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Article
Glucose 6 phosphate dehydrogenase deficiency among neonates with hyperbilirubinaemia in western Iraq

Author: Sahar J Al-Hiali
Journal: Journal of the Faculty of Medicine مجلة كلية الطب ISSN: 00419419 Year: 2008 Volume: 50 Issue: 4 Pages: 431-434
Publisher: Baghdad University جامعة بغداد

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Abstract

Background: Glucose -6-phosphate (G6PD) deficiency seems to be a major cause of neonatal hyperbilirubinaemia. This study was carried out to determine the prevalence of G6PD deficiency among icteric neonates in western Iraq and to evaluate its association with hemolysis in neonatal jaundice.
Patients and Methods: All icteric neonates admitted to Al-Ramadi Maternity and Paediatrics hospital, Al-Anbar governorat, for the period from 1st Feb. to 1st Dec. 2006 were included in the study. Data collected from case records and includes age, sex, total serum bilirubin hemoglobin level, reticulocyte count, blood group and Rh of the mothers and neonates, direct coomb's test and peripheral smear. G6PD enzymewas measured also.
Results: eight out of 100 icteric neonates had G6PD deficiency, with male to female ratio of 7:1. A significant higher total serum bilrubin (TSB) level was among G6PD deficient icteric neonates than that among non deficient icteric neonates. Reticulocytes count and haemoglobin level was not significantly differ between G6PD deficient and non deficient icteric neonates.
Conclusion: Neonatal screening for G6PD deficiency is a need in order to control genetic blood diseases.

Keywords

G6PD deficiency --- haemolysis --- TSB


Article
The effect of sever glucose-6-phosphate dehydrogenase(G6PD) deficiency on the activity of white blood cells for a female medical students in Basrah University
دراسة تأثير النقص الحاد لنازعة هدروجين فسفات-6-كلوكوز على فعالية الكريات البيضاء لطالبات كلية الطب/ جامعة البصرة

Authors: Nawal K. Ibraheem نوال خليل ابراهيم --- Gania.S.Gadban غنية سالم غضبان
Journal: Thi-Qar Medical Journal مجلة ذي قار الطبية ISSN: 19929218 Year: 2010 Volume: 4 Issue: 3 Pages: 100-106
Publisher: Thi-Qar University جامعة ذي قار

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Abstract

ABSTRACT : This study involved ( 57) female medical student, aged between ( 19-24) years, subdivided into two groups, control group that consist of (30) female with normal level of G6PD enzyme and case group that consist of (27) female with severe G6PD deficiency. Both groups have hemoglobin type AA, and white blood cells were estimated for them. We tried in this study to identify the effect of sever G6PD deficiency on the phagocytic activity of non isolated granulocytes from the whole blood, to mirror the in vivo stimulation of granulocytes and the effect of severe G6PD deficiency on their phagocytic activity. We demonstrate a statistically significant proportion ( P < 0.05) between the granulocytes phagocytic activity and severe G6PD deficiency. This could form the basis for drug development in order to prevent or treat G6PD deficiency-related disease and thus unburden the public health system.

الخلاصة:هذه الدراسة شملت (57) طالبة في كلية الطب ، تتراوح أعمارهم بين(19-24) سنة، قسموا إلى مجموعتين إحصائيتين ، المجموعة الأولى (control) وتتكون من (30) طالبة لهم مستوى طبيعي لنازعة هدروجين فسفات-6-كلوكوز، والمجموعة الثانية ) (case وتتكون من (27) طالبة تعانى من نقص حاد لنازعة هدروجين فسفات-6-كلوكوز. كلا المجموعتين لهم فئة دم (AA) . حاولنا في هذه الدراسة معرفة تأثير النقص الحاد لنازعة هدروجين فسفات-6-كلوكوز على فعالية الكريات البيضاء غير المنفصلة من الدم ، وبرهنا على وجود تناسب رقمي هام(P< 0.05) بين فعالية الالتقاف للكريات البيضاء والنقص الحاد لنازعة هدروجين فسفات -6-كلوكوز. هذا ممكن أن يكون الأساس لتطوير الأدوية من اجل منع أو معالجة الأمراض المتعلقة بنقص نازعة هدروجين فسفات-6-كلوكوز وذلك لإزاحة العبء عن النظام الصحي العام.

