Vol. 6 Issue 2
On the cover: Official Journal of the Mexican Association of Hepatology
The increasing prevalence of obesity in Western countries has led to a significant increase of nonalcoholic fatty liver disease (NAFLD) over the past decades. Being part of the metabolic syndrome, NAFLD is thought to be the most frequent cause of elevated liver enzymes in the United States affecting up to one third of the population. NAFLD is also proposed to be the major cause for cryptogenic cirrhosis and hepatocellular cancer of unknown etiology, and thus, represents one of the most important problems for hepatologists in the future. However, the natural course of NAFLD is highly variable and is influenced by both environmental and genetic factors. Polymorphisms in specific genes have been proposed to increase the risk of fibrosis in patients with NAFLD. The present review article summarizes currently available data from genotype-phenotype studies and defines candidate genes that deserve future investigation.
Obstruction at the level of the gastric outlet by a gallstone is defined as Bouveret's syndrome. It is an uncommon form of gallstone ileus. A single gallstone of at least 2.5 cm in diameter is the most common underlying cause of Bouveret's syndrome. Diagnosis is based on the clinical manifestations, existence of pneumobilia, visualization of lithiasis and demonstration of duodenal obstruction. Enterotomy or gastrotomy with or without cholecystectomy and fistula repair is the most common surgical therapy. It has high success rate, with acceptable surgical morbidity and mortality. Heightened awareness of this syndrome may lead to decreased morbidity and mortality.
HepG2 human hepatoma cells were incubated for 24 or 48 h with various concentrations of YHK solution. After 24 h incubation, cell proliferation and cytotoxicity were determined by 3-(4,5-dimethylthiazol-2- yl)-5-(3- carboxymethoxyphenyl)-2-(4-sulfophenyl)-2Htetrazolium (MTT) assay. Cytotoxicity or necrosis was expressed as lactate dehydrogenase (LDH) release. After exponential growth phase HepG2 cells were treated with different doses of YHK and apoptosis was assessed by using an Annexin V-FITC kit. Further, oxidative stress was measured by dichlorofluorescein-diacetate (DCFH-DA) assay. As compared to control, YHK-treated cultures showed a significant time-course decrease of the proliferation rate of HepG2 cell growth (p < 0.01). This is likely to be due to an enhanced cytotoxicity (MTT and LDH tests) (p < 0.001). On the other hand, YHK showed in vitro to significantly enhance the oxidative stress of HepG2 cell (p < 0.01) while also markedly increasing apoptosis at 72 h with cells G2/M phase arrest (p < 0.01). These data suggest that YHK seem to modulate the extrinsic and intrinsic regulators of apoptosis and sensitize tumour cells to apoptosis. These preliminary data are worth interest when considering that this nutraceutical has been shown in vitro and in vivo to exert protective anti-tumour effect by redox statusmodulating and immuno-regulatory actions. Given its lack of toxicity so far reported, such natural product might represent an effective nutritional supplement in a number of pathological conditions where a chemopreventive strategy is planned.
Background and study aims: Increased alanine aminotransferase (ALT) levels with negative hepatitis B virus (HBV) DNA by hybridization is a common problem in Turkey where is a mild endemic region. We aimed to evaluate the causes of elevated ALT levels in patients who are negative for hepatitis B e antigen (HBeAg) and HBV DNA (by hybridization) for at least 6 months. Patients-methods: Forty-nine patients were enrolled in this study. Histological changes [histological activity index (HAI), and the extent of fibrosis] were assessed according to the Knodell scoring system and steatosis were graded by Brunt's classification for NAFLD in all patients. Results: A mean age of the patients was 34.9 ± 12.1 years (16-70). 43 (87.8%) of them were male. Mean ALT level was 95 ± 39.7 IU/L (50- 258). Hyperglycemia (>100 mg/dL) and hyperlipidemia were found in 12 and 24 patients, respectively. Hepatic steatosis (7 patients grade 1; 5 patients grade 2; and 7 patients grade 3), ground-glass hepatocyte, chronic hepatitis, and Wilson disease were found in liver biopsy in 38.8%, 32.6%, 26.6%, 2%, respectively. Mean HAI was 6.5 ± 3.6 (4-12) in chronic hepatitis. Seven patients (53.9%) were in stage 1 and 2 while 6 patients (46.1%) were in stage 3 and 4. Conclusions: Nonalcoholic fatty liver disease is the most common cause of elevated ALT levels in HBeAg negative/HBV DNA negative patients. Chronic hepatitis B was found in 26.6% of these patients.
