Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver involvement in tuberculosis in absence of miliary tuberculosis is rare. This study was performed to analyse the spectrum and response to treatment of hepatic tuberculosis in the absence of miliary abdominal tuberculosis. Retrospective analysis of seven cases of hepatic tuberculosis without miliary abdominal tuberculosis who presented at the single tertiary referral center were analyzed. All patients presented with fever and hepatomegaly. Five of them had pain in upper abdomen and vomiting. HIV serology was positive in one patient. All patients had normocytic normochromic anaemia, raised erythrocyte sedimentation rate (Mean 65). Mild elevation of liver enzymes and low albumin (Mean 2.4 gm%) with reversal of albumin globulin ratio (Mean 0.6) were seen in all. Two had jaundice. Prothrombin time was normal in all and lactate dehydrogenase values were elevated in all (Mean 794 IU/L). On ultrasonography, 2 had multiple hypodense lesion, 1 had coarse echotexture of liver, 1 had hyperechoic pattern and 3 had just hepatomegaly. Complete resolution of liver lesions on treatment with 4-drug anti-tuberculosis drug chemotherapy was seen. In conclusion, liver tuberculosis has protean manifestations with nonspecific alteration of liver function tests and is best diagnosed on liver biopsy. Overall response to therapy is satisfactory.
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PMID:Hepatic tuberculosis in absence of disseminated abdominal tuberculosis. 1653 64

Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a kind of inborn errors of metabolism, with the main clinic manifestations of jaundice, hepatomegaly, and abnormal liver function indices. As a mitochondrial solute carrier protein, citrin plays important roles in aerobic glycolysis, gluconeogenesis, urea cycle, and protein and nucleotide syntheses. Therefore citrin deficiency causes various and complicated metabolic disturbances, such as hypoglycemia, hyperlactic acidemia, hyperammonemia, hypoproteinemia, hyperlipidemia, and galactosemia. This paper reported a case of NICCD confirmed by mutation analysis of SLC25A13, the gene encoding citrin. The baby (male, 6 months old) was referred to the First Affiliated Hospital with the complaint of jaundice of the skin and sclera, which it had suffered from for nearly 6 months. Physical examination showed obvious jaundice and a palpable liver 5 cm below the right subcostal margin. Liver function tests revealed elevated enzymatic activities, like GGT, ALP, AST, and ALT, together with increased levels of TBA, bilirubin (especially conjugated bilirubin), and decreased levels of total protein/albumin and fibrinogen. Blood levels of ammonia, lactate, cholesterol, and triglyceride were also increased, and in particular, the serum AFP level reached 319,225.70 microg/L, a extremely elevated value that has rarely been found in practice before. Tandem mass analysis of a dried blood sample revealed increased levels of free fatty acids and tyrosine, methionine, citrulline, and threonine as well. UP-GC-MS analysis of the urine sample showed elevated galactose and galactitol. The baby was thus diagnosed with suspected NICCD based on the findings. It was then treated with oral arginine and multiple vitamins (including fat-soluble vitamins A, D, E, and K), and was fed with lactose-free and medium-chain fatty acids enriched formula instead of breast feeding. After half a month of treatment, the jaundice disappeared, and the laboratory findings, including liver function indices, blood levels of ammonia, lactate and AFP, were returned to normal level. The baby was followed up for 6 months. It developed well, and the abnormal laboratory findings, including MS-MS and UP-GC-MS analysis results, have been corrected, except a slightly elevated lactate level sometimes. SLC25A13 gene mutation analysis for the patient revealed a compound heterozygote of mutation 851del4 and 1638ins23 and therefore NICCD was definitely diagnosed.
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PMID:[A difficult and complicated case study: neonatal intrahepatic cholestasis caused by citrin deficiency]. 1661 6