Keywords

G6PD --- granulocyte --- Phagocytosis.


Article
PREVALANCE OF SALMONELLA TYPHI CARRIER STATE PATIENTS WITH GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY
انتشار صفة الحامل للجرثومة المسببة للحمى التايفوئيدية في الاشخاص المصابين بنقص انزيم محلل الكلوكوز

Author: Rahman K.Mohsen رحمن كاظم محسن
Journal: Basrah Journal of Veterinary Research. مجلة البصرة للابحاث البيطرية ISSN: Print:18138497 E; 24108456 Year: 2005 Volume: 4 Issue: 1 Pages: 17-21
Publisher: Basrah University جامعة البصرة

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A case control study was conducted in Busrah at the period from March toSeptember 2002 . The population included in this study was divided into two groups . Thefirst group was included patents with G6pD deficiency and the second group was includednormal individuals as a control group .Stool samples were collected from both groups for bacteriological e.'amination .This study revealed that ; there was an association between G6pD deficiency andSalmonella typhi carrier state and this association was statistically significant in urbanrather than rural area .

Keywords

G6pD --- salmonella --- Infection


Article
DETECTION OF A, A- MUTATIONS OF G6PD GENE ON MOLECULAR LEVEL IN IRAQI POPULATION
الكشف عن طفرات A, A- المصاحبة لأنزيم نازع هيدروجين الكلوكوز-6- فوسفات (G6PD) على المستوى الجزيئي بإستعمال تقنية PCR/RFLP في عينات محلية

Author: Rana A. Al-Temmemy
Journal: Iraqi Journal of Biotechnology المجلة العراقية للتقانات الحياتية ISSN: 18154794 Year: 2012 Volume: 11 Issue: 2 Pages: 357-368
Publisher: Baghdad University جامعة بغداد

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Abstract

The study involved the extraction of deoxyribonucleic acid (DNA) from 71 samples of random G6PD patients and 85 samples apparently healthy individuals from different Iraqi populations respectively, which was then amplified by polymerase chain reaction (PCR) and later subjected to digestion by restriction enzymes (Nla III and Fok I) to create restriction fragment length polymorphism (RFLP) to enable the detection of mutation that caused G6PD deficiency namely A and A-. The results of the current study showed that Iraqis were affected by G6PD deficiency in a percentage 7.2% and showed that the affected cases were attributed to A mutation in 4.2% while 0% was recorded for A- mutation.

تضمنت الدراسة إستخلاص الدنا من 71 عينة مصابة سرسرياً بنقص نازع هيدروجين الكلوكوز-6-فوسفات (G6PD) و 85 حالة من الاصحاء ظاهرياً ثم أخضعت هذه العينات لتفاعل التضاعف التسلسلي ((PCR بعدها تم إستعمال احد الطرق المعتمدة (RFLP) وذلك باستعمال انزيمات قاطعة (Nla III and Fok I ) للكشف عن الطفرتين قيد الدراسة. بينت نتائج الدراسة الحالية إن نسبة الإصابة بمرض نقص نازع هيدروجين الكلوكوز-6-فوسفات في العراق هي 7.2% وان الطفرة نوع A قد تسببت ب 4.2% من مجمل حالات الإصابة في حين لم تسجل أي إصابة بالطفرة من نوع A-.

Keywords

G6pd Detection --- Mutations --- Rflp


Article
Molecular Basis of G6PD Deficiency in Babylon : Iraq

Authors: Munaf S. Dauod --- William M. Frankool --- Fadhil J. Al-Touma
Journal: Iraqi National Journal Of Chemistry المجلة العراقية الوطنية لعلوم الكيمياء ISSN: 22236686 Year: 2010 Issue: 39 Pages: 571-588
Publisher: Babylon University جامعة بابل

