Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A parasitological survey of stool and urine of 2577 from 3281 individuals living in Abis villages, Alexandria was undertaken in 1998 in order to investigate the prevalence of schistosomiasis in this area and risk factors for hepatic morbidity. A random sample of 1082 individuals was interviewed using a questionnaire regarding risk factors for liver morbidity. All interviewed adults (total: 728) were clinically examined for evidence of organomegally (hepatomegally and/or splenomegally). Individuals with clinically detected organomegally were referred for detailed investigations (total: 65). The criteria for severe hepatic morbidity were AST/ALT ratio higher than 1, prothrombin activity < 70%, and evidence of portal hypertension. The results revealed that prevalence of S. mansoni accounted for 20.5%, with low intensity of infection and increased with age to reach a maximum of 40-46.3% at 15-30 years of age. Intensity of infection followed the same pattern. All tested urine samples were negative for S. haemato-bium. The prevalence of clinically detected organomegally was 10.3% among adults (75/728). Significant risk factors for developing organomegally were age > or = 35 years (2.2 folds), farming occupation (1.7 fold), history of parenteral anti-schisto-somal treatment (PAT) with or without tablets (2.03 folds), and heavy water canal exposure (2.85 folds). Detailed morbidity study on 65 individuals with clinically detected organomegally showed that 52.3% reported heavy score for water canal exposure, 33.8% were positive for HCV antibodies, and 7.7% for HBV antibodies. Procollagen level was higher than 5.5 microg/l in 26.2% of this group. The results of Doppler ultrasonography showed that 33.3% recorded a portal vein diameter > or = 13 mm, 26.2% periportal fibrosis more than grade 2 (> 5 mm), 19% hepatofugal direction of portal blood flow, 30.2% collaterals, 28.6% splenomegaly, and 17.5% hepatofugal direction of splenic blood flow. The burden of severe hepatic morbidity was alarming among this group: 33.8% with portal hypertension, 24.6% with prothrombin activity < 70, and 13.8% with AST/ALT ratio > 1. There was a 4.44 and 3.7 fold increased risk for portal hypertension with elevated levels of PIIIP and positive serologic tests for HCV and/or HBV infections, respectively. Similarly, a 4.58 and 18.35 fold increased risk for AST/ALT more than one was attributed to these two factors, respectively. Elevated procollagen level was significantly associated with viral infection (HCV and/or HbsAG). Seropositivity for HCV antibodies was found strikingly high in adults above 35 years (positive HCV antibodies in 45.9% of individuals). This indicates a high level of endemicity in the study area which is also endemic for S. mansoni. So, a heavy burden of severe liver disease exist in rural Alexandria is attributed to combined infection of S. mansoni and hepatitis viruses. This emphasizes the need for intervenetion strategies targeting these two main liver offenders.
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PMID:Morbidity of schistosomiasis mansoni in rural Alexandria, Egypt. 1470 47

We evaluated the role of liver biopsy in the management of chronic hepatitis C in HIV-infected persons. Patients included had abnormal alanine transaminase (ALT) levels, detectable HCV RNA, and an interpretable liver biopsy. Demographic, epidemiologic, clinical, laboratory, histological, and therapeutic data were recorded in all patients. We also registered the clinical diagnosis of cirrhosis (previous to biopsy) and whether the biopsy result deferred the decision of initiating therapy. During the 33-month duration of the study, 112 patients were included. The degree of fibrosis in liver biopsies was none or mild (F0 or F1) in 47 patients (42%) and was significant or severe in 65 (58%). Seventeen patients (15%) had histological cirrhosis. By logistic regression analysis, only portal hypertension (odds ratio [95% confidence interval], 5.3 [1.05-25.9], P = 0.04) was independently associated with significant fibrosis. Overall, cirrhosis was predicted before biopsy in 29 patients (26%) by the caregiving physician, but only 8 of these were confirmed histologically. The clinical prediction of cirrhosis before biopsy had a sensitivity of 47%, a specificity of 78%, a positive predictive value of 28%, and a negative predictive value of 89%. Histological findings changed the decision to initiate HCV therapy in 19 patients (17%) because of little or no fibrosis. Liver biopsy is a useful tool in the management of HCV-HIV-coinfected persons. In addition to allowing grading and staging of the disease far better than any other method or combination of methods, it is important for making management decisions for patients coinfected with HCV and HIV.
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PMID:The role of liver biopsy in the management of chronic hepatitis C in patients infected with the human immunodeficiency virus. 1534 9