Secondary amyloidosis is a progressive systemic disease for which there is no reliable diagnostic assay, preventive measure, or treatment. In an attempt to elucidate an antemortem diagnosis, 30 female pig-tailed macaques (Macaca nemestrina) at the Washington National Primate Research Center were surveyed for amyloidosis. Amyloid was demonstrated histologically in 47% (14 of 30) of the animals. The distribution and severity of amyloid deposition was variable. Affected animals had a mean age (+/-1 standard deviation) of 13.2 +/- 4.9 y, which was significantly greater than the mean age of unaffected animals (9.3 +/- 4.1) y. Twelve tests were evaluated for detection of amyloidosis; the diagnostic value of each was determined through comparison of histologically positive and histologically negative animals. Diagnostic tests evaluated were endoscopic examination and biopsy of the stomach and colon, abdominal ultrasonography, hepatic radiology, serum amyloid A (SAA), endothelin 1, alpha-fetal protein, aspartate aminotransferase (AST), alanine aminotransferase, gamma-glutamyltransferase (GGT), alkaline phosphatase, cholesterol, blood urea nitrogen, total bilirubin, C-reactive proteins, and erythrocyte sedimentation rate. Amyloidotic animals demonstrated a distinctive serologic profile: elevated SAA, GGT, and AST in combination with decreased total protein and albumin. Radiology demonstrated hepatomegaly in animals with hepatic amyloid deposition. In the absence of known infection or trauma, an amyloidotic serologic profile and radiologic hepatomegaly are consistent with systemic amyloidosis in M. nemestrina.
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PMID:Detection of systemic amyloidosis in the pig-tailed macaque (Macaca nemestrina). 1663 79

Soluble intercellular adhesion molecule-I (sICAM-1) is an important early marker of response to inflammatory mediators and immune activation released from a variety of cells including hepatocytes. At present, the most reliable determination of severity and prognosis in chronic viral hepatitis is the histological staging of the disease which is an invasive procedure and is often not well accepted by patients. The search for alternative non-invasive methods is mandatory especially in follow ups after initial assessment by biopsy. Serum sICAM-1 level was measured in 19 patients with chronic HCV, 19 patients with non-B, non-C chronic liver diseases (NBNC-CLD) and in 19 healthy control subjects using ELISA. Serum sICAM-1 levels were significantly higher in patients with chronic HCV and in NBNC-CLD patients compared to normal subjects (mean +/- SD, [1003 +/- 453 vs. 232 +/- 177, p<0.001], and [881 +/- 328 vs. 232 +/- 177, p<0.001]), respectively. Furthermore, serum levels of sICAM-1 were significantly higher in HCV-RNA positive patients than in HCV-RNA negative patients (p<0.001). Positive correlations were detected between serum levels of sICAM-1 and serum alanine aminotranseferase (ALT) (p<0.001), aspartate aminotranseferase (AST) (p<0.001), prothrompin time (p<0.001), and alkaline phosphatase (p<0.001), while, a negative correlation with albumin was found (p<0.001). Also, there was a significant correlation between clinical, ultrasonic findings and the level of sICAM-1 in chronic HCV patients as regards hepatomegaly, splenomegaly and normal liver echogenecity. High knodell score was significantly associated with high sICAM-1 level (p<0.001) in both patient groups. while no association between sICAM-1 and fibrosis was found. In conclusion, the measurement of sICAM-1 serum levels in chronic hepatitis C and NBNC-CLD patients is a useful non-invasive marker for monitoring liver disease activity that could replace follow up liver biopsies that are mostly not welcomed by the patients.
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PMID:Soluble ICAM-1 in patients with chronic hepatitis C infection: a prognostic marker of disease activity. 1673 23

The clinical outcome of nonobstructive neonatal cholestasis (NC) cases varies greatly and the prognosis is generally unpredictable. In this study, we aimed to evaluate the prognostic benefits of qualitative analysis of histopathological changes in nonobstructive NC cases. A total of 28 nonobstructive NC cases (18 neonatal hepatitis; 10 intrahepatic bile duct paucity) were studied. We analyzed the relationship between histopathological and clinical parameters. Hepatic inflammation, bridging necrosis, pericellular fibrosis, giant cell transformation, and extramedullary hematopoiesis were evaluated and scored according to their absence or presence in each case. The sum of the histopathological scores was accepted as "total pathological injury score." The height percentiles, the presence and the degree of hepatomegaly and ascites, and serum alanine aminotransferase (ALT), albumin, and bilirubin levels and prothrombin time were also evaluated and scored. The patients were divided into 2 clinical course groups considered "good" or "bad" according to the total clinical scores. For statistical analysis, Pearson's chi-square test, Mann-Whitney U-test, and receiver operating characteristic curve were used. We found a statistically significant negative relation between the clinical course and total pathological injury score (P = 0.042) and pericellular fibrosis (P = 0.016). In conclusion, during the interpretation of liver biopsies of nonobstructive NC, scoring of histopathological changes should be done for assessing the clinical prognostic outcome.
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PMID:Nonobstructive neonatal cholestasis: clinical outcome and scoring of the histopathological changes in liver biopsies. 1680 34