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Abstract

AbstractObjective: The objective of this study was to investigate the molecular basis of glucose-6-phosphate dehydrogenase (G6PD) genes in hyperbilirubinemic neonates in Babylon province of Iraq by using molecular methods (genomic DNA extraction, PCR and RFLP analysis) and then to investigate the type of G6PD variant predominantly present. Methods: The study included a total of 236 full-term male neonates, 183 of them were associated with severe hyperbilirubinemia which were admitted in Teaching Hospital of Pediatric and Maternity / Babylon during 1st , Oct., 2007 to 14th , July, 2008 with age ranged between 1 – 28 days, their TSB levels ≥ 15 mg/dl , while another 53 neonates were used as control group. The blood sample taken from each neonate was divided into two aliquots: the first aliquot was used for hemoglobin (Hb), total and conjugated bilirubin (TSB and SCB), G6PD activity. The second aliquot was used for molecular analysis including genomic DNA extraction and then application of polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) protocols. Results and Discussion: Severe hyperbilirubinemic neonates were screened for erythrocyte G6PD enzyme activity measurements, severe G6PD deficiency was detected in 22 of the total 183 hyperbilirubinemic neonates included and their activity levels was significantly decreased (P < 0.05) to 0.34 ± 0.17 U/g Hb as compared with control value 10.02 ± 1.17 U/g Hb. The incidence of severe G6PD deficiency in neonatal hyperbilirubinemic neonates identified was 12.02 %. TSB levels were markedly elevated to (23.01 ± 5.0 mg/dl), whereas the control value was 0.75 ± 0.23 mg/dl. The mean ± SD values of each of SCB and Hb were significantly lower than that found in controls (P < 0.05) and reached to 0.063 ± 0.036 mg/dl ; 13.32 ± 0.94 g/dl as compared with that found in control neonates 0.19 ± 0.11 mg/dl ; 15.91 ± 1.62 g/dl respectively. Conjugated bilirubin was undetectable in sera of 10 of 22 neonates (45.5%) with severe G6PD deficiency which imply a partial defect of bilirubin conjugation. The molecular part of the study involved the extraction of genomic DNA from hyperbilirubinemic neonates with severe G6PD deficiency which detected by agarose electrophoresis and then amplified by PCR and finally was subjected to digestion by endonuclease restriction enzymes to create RFLP to enable the detection of mutation that caused G6PD deficiency. The overall majority of affected severe G6PD-deficient neonates with hyperbilirubinemia in Babylon province : Iraq were due to G6PD Med variant (C563T, Ser 188 Phe) in which 19 out of 22 (86.4%) have this type of gene mutation, and only one G6PD A- variant (4.55%) (G202A ; A376G mutations) was diagnosed, whereas 2 of 22 (9.1%) remain with unknown G6PD variants. Conclusion: The predominant G6PD gene detected in hyperbilirubinemic neonate with severe G6PD deficiency in Babylon province was G6PD Med.