Background: Congenital hypopituitarism is an uncommon cause of neonatal cholestasis. Little is known about the effect of anterior pituitary hormone on hepatic functions. Methods: A retrospective review of the medical charts of eight infants with congenital hypopituitarism and neonatal cholestasis was performed. The results of endocrinological investigations, eye examinations, and magnetic resonance imaging were used to classify these infants. Results: Eight infants (4 male and 4 female; mean age, 1.7 weeks) who presented with cholestatic jaundice subsequently (mean age, 7.6 weeks) developed isolated or multiple anterior pituitary hormone deficiencies. Persistent hypoglycemia, ocular abnormalities, and microphallus were often clinical signs prompting further endocrinological and radiological investigations. Septo-optic dysplasia was prevalent, occurring in five cases. Cholestasis and hepatosplenomegaly resolved within a mean of 9.7 and 10 weeks, respectively, in the majority of cases after replacement of glucocorticoid and thyroid hormones. However, transaminase levels remained high after hormone replacement. Cortisol deficiency and hypoglycemia were noted in all cases, often following stress. Hyperlipidemia persisted in one case after the resolution of cholestasis and after corticosteroid and thyroid hormone replacement therapy. Growth hormone deficiency was not corrected due to the absence of hypoglycemia after corticosteroid hormone, an infant's age, and/or a lack of financial resources. Conclusions: In our series, it appears that glucocorticoid and thyroid hormones play a significant role in the resolution of cholestasis and hepatosplenomegaly. A persistently elevated transaminase level and hyperlipidemia after corticosteroid and thyroid hormone replacement may indicate the need for long-term follow-up and/or growth hormone therapy.
Background: Autonomic dysfunction has been documented in cirrhosis liver. Its influence on variceal bleed is not known. Aim: To determine the autonomic function amongst variceal bleeders in cirrhosis of the liver. Materials and methods: Fifty cirrhotics (variceal bleeders: 34) belonging to either sex, Childs B, age more than 15 years and non diabetic constituted the study group. Parasympathetic function tests included valsalva ratio (E:I ratio) and deep breathing test. (Max.-Min. heart rate); sympathetic function included postural fall of B.P and a rise in diastolic B.P. with sustained hand grip. A cirrhotic was considered to have 'True' autonomic dysfunction when both parasympathetic and one of the two sympathetic tests were abnormal. Results: The mean age for men was 39.64 + 10.6 yrs and for women 39.54 + 15.8 yrs. The male female ratio was 3.5:1. Only 10 of the 50 patients (all bleeders) had 'true' autonomic dysfunction i.e. 20%. Parasympathetic dysfunction alone was positive in 19 (38%) and sympathetic in 10 patients (20%). The E:I ratio (p < 0.001) and an increase in diastolic B.P. during sustained hand grip (p < 0.04) were significantly positive amongst variceal bleeders. Conclusion: 'True' autonomic dysfunction can predispose a cirrhotic to variceal bleed.
Hepatitis D virus (HDV) is an RNA virus that can cause hepatitis. Development and approval of new vaccines are the hope for control of the possible emerging pandemic of this infection. Recently, the possible epitope as 174 to 195 of HDAg was mentioned. Here, the author reports the preliminary data from the computational analysis to find binding affinity of the candidate HDV epitope using new bioinformatics technique. For LHDAg, the binding affinity for A0203, A0301, A1101, A6801 and DRB0101 are acceptable. For S-HDAg, the binding affinity for A0203, A0301, A1101, A6801 and DRB6802 are acceptable. The binding affinity for A0203 is the most for both L-HDAg and S-HDAg.