver Journal, 2004, vol 3, No2, (July), pp 41-52.
41. Alter MJ. Epidemiology of hepatitis C virus infection.World journal of gastroenterology 2007, 13 (17): 2436–41. PMID 17552026
Adrenocortical carcinomas are highly malignant rare tumors that can occur in adults, adolescents or children, Whil they can affect both sexes the incidence is higher among girls. Hormone-secreting tumors and the associated classic endocrine syndromes (virilizing, feminizing, Cushing’s and Conn’s syndromes) represent the most common presentation in this age group. Both genetic and environmental factors have been implicated in its etiology. Diagnosis is done by imaging studies including Computerized tomography scan an/ord magnetic resonance imaging of abdomen in addition to ultra-sound examination, histological confirmation is done by excisional biopsy or in exceptional conditions by fine needle aspiration. Regarding functional state of the tumor hormonal study is needed. Treatment includes; complete radical surgical resection which might be curative in case of small tumors, in patients with incomplete resection or metastatic spread treatment options include mitotane and/or chemotherapy. radiation therapy is recommended in the treatment of bone, brain and other metastases, radiation therapy is also recommended in the treatment of symptomatic local recurrences. Regarding prognosis It has been reported that patients with untreated adrenocortical carcinoma have a median survival of 3 months only. In treated adrenocortical carcinoma, overall 5-year survival ranged between 23% and 60% in different series. We present a 17 years old girl, she presented with generalized acne, virilizing features, primary amenorrhea and hemoptysis, Investigations revealed adrenocortical carcinoma. In the light of this case, the literature about adrenocortical carcinoma was reviewed.
Conclusion: Adrenal carcinoma can occur in our locality and the diagnostic keys are hormonal and imaging studies.
Keywords: Adrenal gland, Neoplasm, Endocrine.
1. D E Schteingart, G M Doherty1, P G Gauger1, T J Giordano2, G D Hammer, M Korobkin3 and F P Worden. Management of patients with adrenal cancer: recommendations of an international consensus conference. Society for Endocrinology.2005,1351-1388.
2. R.C. Ribeiro E.L. Michalkiewicz1,4.B.C. Figueiredo5,L. DeLacerda5, F. Sandrini5, M.D. Pianovsky6,G. Sampaio7 and R. San drini5. Adrenocortical tumors in children. Brazillian journal of medical and biological research. 2000.(33):1225-1234
3. Sergio Gugisch Moreira, Jr, MD, and Julio M. Pow- Sang, MD. Evaluation and Management of Adrenal Masses. Cancer Control.. 2002. Vol.9, No.4.326-334
4. Dieter Nürnberg, Ruppiner Kliniken GmbH .Christoph F. Dietrich.. Ultrasound of the adrenal glands. 2011,12. 20 (1-31)
5. Bruno Allolio, Stefanie Hahner, Dirk Weismann and Martin Fassnacht. Management of adrenocortical carcinoma. .Clinical Endocrinology. 2004. (60); 273-287
6. Dimitrios A. Linos.. Adrenal incidentaloma (adrenaloma).. Hormones. 2003..2(1) 12-21
7. Jill Hudson – PGY. Lawen.. Adrenocortical Carcinoma Controversies and Consensus. march; 2011.(Internet ppt-file) Accessed at 10th September 2011
8. Bernadette Bernnan.Adrenacortical carcinoma. Orphanet encyclopedia. 2003. review 2004.1-5
9. Shuen-Fu Weng, Ching-Chung Chang, Deng-Huang Su1, Yih-Leong Chang2.,.An Adrenocortical Carcinoma Patient with Multiple Lung Metastases — A Case Report TaiwanTzu Chi Med J. 2005 .17-No.