الخلاصة يعتبر مرض عوز نازعة هيدروجين الكلوكوز- 6- فوسفات (G6PD deficiency) من الأمراض المنتشرة في مناطق مختلفة من دول العالم حيث أن عدد المصابين يتجاوز اﻠـــ 400 مليون من اﻠﺬكور والإناث ومن حديثي الولادة والأعمار الأخرى و يعتبر من الأسباب المؤدية إلى حدوث مرض اليرقان الولادي اﻠﺬي يسبب مضاعفات سريرية خطيرة تؤدي إلى تلف الدماغ ومن ثم الموت. وقد تم تشخيص أكثر من 442 نوع من أنماط الإنزيم (G6PD Variants) باستعمال عدد كبير من التقنيات الحيوية ومنها التقنيات الجزيئية Molecular analytical methods والتي تحدد الطفرات الوراثية التي تحدث في الجينات المسئولة عن التصنيع الحيوي للأنماط المختلفة من الإنزيم . إن أحد أهم أهداف ﻫﺬه الدراسة هو تحديد نسبة انتشار المرض لدى حديثي الولادة من اﻠﺬكور ﺬو النمو الجنيني المتكامل والمصابين بمرض اليرقان الولادي في محافظة بابل وتحديد الطفرات الوراثية في تتابع القواعد النتروجينية للجينات المسئولة عن تصنيع الأنماط الإنزيمية المختلفة (G6PD Variants) والتي تسبب حدوث مرض اليرقان الولادي الحاد باستعمال طرق جزيئية وباستعمال236 عينة من الذكور حديثي الولادة للفترة من 1/ 10 2007/ولغاية 12/ 7/ 2008 ولأعمار تراوحت ما بين 1 – 28 يوما حيث تم توزيعهم إلى مجموعتين اعتمادا على تركيز البيليروبين الكلي TSB وكما يلي:- - المجموعة الأولى وهي مجموعة السيطرة والتي شملت 53 (22.46%) حديث الولادة وكان تركيزالبيليروبين الكلي طبيعيا (1 mg/dl (TSB <. - المجموعة الثانية والتي شملت 183 (77.54%) حديث الولادة مصابين باليرقان الولادي وكان تركيز البيليروبين قد ارتفع وبشدة ≥15 mg /dl) TSB). وتضمنت ﻫﺬه الدراسة متابعة تأثير العوز الحاد للإنزيم على تركيز كل من الهيموكلوبين , البيليروبين الكلي TSB والبيليروبين المقترن SCB في مصل الدم. ولقد وجد أن نشـــــــــــــاط الإنزيم قد انخفض معنويا بشكل حاد في 22 حالة من حالات اليرقان الولادي ووصل إلى IU/g Hb 0.34 ± 0.17 مقارنة مع المعدل الطبيعي وان معدل الـ TSB قد ارتفع إلى 23.01 ± 5.0 mg/dl . وان نسبة انتشار النقص الحاد للإنزيم في محافظة بابل كانت 12.02%) ). وقد اقترن ﺬلك بانخفاض معنوي في تركيز البيليروبين المقترن SCB وﻫﺬا يوضح عدم حدوث عملية الاقتران للبيليروبين في خلايا الكبد لغــــــــرض التخلص منه بسبب عدم نضج ميكانيكية الاقتران إضافة إلى وجود نقص في بعض الإنزيمات المسئولة عن ﺬلك ومنها إنزيم اﻠـــ UGT1A1 . وقد وجد أن هناك ارتباط معنوي(P<0.05) سالب مابين نشاط إنزيم الــ G6PD المنخفض بشدة وتركيز البيليروبين الكلي TSB اﻠﺬي ارتفع إلى أكثر من .15 mg/dl وقد تضمن المحور الجزيئي التحري عن الطفرات الوراثية للقواعد النتروجينية التي تحدث في الجينات المسئولة عن التصنيع الحيوي لإنزيم اﻠـــ G6PD باستعمال التقنيات الجزيئية Molecular Analysis والتي تعتمد على استخلاص جزيئة اﻠـحامض النووي منقوص الأوكسجين Genomic DNA التي تم استخلاصها من دم الذكور حديثي الولادة والمصابين بالنقص الحاد في نشاط إنزيم اﻠـــ G6PD باستعمال طقم خاص تم استيراده من شركة Roche الألمانية ومن ثم متابعة دراسة التحليل الجيني للطفرات الوراثية حيث أخضعت العينات المرضية مع مجموعة السيطرة إلى تفاعل التضاعف التسلسلي Polymerase Chain Reaction للحامض النووي بعدها تم استعمال طريقة الهضم بالأنزيمات المعتمدة (RFLP) للكشف عن الطفرات في الجينات المسئولة عن التصنيع الحيوي لنمطي الإنزيم G6PD Med and G6PD A- . وقد بينت الدراسة أن الطفرات التي تم تشخيصها والتي تحدث في الجينات المسئولة عن التصنيع الحيوي للإنزيم والتي تسبب نقصان حاد في نشاطه الحيوي في مصل الدم باستعمال الطرق الجزيئية ومن ثم إحداث اليرقان الولادي في حديثي الولادة بمحافظة بابل كانت 19 حالة من النمط المتوسطي للإنزيم G6PD Med(C563T) ونسبته% (86.4 ) بينما تم تشخيص حالة مرضية واحدة من النمط الأفريقي G6PD A- (G202A ; A376G) وكانت نسبته هي ( %4.55) ولكن بقيت حالتين (% 9.1) لم يتم تشخيص نوع الطفرة الوراثية في الجين المسئول عن النمط الإنزيمي لهما .