In alcoholic steatohepatitis, hepatic microvascular changes have pathogenic significance for hepatocellular function, perisinusoidal fibrosis, and portal hypertension. It is unclear whether similar changes occur in other forms of steatohepatitis. We therefore examined whether hepatic microvascular dysfunction occurs in fibrosing steatohepatitis induced by feeding mice a high-fat methionine- and choline-deficient (MCD) diet. Using in vivo microscopic--as well as histological and electron microscopic--methods, together with measurements of alanine aminotransferase (ALT), lipid content, and oxidative stress, hepatic microvascular structure and function were studied in relation to inflammatory and fibrotic changes during evolution of steatohepatitis. At 3 weeks of MCD diet intake, serum ALT was elevated and hepatic steatosis was pronounced. By 5 weeks, necroinflammatory change was noteworthy, and by 8 weeks perisinusoidal fibrosis was established. Compared with mice receiving the high-fat diet supplemented with methionine and choline (controls), levels of hepatic lipid and lipoperoxides were elevated at 3 weeks and beyond. The numbers of perfused sinusoids were significantly reduced at each time point. Enlarged, fat-laden hepatocytes together with perivascular fibrosis narrowed sinusoidal lumens, making vessels tortuous and impairing sinusoidal perfusion. At 3 and 5 weeks, MCD diet caused significant increases in phagocytic activity of macrophages in centrilobular regions. By 8 weeks, macrophage activity was less striking, but the number of leukocytes adherent to the sinusoidal lining had increased 5-fold compared with controls. In conclusion, these results are consistent with a dysfunctional hepatic microvasculature. Thus, microvascular changes may contribute to progressive liver injury in metabolic and toxic forms of steatohepatitis.
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PMID:Hepatic microvascular dysfunction during evolution of dietary steatohepatitis in mice. 1536 43

Live donors are becoming an increasingly important source of donor organs in liver transplantation; however, long-term functional aspects of recovery from donor right hepatectomy are unknown. We analyzed donor outcomes at 1-year follow-up. We performed a single-center retrospective analysis of 70 right hepatectomy donors. Six-week and 1-year postoperative follow-up results were compared to preoperative baseline values. Ultrasonography was performed in all donors at 6 weeks and as clinically indicated. All donors were alive and well at the end of the study period. Of 66 right hepatic donors, only 22 (32%) were fully compliant with a 1-year follow-up visit. All those not compliant were contacted by phone. All complications except 1 (late finding of portal vein thrombosis) occurred in the perioperative (90-day) period. The incidence of bile leak was 4.3%, incisional hernia 20%, and autologous transfusion 1.0%. There were no aborted procedures. In those compliant with full 1-year follow-up, total bilirubin, aspartate aminotransferase, and alanine aminotransferase were normal in 97%. A total of 5 donors were noted to have persistence of asymptomatic thrombocytopenia beyond the perioperative period (90 days). These were investigated with Doppler sonography. Sonography was unremarkable in 3 of the 5, while 2 had abnormal findings: splenomegaly alone in 1, and splenomegaly with portal vein thrombosis in the other. Magnetic resonance angiography was performed in both, and the patient with portal vein thrombosis underwent endoscopy, which failed to reveal varices. Neither has clinical portal hypertension. Both remain asymptomatic albeit with stable thrombocytopenia. In conclusion, the majority of complications after donor right hepatectomy occur in the perioperative period. Later findings may include asymptomatic thrombocytopenia, with an incidence possibly as high as 23%, though the significance of this finding remains uncertain. Larger-scale studies are needed to confirm the true incidence and clinical significance of persistent thrombocytopenia in the donor hepatectomy population. Strategies to improve compliance with 1-year follow-up visits need to be developed.
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PMID:One-year morbidity after donor right hepatectomy. 1549 45

