Mona A. Hegazy

Egyptian experience of reliability of 4T's score in diagnosis of heparin induced thrombocytopenia syndrome.

To evaluate the utility of the 4Ts clinical scoring system as a pretest probability method for detection of heparin-induced thrombocytopenia (HIT). Medical and surgical inpatients and outpatients at Kasr El Eini hospital. This single-centre series of 50 HIT testing referrals assessed combination of clinical score (thrombocytopenia, timing, thrombosis, other causes of thrombocytopenia not evident; 4Ts), Heparin platelet factor 4 (H-PF4) rapid particle gel immunoassay (PaGIA) and 14C serotonin release assay (SRA) to develop a practical and well tolerated diagnostic strategy for HIT. Sixteen patients (32%) had a low 4Ts score, 26 (52%) had an intermediate score and only eight (16%) had a high score. A positive H-PF4 by PaGIA was seen in seven patients (14%). As might be anticipated, the likelihood of obtaining a positive H-PF4 by PaGIA increased with an increasing clinical score, with positive H-PF4 by PaGIA results in low, intermediate and high scoring patients of 6.25, 7.7 and 50%, respectively. The positive predictive value of a positive PaGIA was 92%. The negative predictive value was 100%. Five patients (10%) in our cohort had a positive SRA. All patients with a positive SRA were included in the intermediate (two of 26 patients, 7.7%) or high (three of eight patients, 37.5%) score groups. The negative predictive value of a low 4Ts score was 100%, effectively ruling out HIT. A low 4Ts score supports low probability of HIT based on the results of the PaGIA and SRA. Overall, the interrater reliability of the scoring system was fair.

Liver ultrasound is more sensitive in assessing the severity of nonalcoholic fatty liver disease with homeostasis model assessment-insulin resistance

Objective To evaluate the association between different grades of nonalcoholic fatty liver disease (NAFLD) as assessed by a liver ultrasound scan and homeostasis model assessment-insulin resistance (HOMA-IR) and also to investigate the possibility of using a noninvasive objective method to both diagnose and predict the severity of NAFLD in Egyptian obese nondiabetic patients. Methods The present study examined 57 obese, nondiabetic participants, aged 18–57 (34.3±10.5) years. Their BMI ranged from 32 to 48.3 (37.9±4.6) kg/m2. Complete medical history, anthropometric measurements, biochemical studies, and abdominal ultrasonography were carried out for each participant. HOMA-IR was calculated using the formula fasting plasma glucose (mmol/l)×fasting insulin (mIU/l)/22.5. Liver steatosis was evaluated using an ultrasound scan and categorized into four grades of severity according to an international guideline. Results NAFLD diagnosed using an ultrasound scan was associated significantly with a high level of insulin resistance expressed by HOMA-IR in obese nondiabetic patients as compared with participants with normal liver (10.54±4.99 vs. 3.303±0.90, P=0.000). HOMA-IR showed a significant positive correlation with the severity of fatty liver as diagnosed and graded by a liver ultrasound scan (7.14±4.3, 10.62±4.57, 11.93±4.98, and 14.69±5.35 in grade 1, 2, 3, and 4 steatosis, respectively). Conclusion NAFLD and its different grades of severity as assessed by liver ultrasound shows a strong positive association with a high level of insulin resistance expressed by HOMA-IR in obese nondiabetic Egyptian patients. The combination of HOMA-IR and liver ultrasound is a highly sensitive and specific method not only in diagnosis of NAFLD but also in predicting its severity.

Combined Adiponectin Deficiency and Resistance in Obese Patients: Can It Solve Part of the Puzzle in Nonalcoholic Steatohepatitis