Article
Molecular Basis of G6PD Deficiency in Hyperbilirubinemic Neonates in Middle Euphrates Province : Iraq

Authors: William M. Frankool --- Fadhil Jawad Al-Tu'ma
Journal: Karbala Journal of Medicine مجلة كربلاء الطبية ISSN: 19905483 Year: 2010 Volume: 3 no.3, 4 Issue: 7 Pages: 867-881
Publisher: Kerbala University جامعة كربلاء

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Abstract


Background: Neonates G6PD deficiency screening has been recognized as an essential component of public health care in most developed and some Mediterranean countries. However, such screening is yet to be widely embraced in Iraq. More than 442 variants of G6PD have been identified by various molecular methods. The aim of the present study was to determine the normal values of G6PD and deficiency prevalence of this enzyme in male neonates and then determination of the type molecular variant of G6PD prevalence in Middle Euphrates Province of Iraq.
Objective: The objective of this study was to investigate the molecular basis of glucose-6-phosphate dehydrogenase (G6PD) deficiency in hyperbilirubinemic neonates in Middle Euphrates province of Iraq. Molecular methods (genomic DNA extraction, polymerase chain reaction and restriction fragment length polymorphism analysis) and then investigate the type of G6PD variant predominantly present have been performed.
Methods: The study included a total of 917 full-term male neonates which were divided into two groups:
The first group which include 704 neonates (76.8%) associated with severe hyperbilirubinemia were admitted in Middle Euphrates Province Teaching Hospitals of Maternity and Pediatrics during 1st Oct., 2007 to 12th July, 2008 with age ranged between 1 – 28 days, their total serum protein , TSB levels ≥ 15 mg/dl.
The second group which include 213 neonates (23.2%) with the same age ranged were used as control group, their TSB levels ˂ 1 mg/dl. The blood sample taken from each neonate was divided into two aliquots: the first aliquot was used for the determination of total and serum conjugated bilirubin (TSB and SCB), and G6PD activity. The second aliquot was used for molecular analyses including genomic DNA extraction and then application of polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) protocols.
Results and Discussion: Severe hyperbilirubinemic neonates were screened for erythrocyte G6PD enzyme activity, severe G6PD deficiency was detected in 75 of 704 hyperbilirubinemic neonates included and their activity levels was significantly decreased (P < 0.05) to less than 10% of that found in control group. Therefore, the incidence of severe G6PD deficiency identified in Middle Euphrates Province of Iraq was 10.65%. TSB levels were markedly elevated to ( ≥ 15 mg/dl), whereas the mean ± SD values of SCB were significantly lower than that found in controls (P < 0.05) , SCB was undetectable in 32 of 75 (42.67%) of hyperbilirubinemic neonates with severe G6PD deficiency which imply a partial defect of bilirubin conjugation. The molecular part of the study involved the extraction of genomic DNA from hyperbilirubinemic neonates with severe G6PD deficiency which was detected by agarose gel electrophoresis and then amplified by PCR and finally was subjected to digestion by endonuclease restriction enzymes to create RFLP and to enable the detection of mutation that caused G6PD deficiency. The majority of affected severe G6PD deficient neonates with hyperbilirubinemia in Middle Euphrates province – Iraq, were due to G6PD Med variant (C563T, Ser 188 Phe) , of such 67 of 75 neonates (89.3%) have this type of mutation, and 5 of 75 (6.67%) have G6PD A- variant (G202A ; A376G mutations), whereas only 3 of 75 (5.3%) remain unknown G6PD variants which require future molecular studies.
Conclusion: The predominant G6PD gene detected in hyperbilirubinemic neonate with severe G6PD deficiency in Middle Euphrates province was G6PD Med.variant.
Keywords : Hyperbilirubinemia, G6PD gene, Polymerase Chain Reaction , RFLP.


Article
The in Vitro Effect of Chloramphenicol and Salicylate on Erythrocytes of Patients with Favism

Authors: Zuhair M. Al-Musawi --- Mohammad Sh. Ali --- Ahmmed H. Matloob
Journal: Iraqi Academic Scientific Journal المجلة العراقية للاختصاصات الطبية ISSN: 16088360 Year: 2010 Volume: 9 Issue: 1 Pages: 95-100
Publisher: The Iraqi Borad for Medical Specialization المجلس العراقي للاختصاصات الطبية