Biliary atresia (BA) is a neonatal obliterative cholangiopathy of unknown etiology. Despite the Kasai procedure, hepatic fibrosis and portal hypertension (PH) still occur. Interleukin-8 (IL-8) is an important mediator of inflammation and immune response in human disease. The objective of this study was to investigate the potential role of IL-8 in the pathogenesis of the progressive, sclerosing, inflammatory process and fibrosis in BA. A total of 60 pediatric patients with BA and 15 healthy children were evaluated. The mean ages of BA patients and controls were 6.3 +/- 0.6 and 6.7 +/- 1.1 years, respectively. The patients were classified into two groups according to their clinical outcomes: patients with jaundice (total bilirubin +/- 25.5 micromol/l) and patients without jaundice (total bilirubin < 25.5 micromol/l). The IL-8 levels in serum samples were determined by commercially available enzyme-linked immunosorbent assay. Serum IL-8 levels were higher in the BA patients than in healthy children (236.2 +/- 60.1 vs. 34.5 +/- 12.1 pg/ml, P < 0.001). Patients with jaundice had lower levels of albumin but had greater levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase compared with patients without jaundice. Serum IL-8 levels in the jaundice group were significantly higher than in those without jaundice (516.5 +/- 130.0 vs. 49.3 +/- 10.4 pg/ml, P < 0.0005). Furthermore, patients with PH had higher IL-8 levels than those without PH (378.1 +/- 102.2 vs. 106.6 +/- 48.4 pg/ml, P < 0.005). In the jaundice-free group, IL-8 levels were elevated in patients with PH compared with those without PH (79.0 +/- 17.4 vs. 19.7 +/- 5.8 pg/ml, P < 0.005). The present study demonstrated elevation of serum IL-8 levels in children with BA. Serum IL-8 levels were also higher in patients with jaundice compared with patients without jaundice. These findings suggest that IL-8 may play a significant role in the pathogenesis of BA.
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PMID:Serum interleukin-8 in children with biliary atresia: relationship with disease stage and biochemical parameters. 1561 91

Since 1975, our experience in the treatment of biliary atresia with Kasai's technique has improved little by little, achieving 65% favourable outcome in the last five years. We define "good results" as the complete restoration of biliary flow and normalization of bilirrubin levels. The long-term evolution of these good results can be diverse. The objective of the present work is to analyze the outcome of patients in our series in whom a favourable initial response was achieved, as well as evaluating their present situation and future perspectives. The authors present a total of 17 patients operated by Kasai's technique since 1985, that constitutes the group with good results in our series. The controls were based on general analysis, liver function and periodic ultrasound explorations. All received a standardized medical treatment consisting of vitamin supplements (A, D3, E, K) minerals (zinc, calcium, phosphate, iron) ursodexoxicolic acid, luminal,as well as close control of calorie intake. In two patients the levels of bilirrubine were progressively increased with time, stabilizing at between 5/6 mgs/100 ml, with progressive hepatic hardening, appearance of splenomegalia, indirect signs of portal hypertension and a slight deterioration of hepatic function. One received a transplant at age 12 with Quick levels below 50%. The other, aged 16, continues with an acceptable hepatic function and good quality of life under recommendation of transplant. Eleven patients with ages ranging from fourteen months to seventeen years presented slight and firm hepatomegalia, moderate portal hypertension, GOT 71 +/- 8 mg/100 ml, GPT 97 +/- 11 mg/100 ml and normal bilirrubine levels. From this group, 3 patients, all under five years of age, experienced bleeding from esophageal varices which were controlled by sclerosis and medical treatment (propanolol and isosorbide dinitrate). Recently, one three year-old patient developed a hepatocarcinoma of rapid, mortal evolution. Since then, the determination of alfa-feto protein in follow-up controls has been introduced. Four other patients of 5, 6, 14, 16, years of age are completely assymptomatic with an excellent clinical evolution. In our experience,the patients that overcome the third year after surgery without serious complications seem destined to reach puberty with a good quality of life. However, some cases show signs of hepatic fibrosis and portal hypertension, 77% in our series. Only 23% of patients with a favorable initial evolution appear to present a complete normalization of their hepatic lesion in the long term.
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PMID:[Biliary atresias operated with favourable results: predictable outcome]. 1590 Nov 4

In order to assess the effects of significant cystic fibrosis-related liver disease (CFLD) on bone health, we compared the bone mineral status of older children and adolescents with CFLD to those with cystic fibrosis (CF) alone. Thirteen children (age range, 10-19 years) from our clinical CF services were identified with significant CFLD (9 of these 13 patients had clinical and radiological evidence of portal hypertension). This cohort was then matched by age, gender, and anthropometric measurements with equal numbers of patients with CF alone. All patients had a dual-energy X-ray absorptiometry (DEXA) scan to determine bone mineral content (BMC), bone area (BA), bone mineral density (BMD), and bone mineral apparent density (BMAD) in the region of the lumbar spine. Blood was drawn to determine serum vitamin A, D, E, and K status and liver function tests. The best forced expired volume in 1 sec (FEV1) for each patient in the 12 months around the time of the scan was also documented. Patients with CFLD had slightly worse FEV1 (82 +/- 20% vs. 91 +/- 16%, P = 0.05) and significantly higher alanine aminotransferase (65.5 +/- 35 IU/l vs. 30 +/- 20 IU/l, P = 0.01) than those with CF alone. The mean lumbar spine BA, BMC, BMD, and BMAD were not different between children with CFLD and CF. In conclusion, the presence of significant liver disease in children with CF does not appear to be an additional risk factor for the development of abnormal bone mineralization.
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PMID:Is significant cystic fibrosis-related liver disease a risk factor in the development of bone mineralization abnormalities? 1647 57