In this study we retrospectively assessed the prevalence of impaired liver function in all 49 patients suffering from Mediterranean Spotted Fever (MSF) consecutively admitted to our department over the last four years. The main parameters of liver function and ultrasound of upper abdomen were performed at entry and at the end of treatment. At admission mean values of transaminases were above the normal limits and significantly higher when compared to mean serum levels at recovery. 55% and 51% of patients had serum values of GOT and GPT, respectively, above the normal limits versus 1% and 2% at the end of treatment. Mean serum values of alkaline phosphatase (AP) were within the normal limits at entry in hospital, but 22 of them had serum values above the normal limits. The same proportion was seen for gamma glutamiltranspeptidase values. Eighteen patients (36.7%) had both transaminases and AP above the normal limits. There were no significant differences among serum values of albumin, bilirubin and gamma globulin before and after therapy. Platelet count, on the contrary, was significantly reduced at admission (p < 0.0001). At ultrasound half of the patients showed hepatomegaly with a hepatitis-like pattern and 39% of patients had splenomegaly. In conclusion, this study confirms previous data from the literature showing a high frequency of liver impairment during the course of MSF, which is usually mild-moderate. In a few cases, however, the increase of transaminases could be serious and the recovery delayed, but never, in our experience, has there been progression toward chronic liver disease.
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PMID:[Abnormal liver function in Mediterranean spotted fever]. 1759 97

The present study tested the hypothesis that mice exposed to Schistosoma mansoni and treated with the insecticide Larvin have an increased risk of accelerated liver damage. To investigate this hypothesis, adverse effects resulting from treatment with Larvin were compared between S. mansoni-exposed and nonexposed outbred albino mice. The effects of concurrent treatment with Larvin on the progress and outcomes of S. mansoni infection were assessed via macroscopic and microscopic examination of liver and spleen, evaluation of several hematological, biochemical and hepatic enzymes parameters, and effect on worm burden. Oral administration of 1/5 and 1/10 LD(50) of Larvin to S. mansoni-exposed mice induced (1) hepatomegaly and splenomegaly; (2) prominent lymphocytic aggregation in liver replacing large areas of bridging necrosis; (3) increased serum level of bilirubin and alanine aminotransferase-aspartate aminotransferase enzymes; (4) decreased serum level of albumin and total proteins; and (5) decreased RBC, hemoglobin content, leukocyte, and lymphocyte counts. No significant effect on worm burden or oviposition was noted as a result of Larvin treatment compared to controls. All doses used in mice either for infection with S. mansoni cercariae or treatment with Larvin resulted in dose dependent alterations in hepatic functions of the tested mice. These alterations were most profound in mice exposed to S. mansoni and receiving Larvin treatment. The present findings support our hypothesis and show that concurrent S. mansoni infection with exposure to Larvin adversely affect liver functions and seriously alter hematological, biochemical, and hepatic enzymes parameters in outbred albino mice. These findings warrant further investigation and reinforce the need to minimize exposure to insecticide in both natural field settings and the broader environment.
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PMID:Outcomes of Schistosoma mansoni infection in outbred albino mice exposed to Larvin contaminant. 1851 77