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ABSTRACT:BACKGROUND:Glucose 6-phosphate dehydrogenase (G6PD) deficiency is the most common of all clinically significant enzyme defects. A long list of drugs thought to cause haemolysis in patients with this enzyme defect.OBJECTIVE:To determine whether chloramphenicol and salicylate can act as in vitro exogenous oxidizing agents and subsequently cause haemolysis of G6PD deficient erythrocytes and matching the result with the data obtained from the clinical observations which includes the intake of trimethoprim-sulfamethoxazole, salicylate or nalidixic acid by favic patient.PATIENTS AND METHODS:Sixty six patients admitted to the hospital (Karbala teaching hospital for Children, Karbala, Iraq) with history of sudden onset of pallor and dark urine after fava beans ingestion were studied. Each patient was fully examined and his parents were asked about the type of fava beans ingested and the past drug history.Of the sixty six patients, ten were evaluated 1-3 months later and blood samples were taken from them along with blood samples from ten healthy volunteers. Blood samples from both groups were incubated in vitro with chloramphenicol and salicylate separately.RESULTS:Mean (SD) of methaemoglobin concentrations at baseline and after incubation with therapeutic and toxic concentrations of chloramphenicol (15 μg/ml and 25 μg/ml) and salicylate ( 150 μg/ml and 300 μg/ml) were calculated for both the control and the study groups. Paired t-test showed no significant differences (P> 0.05) in methaemoglobin concentrations at baseline and after incubation with therapeutic and toxic concentrations of these drugs. Mean percentage differences from baseline for G6PD deficient group were not significantly different from control group at both concentrations of these drugs as tested by student t-test.CONCLUSION: Hemolysis in G6PD deficient patients occurs mainly after fresh fava beans ingestion. chloramphenicol and acetylsalicylic acid do not cause significant hemolysis in G6PD deficient erythrocytes in vitro


Article
Molecular Characterization of Severe G6PD Deficiency in Hyperbilirubinemic Neonates in Karbala : Iraq……

Authors: Fadhil J. Al-Touma --- William M. Frankool
Journal: Karbala Journal of Medicine مجلة كربلاء الطبية ISSN: 19905483 Year: 2009 Volume: 2 no.8, 9 Issue: 5 Pages: 663-680
Publisher: Kerbala University جامعة كربلاء

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Objective: The objective of this study was to investigate the molecular basis ofglucose-6-phosphate dehydrogenase (G6PD) genes in hyperbilirubinemic neonates inKarbala province of Iraq by using molecular methods (genomic DNA extraction, PCRand RFLP analysis) and then to investigate the type of G6PD variant predominantlypresent.Methods: The study included a total of 253 full-term male neonates, 197 of themassociated with severe hyperbilirubinemia which were admitted in Karbala TeachingHospital of Pediatrics during the period from 1st October 2007 to 14th July 2008 withage ranged between 1 – 28 days, their TSB levels ≥ 15 mg/dl, and another 53 neonateswere used as control group. The blood sample taken from each neonate was dividedinto two aliquots: the first aliquot was used for total and conjugated serum bilirubin(TSB and SCB), G6PD activity. The second aliquot was used for molecular analysisincluding genomic DNA extraction and then application of polymerase chain reaction(PCR) and restriction fragment length polymorphism (RFLP) protocols.Results and Discussion: Severe hyperbilirubinemic neonates were screened forerythrocyte G6PD enzyme activity measurements, severe G6PD deficiency wasdetected in 18 of the total 197 hyperbilirubinemic neonates included and their activitylevels was significantly decreased (P < 0.05) to 0.56 ± 0.32 U/g Hb. The incidence ofsevere G6PD deficiency identified was found 9.14%. TSB levels were markedlyelevated to (20.26 ± 4.96 mg/dl), whereas the mean ± SD values of SCB weresignificantly lower than that found in controls (P < 0.05) and reached to 0.053 ± 0.046mg/dl , and it was undetectable in 5 of 18 neonates (27.78%) with severe G6PDdeficiency which imply a partial defect of bilirubin conjugation. The molecular part ofthe study involved the extraction of genomic DNA from hyperbilirubinemic neonateswith severe G6PD deficiency which detected by agarose electrophoresis and thenamplified by PCR and finally was subjected to digestion by endonuclease restrictionenzymes to create RFLP to enable the detection of mutation that caused G6PDdeficiency. The overall majority of affected severe G6PD neonates withhyperbilirubinemia in Kerbala province : Iraq were due to G6PD Med variant(C563T, Ser 188 Phe) in which 17 out of 18 (94.4%) have this type of mutation, andonly one G6PD A- variant (5.56%) (G202A ; A376G mutations) was diagnosed.Conclusion: The predominant G6PD gene detected in hyperbilirubinemic neonatewith severe G6PD deficiency in Kerbala province was G6PD Med.