NAFLD likely is the most common liver disease in children and is responsible for significant progression to cirrhosis, portal hypertension, and the need for liver transplantation in adults and even in some adolescents. Early diagnosis and lifestyle interventions appear to be our best hope for controlling progression of disease. The pediatrician is responsible for screening all obese children with measurement of aminotransferases. Those with elevated enzymes (particularly ALT) for longer than 3 months, in the absence of markers of hepatitis B or C, autoimmune chronic active hepatitis, Wilson's disease, hemochromatosis, or alpha-1-antitrypsin deficiency, should follow up with an abdominal ultrasound. In patients with a BMI in the morbidly obese range, an ultrasound to search for a diffusely echogenic liver should be performed even if the liver enzymes are normal. Findings suggestive of NAFLD should prompt the institution of appropriate dietary and exercise regimens. If these are unsuccessful after a 3-month trial, the patient should be referred to a pediatric gastroenterologist and hepatologist for further work-up and treatment, preferably in the context of a controlled therapeutic trial. Only by aggressively engaging this current epidemic will we be able to decrease the mounting human cost of NAFLD.
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PMID:Nonalcoholic fatty liver disease. 1663 58

The purpose of this study was to determine the possible role of serum levels of tissue inhibitors of metalloproteinase-1 (TIMP-1) in the pathogenesis of the progressive inflammation and fibrosis in biliary atresia (BA). Serum concentrations of TIMP-1 were measured in 57 BA patients and 15 healthy controls using commercially available enzyme-linked immunosorbent assays. The mean ages of the BA patients and the controls were 6.1 +/- 0.6 and 6.7 +/- 1.1 years, respectively. The patients were categorized into two groups according to their clinical outcomes: patients with jaundice (total bilirubin > or = 2 mg/dl) and patients without jaundice (total bilirubin < 2 mg/dl). In our study, serum levels of TIMP-1 were significantly higher in the BA patients than in healthy subjects (4.8 +/- 0.4 vs. 3.5 +/- 0.3 ng/ml, respectively; p < 0.05). Additionally, serum levels of TIMP-1 significantly increased in the BA patients with jaundice in comparison to those without jaundice (6.3 +/- 0.7 vs. 3.1 +/- 0.3 ng/ml, respectively; p = 0.001). Patients with persistent jaundice had lower levels of albumin but had greater levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase compared with patients without jaundice. Furthermore, patients with portal hypertension (PH) had higher TIMP-1 levels than those without PH (5.3 +/- 0.4 vs. 1.9 +/- 0.3 ng/ml, respectively; p < 0.001). It is concluded that serum levels of TIMP-1 increased in patients with BA. The significant increase in TIMP-1 levels is related to the presence of PH and the severity of jaundice. The elevated TIMP-1 levels may reflect the degree of hepatic fibrosis and development of PH. The data suggest that TIMP-1 may play a role in the pathophysiology of post-Kasai BA.
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PMID:Association of serum levels of tissue inhibitors of metalloproteinase-1 with clinical outcome in children with biliary atresia. 1713 82

Sixty four children (38 boys and 26 girls), aged 1 yr to 14 yr, presenting with fever, splenomegaly and positive LD body in splenic smear examination, admitted to pediatric ward of Nalanda Medical college and Child care center between 1st July 03 to 30th June 04 were taken for study. Patients were categorized into two groups: 44 were in Group I (Patients who had not received prior antileishmanial drug) and 20 in Group II (Patients who had received 30 days course of SAG; 20 mg per kg per day). All patients were given Miltefosine in dose of 2.5 per kg per day od or bid per orally to a maximum of 100 mg and were followed at completion of therapy, 1 month and 6 months for clinical response, splenic size and parasite density. 63 patients had parasitological cure with relapse in one patient of Group I during follow up. One patient in Group II had no response with first course but became parasitologically negative with 2nd course of Miltefosine. In Group I, one patient had persistent splenomegaly and found to have associated portal hypertension. GI side effects i.e. diarrhea and vomiting were observed in 26 and 23 patients respectively. Majority of patients had pancytopenia. Elevated ALT (> 3 times of normal) were seen in 28 and 11 patients of Group I and Group II respectively which returned to normal in subsequent follow up. The final cure rates were 93.2 percent and 95 percent in Groups I and II respectively.
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PMID:Miltefosine in children with visceral leishmaniasis. 1720 5


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