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent cause of liver disease, nonalcoholic steatohepatitis (NASH) and fibrosis in obese patients identifies the risk group with increased incidence of liver-related deaths. AIM: To clarify the role of serum adiponectin and its receptor liver gene expression in the progression of liver damage in NAFLD. METHODS: Fifty four (54) obese patients with NAFLD preliminary diagnosed by liver ultra-sound were recruited. Full medical history, anthropometric measurement, biochemical studies, serum adiponectin level, liver biopsy for histological examination and NAS score to identify NASH patients, and assessment of adiponectin receptor gene expression by RT-PCR, were conducted for each patients. Fifteen ages matched average weight healthy adult had been chosen as a control for serum adiponectin level. RESULTS: According to NAS score, patients were divided into non- NASH (8 patients), and NASH (46 patients). Serum adiponectin level was significantly lower in NAFLD patients compared to normal participants (p < 0.004). Serum adiponectin level was lower in NASH patients (4.437 ± 2.569 ng/dl in NASH vs. 5.138 ± 2.841 ng/dl in non-NASH). Adiponectin receptor liver gene expression was lower in NASH patients (0.8459 ± 0.4671 vs. 1.0688 ± 0.3965 in non-NASH). CONCLUSION: Both adiponectin deficiency and resistance had a role in progression of simple liver steatosis to severe injury in obese patients.

Serum Resistin Level and Its Receptor Gene Expression in Liver Biopsy as Predictors for the Severity of Nonalcoholic Fatty Liver Disease

ABSTRACT Background Liver histology remains the gold standard for assessing nonalcoholic fatty liver disease (NAFLD). Noninvasive serological markers have been developed to evaluate steatosis to avoid biopsy. In NAFLD patients, serum resistin was higher than those in control lean and obese patients. Objective of the study To investigate serum resistin and its receptor gene expression in liver biopsy as predictors for NAFLD severity. Patients and methods This study was conducted on 54 obese patients, with suspected fatty liver by ultrasound (excluding diabetic, alcoholic, hepatitis C virus antibody (HCVAb) or hepatitis B surface antigen (HBsAg) positive patients). They were subjected to anthropometric measurements, laboratory studies including serum resistin, abdominal ultrasonography (US) and liver biopsy. The 15 lean subjects were included as a control group. According to biopsy results, patients were subdivided into nonalcoholic steatohepatitis (NASH) group (46 patients) and non-NASH group (8 patients). Results Significantly higher levels of resistin were detected in NAFLD patients compared to control subjects (p = 0.0001). Also, higher levels of resistin were recorded in NASH group compared to the non-NASH group; however, the difference was not statistically significant (p = 0.584). Serum alanine aspirate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (GGT) were higher in NASH patients than non-NASH group (p = 0.223, p = 0.005 and p = 0.006 respectively). Abdominal US showed high sensitivity in NAFLD diagnosis (sensitivity of sonar in detecting steatosis grade compared to biopsy was 61% in grade 1, 25% in grade 2 and 75% in grade 3). Conclusion Serum resistin can be combined with other noninvasive markers to predict the presence of NASH as an alternative to liver biopsy. How to cite this article: Hegazy M, Abo-Elfadl S, Mostafa A, Ibrahim M, Rashed L, Salman A. Serum Resistin Level and Its Receptor Gene Expression in Liver Biopsy as Predictors for the Severity of Nonalcoholic Fatty Liver Disease. Euroasian J Hepato-Gastroenterol 2014;4(2):59-62.

Association of the Leu72Met polymorphism of the ghrelin gene and ghrelin level with type 2 diabetes mellitus and obesity

The aim of the study is to resolve the debated association between ghrelin level and polymorphism of ghrelin gene (Leu72Met) with obesity and type 2 diabetes mellitus. The present study was conducted on 30 diabetic middle-aged patients with normal body mass index (BMI) and 40 age-matched non-diabetic participants (20 with normal BMI and 20 obese). All participants were subjected to full medical history and examination, anthropometric measurements, and laboratory investigations which include complete lipid profile, fasting plasma glucose, glycated hemoglobin, fasting serum insulin and HOMA-IR was calculated, fasting plasma ghrelin level was determined using ELISA method, and the Leu72Met polymorphism of the ghrelin gene was screened using PCR-RFLP. The median level of fasting plasma ghrelin was higher in the diabetic group than those of the non-diabetic group (P = 0.157). However, lower median fasting plasma ghrelin level was reported in the obese group compared to those with normal BMI, yet not statistically significant (P = 0.289). In the present study, Leu72Met polymorphism was present in 13% of the diabetic subjects, 20% of the non-diabetic subjects with normal BMI, and in 30% of the obese non-diabetic participants. No statistically significant association was found between the ghrelin level and the Leu72Met polymorphism in preproghrelin gene with either obesity or type 2 diabetes mellitus.