Article
Levels of Glucose-6-phosphate Dehydrogenase in Type 1 Diabetes Mellitus patients with Nephropathy and Cardiovascular disease complication
مستويات إنزيم الكلوكوز 6 فوسفات ديهايدروجينيز في مرضى السكري من النوع الاول مع مضاعفات الكلى والامراض الوعائيه

Authors: Israa B. Raoof اسراء برهان رؤوف --- Saad M. Nida سعد محمد ندا --- Perry H. Saifullah بري حبيب سيف الله
Journal: Baghdad Science Journal مجلة بغداد للعلوم ISSN: 20788665 24117986 Year: 2014 Volume: 11 Issue: 2 عدد خاص بالمؤتمر النسوي الثاني Pages: 461-468
Publisher: Baghdad University جامعة بغداد

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Abstract

The aim of this study is to evaluate oxidative stress in diabetes mellitus (DM) Type1 by the measurement of Glucose-6-phosphate Dehydrogenase (G-6-PD), an enzyme expressed in human RBCs, is important in the generation of reduced glutathione which is the key product in oxidative stress controls. The Study was carried on 80 samples of blood and serum of National Diabetes Center (NDC). The study groups under fasting conditions and they divided as:20 samples of diabetes mellitus patients without complications and 20 samples of diabetes mellitus with cardiovascular (CV) complications and 20 samples of diabetes mellitus with Nephropathy (Neph) complications compared with 20 control group with average age (13-67) years.. The results showed an elevation in the lipid profile and urea levels in patients groups compared with control group and a decrease in glucose-6-phosphate Dehydrogenase, HDL levels in all patients groups compared with control group.

الهدف من هذه الدراسه هو تقدير قياس مستوى إنزيم الكلوكوز 6 فوسفات لمرضى السكري من النوع الاول بواسطه قياس مستوى انزيم G6PDالموجود في كريات الدم الحمراء والمسؤول عن اختزال الكلوتاثايون المفتاح الرئيسي للسيطره على الجهد التاكسدي اجريت الدراسه على80 عينه من الدم والمصل من النساء وقد تم تقسيمهم كالاتي: 20عينه للمرضى المصابات بالسكري ,20 عينه للمرضى المصابات بالسكري مع مضاعفات الامراض الوعائيه و20 عينه للمرضى المصابات بالسكري مع المضاعفات الكلويه مقارنه ب 20 عينه من الاصحاء سريريا وقد تمت الدراسه في المركزالوطني لابحاث السكري ومركز بحوث التقنيات الاحيائيه /جامعه النهرين وكان معدل اعمارهم مابين (13-67) سنه اظهرت النتائج وجود ارتفاع في مستوى الدهون واليوريا في مرضى السكري من النوع الاول مقارنه بمجموعة الاصحاء(مجموعه السيطره) كما اظهرت الدراسه وجود انخفاض في نسبه انزيم G6PD و HDLفي مريضات السكري من النوع الاول مقارنه بمجموعة السيطره .


Article
PHYSIOLOGICAL AND BIOCHEMICAL STUDY FOR SPECIMEN OF CHILDREN SUFFERING OF ENZYME G6PD DEFICIENCY AT RAMADI CITY
دراسة فسلجية كيموحيوية لعينة من الأطفال المصابين بنقص أنزيم G6PD في مدينة الرمادي