We assessed the prevalence of impaired liver function in 47 patients suffering from brucellosis consecutively admitted to our department over the last five years. Parameters of liver function and ultrasound of the upper abdomen were performed at entry and at the end of treatment. On admission, mean transaminase values were elevated and significantly higher than at recovery (p 0.001): 38 percent and 53 percent of patients had elevated baseline values of GOT and GPT vs 13 and 19% at the end of treatment, respectively. Mean serum values of alkaline phosphatase (AP) were within normal limits on admission, although in 12 of them serum values were elevated. The same proportion was seen for gamma-glutamyltranspeptidase. Both transaminases and AP were elevated in 8 patients (17 percent). There were no significant differences in serum values of albumin and bilirubin before and after therapy. The platelet count slightly decreased, but not significantly, during the acute phase of disease. At ultrasound one third of the patients showed hepatomegaly with a hepatitis-like pattern and 40 percent of patients had splenomegaly. In conclusion, this study confirms data in the literature showing a high frequency of liver impairment during the course of brucellosis, which is usually mild-moderate.
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PMID:[Abnormal liver function in brucellosis]. 1884 12

Male rats were administered one of three biodiesels - soy oil methyl ester (SoME-2), canola oil methyl ester (CaME-2), and methyl ester of animal frying oil (FrAME-1) at 5, 50 and 500 mg/kg, or ultra-low sulphur diesel (ULSD) at 500 mg/kg. Control was administered the vehicle (corn oil) only. After 4-week treatment, serum methanol and formic acid were unchanged or minimally elevated in all treatment groups. Mild histopathological changes in the liver were observed in animals receiving 500 mg/kg biodiesels and ULSD but hepatomegaly, increased phase I and II drug-metabolizing enzyme activities and urinary ascorbic acid were found only in the ULSD group. The ULSD group had increased kidney weight, changes in kidney histopathology, and increased urinary albumin and N-acetylgluocosaminidase activity. Biodiesels and ULSD caused increase in hepatic acyl-CoA oxidase activity. ULSD and FrAME-1 caused decrease in serum free fatty acid while CaME-2 caused decreases in both serum triglycerides and free fatty acids. FrAME-1 produced an increase in liver protein carbonyls and ULSD caused increased liver glutathione. The results indicated that ULSD caused more histopathological and biochemical effects than biodiesels. Biodiesels produced lipid effects and oxidative stress that were feedstock-dependent. The mechanisms and significance of increased hepatic acyl-CoA oxidase activity required further study.
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PMID:Short-term oral toxicity of three biodiesels and an ultra-low sulfur diesel in male rats. 1932 20

A 12-year-old, neutered male, mixed-breed dog was presented to The Ohio State University Veterinary Teaching Hospital with a history of weight loss and weakness. Laboratory abnormalities reported by the referring veterinarian during the past year included increased alkaline phosphatase (ALP) activity, hyperalbuminemia, and nonregenerative anemia. On referral, the dog appeared hydrated and had moderate muscle wasting and hepatomegaly. A large lobular hepatic mass was observed ultrasonographically. Laboratory results included mild to moderate nonregenerative anemia, urine-specific gravity of 1.035, 3+ proteinuria, increased serum activities of alanine aminotransferase (229 U/L, reference interval 10-55 U/L), ALP (813 U/L, reference interval 15-120 U/L), and the steroid-induced isoform of ALP (676 U/L, reference interval 0-6 U/L), marked hyperalbuminemia (5.3 g/dL, reference interval 2.9-4.2 g/dL), and an increased A/G ratio (1.7). Hyperalbuminemia was confirmed by reanalysis on 2 different analyzers and by agarose gel electrophoresis, and colloid osmotic pressure (COP) was markedly increased (42.5 mmHg, reference interval 20-25 mmHg). Cytologic examination of a fine-needle aspirate of the hepatic mass indicated hepatocellular proliferation; histologic examination of an excisional biopsy confirmed hepatocellular carcinoma. Three weeks after surgery, the albumin concentration, A/G ratio, COP, and ALT activity had normalized, but ALP activities remained high. We hypothesized that hyperalbuminemia developed secondary to hepatocellular carcinoma due to increased synthesis of albumin by malignant hepatocytes or due to decreased negative feedback from impaired hepatocellular osmoreceptivity. Hepatocellular carcinoma has been associated with paraneoplastic secretion of other proteins, but hyperalbuminemia has been reported only once in a human patient and has not previously in dogs.
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PMID:Hyperalbuminemia associated with hepatocellular carcinoma in a dog. 1947 32


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