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Abstract

Some blood variable and reduced Glutathione (GSH) concentration had been studied besides lipid peroxides (Malondialdehyde (MDA)) and the concentration of trace ions of the element (Fe+2 , Cu+2 , Zn+2) in the blood serum of ill mace children. The study including sixty children suffering of acute hemolytic anemia of ages between (1-10)years ,more over another 30 healthy childs appearance of the some ages as a control group . The result indicated significant decrease at (P ≤ 0.05) of the activity of the enzyme G6PD in the children suffering illness due to the enzymatic deficiency in comparison with healthy children where the value of the enzyme activity recorded illustrated that the suffered children recorded (1.77 ± 0.71) U/g.Hb while the healthy children was (12.64 ± 2.40) U/g.Hb . The result also showed the children suffering G6PD lack recorded low significant result (P ≤ 0.05) at both the concentration of hemoglobin , site of packed red blood cells , reduced Glutathione and the concentration of Zn+2 relatively to healthy, where its concentration for the suffering children (5.82 ± 1.16) g/dl , (18.43 ± 3.81) % , (2.95 ± 0.99) µmol/l and (15.78 ± 4.23) µmol/l while for the healthy were (11.95 ± 0.67) g/dl , (37.76 ± 1.98) % , (7.80 ± 2.20) µmol/l , (20.60±3.06) µmol/l respectively. While it revealed significant elevation (P ≤ 0.05) at both white blood cells and the MDA concentration ,besides the concentration of Fe+2 and Cu+2 at the Infected children regarding the healthy children. Where by its concentration at Infected children (8.46 ± 2.03)*103 cell/mm3 , (20.83 ± 7.75) µmol/l , (81.75 ± 48.58) µmol/l and (44.29 ± 10.88) µmol/l. while for healthy were (16.14 ± 5.57)*103 cell/mm3 , (8.98 ± 2.47) µmol/l , (33.48 ± 5.23) µmol/l and (33.19 ± 6.76) µmol/l. respectively.

درست بعض المتغيرات الدمية وتركيز الكلوتاثايون Glutathione (GSH) و بيروكسدة الدهن(MDA) Malondialdehyde وتركيز بعض ايونات العناصر النزرة الزنك والنحاس والحديد (Fe+2 , Cu+2 , Zn+2) في مصل دم الاطفال الذكور المصابين بنقص انزيم G6PD الحاد في مستشفى الرمادي للنسائية والاطفال . شملت الدراسة 60 طفل مصاب بفقر دم انحلالي حاد بأعمار تتراوح بين (10-1) سنه اضافة الى 30 طفل اصحاء ظاهريا من نفس الفئة العمرية كمجموعة سيطرة. أظهرت النتائج وجود انخفاض معنوي عند مستوى الاحتمالية (P≤0.05) في فعالية أنزيم G6PD في الاطفال المصابين بالنقص الأنزيمي مقارنة مع الأطفال الأصحاء اذ سجلت قيمت فعالية الأنزيم في الأطفال المصابين معدل بلغ(1.77±0.71) وحدة دولية /غم.هيموكلوبين اما في الاصحاء بلغ(12.64±2.40) وحدة دولية /غم.هيموكلوبين. كما وبينت النتائج ان الاطفال المصابين بنقص فعالية انزيم G6PD كانت لديهم مستويات منخفضة معنويا (P≤0.05) في كل من تركيز هيموكلوبين الدم وحجم كريات الدم المتراصة وتركيز الكلوتاثايون المختزل وتركيز عنصر الخارصين مقارنة بالاصحاء اذ بلغ تركيزها في الاطفال المصابين(5.82 ± 1.16) غم/100مل , (18.43 ± 3.81)% , (2.95 ± 0.99) مايكرو مول/لتر, (15.78 ± 4.23) مايكرو مول/لتر اما في الاصحاء بلغت (11.95 ± 0.67) غم/100مل , (37.76 ± 1.98) % , (7.80 ± 2.20) مايكرو مول/لتر, (20.60 ± 3.06) مايكرو مول/لتر على التوالي, بينما أظهرت ارتفاع معنوي (P≤0.05) في كل من تعداد كريات الدم البيض تراكيز كل من ال MDA عنصري الحديد والنحاس لدى الاطفال المصابين مقارنة بالاصحاء اذ بلغ مستواها في الاطفال المصابين (16.14 ± 5.57)*103 خلية لكل ملم3 , (20.83 ± 7.75) مايكرو مول/لتر, (81.75 ± 48.58)مايكرو مول/لتر , (44.29 ± 10.88) مايكرو مول/لتر, اما في الاصحاء بلغت (8.46 ± 2.03)*103 خلية لكل ملم3, (8.98 ± 2.47) مايكرو مول/لتر , (33.48 ± 5.23) مايكرو مول/لتر , (33.19 ± 6.76) مايكرو مول/لتر على التوالي

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