Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients, aged 17 to 25 years, obtained lead and opium pills which had been stolen from retail pharmacists. They crushed them, suspended them in water an injected them intravenously. They developed general malaise, vomiting and constipation, and blood tests several weeks after injection of the pills showed raised alkaline phosphatase and aspartate transaminases. All four patients had negative tests for the hepatitis B surface antigen. Liver biopsy specimens showed persistent hepatitis in one and resolving hepatitis in the remaining three. Liver lead levels were grossly elevated in every case. The liver lead levels found it the patients described here were up to 35 times greater than levels which have been reported in industrial lead poisoning. It is postulated that the livers of patients with chronic lead poisoning are able to withstand this insult whereas in the cases described the overwhelming dose of lead was sufficient to cause hepatic damage.
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PMID:Acute lead poisoning: an unusual cause of hepatitis. 55 20

The effect of ip administrated aflatoxin B1 and rubratoxin B, singly and in combination, on dogs was determined by serum tests, by observations of clinical signs and survival times, and by evaluation of gross and microscopic lesions. The dog is sensitive to the toxic effects of both mycotoxins. Glutamic-oxaloacetic transaminase, lactic dehydrogenase and alkaline phosphatase activities and survival time varied in relation to dose and to the mycotoxin(s) administered. All three plasma enzymes were elevated regardless of dose with the combination of aflatoxin B1/rubratoxin B at 24 hr after dosing, except LDH, which was within the normal range but only at the lowest dose level. Several serum constituents including BUN, cholesterol, uric acid, and total bilirubin were elevated, whereas serum glucose was depressed in dogs treated with the multiple-toxin regimen; these changes were not seen in dogs given only aflatoxin B1 but were characteristic in rubratoxin-treated animals. In general, gross findings at necropsy were similar in all dogs regardless of the dose regimen. A striking similarity existed in the histologic changes observed between lesions experimentally induced by the mycotoxin combination and those lesions reported for dogs fed toxic feed in laboratory studies or in natural cases of hepatitis X. Of particular similarity were the severe kidney lesions observed in dogs exposed to the mycotoxin combination and kidney lesions reported in natural outbreaks of hepatitis X. There can be little doubt of an association between hepatitis X and aflatoxin B1, although it is apparent that the disease probably involves more than a single toxic factor. Our results suggest that hepatitis X in dogs includes aflatoxin B1 as a primary etiological factor but that rubratoxin B also may be involved.
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PMID:Acute toxicity of aflatoxin B1 and rubratoxin B in dogs. 58 96

The clinical course is reported in 17 patients in whom the histological picture of subacute hepatic necrosis ("bridging hepatitis") was found on needle liver biopsy or at autopsy. The patients' ages ranged from 10-71 years, 12 patients being less than 40 years old. Ten patients were males. Jaundice lasted 2-4 months in nine cases and over six months in two, one of the latter having developed cirrhosis. In five patients a relapse of jaundice occurred within three months. Hepatitis B antigen was found in one of 13 patients tested. Two patients died in fulminant hepatic failure, one developed cirrhosis. These three patients and an additional two received prednisone therapy. Twelve of the remaining patients were followed for periods of 8-81 months; an additional two patients' follow-up was incomplete. None developed clinical evidence of chronic liver disease, and laboratory data at the last examination were normal except for slight elevation of alkaline phosphatase in six cases. Repeat biopsies showed persistent hepatitis in one case, slight portal fibrosis in one, cirrhosis in one and at autopsy in a patient who died of unrelated causes two years after hepatitis no evidence of chronic liver disease was found. This relatively good outome of subacute hepatic necrosis is probably due to the young average age of the patients, and the low incidence of B hepatitis in this series.
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PMID:The clinical course of subacute hepatic necrosis. 74 11

Silymarin has been claimed to have a benificial effect in various types of liver injury. In a prospective study in patients with acute viral hepatitis (n = 151) the effectiveness of this drug on the cause of the disease was tested. The groups with and without Silymarin (Legalon) were comparable concerning age and sex distribution and the frequency of HBs-antigen positive hepatitis; Laboratory findings (total serum bilirubin, activity of GOT, GPT and alkaline phosphatase and prothrombin time) were determined in intervals of 5 to 7 days over a period of 5 weeks beginning with the onset of jaundice. There were no statistical significant differences between both groups in the decrease of mean values of all parameters tested. The frequency of nearly normalized values of transaminases and serum bilirubin after 10, 20 and 30 days was not higher in the group treated with Silymarin as compared to the controls. It is concluded that Silymarin has no favourable effects on the cause of acute viral hepatitis.
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PMID:[Silymarin for the treatment of acute viral hepatitis? Report of a controlled trial (author's transl)]. 84 Jan 25

I evaluated the diagnostic value of routinely ordered liver-function tests in 175 biopsy-proven cases of hepatic disease by use of stepwise discriminant analysis. The tests studied-total and "direct" bilirubin, alkaline phosphatase, lactate dehydrogenase, and aspartate aminotransferase-correctly classified 45-73% of cases, depending on the homogeneity of the diagnostic groups. Aspartate aminotransferase and alkaline phosphatase were the best discriminators. When all tests were used in the most homogeneous groups (tumors, cirrhosis, and hepatitis), there was a stepwise improvement in diagnostic accuracy from 51 to 73%.
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PMID:Diagnostic effectiveness of biochemical liver-function tests, as evaluated by discriminant function analysis. 84 56

The carried out investigations on 70 patients with epidemic hepatitis, 52 of them treated with prednisolon and 18-symptomatically revealed the following: the normal alkaline phosphatase, established prior to the treatment, was elevated with the applied prednisolon treatment and showed no significant alteration in the patients without cortico-therapy. No correlation was found between leukocyte alkaline phosphatase and serum alkaline phosphatase transaminase, serum bilirubin and thymol test. No relationship was found between the severity of the ailment course and the leukocyte alkaline phosphatase.
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PMID:[Leukocyte alkaline phosphatase in epidemic hepatitis]. 89 26

15 patients with primary biliary cirrhosis (PBC) and 109 patients with chronic aggressive hepatitis (CAH) have been followed. Features of PBC, namely the generalized pruritus, massive rise in alkaline phosphatase, antimitochondrial antibodies and high levels of IgM-globulins, were present in 7 patients with CAH. This group was treated with immunosuppressive drugs for 1-2 years. Clinical, biochemical, immunological and histological parameters were used to assess the therapeutic effect. The pruritus improved and there was a statistically significant reduction in the IgG-hyperglobulinemia. Some resolution of the piecemeal necroses was seen. However, in judging these changes the sampling error must be taken into account. The unknown agent attacks both the hepatocytes and the epithelial cells of the bile ducts. The immunosuppressive treatment protects the liver cells from further damage while the progressive destruction of the bile ducts remains uninfluenced. The results suggest that the smallest possible dose sufficient to suppress the activity of CAH must be selected.
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PMID:[Combined form of chronic aggressive hepatitis primary biliary cirrhosis]. 92 35

Distribution of the alkaline phosphatase and 5'-nucleotidase activity was studied in blood serum by means of gel filtration through Sephadex G-200 with jaundices of different origin. Both enzymes have two forms differing in the molecular weight, 5'-nucleotidase presenting mainly a high-molecular form in contrast to alkaline phosphatase. This form activity for both enzymes is higher with obturative jaundices as compared to liver cirrhosis and virus hepatitis. The results of incubating sera with desoxicholate and the subsequent gel filtration in its presence, as well as polyacrylamide gel electrophoresis of butanol extracts of the fractions containing high-molecular fragments, evidence for the fact that these fragments are lipoproteid complexes.
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PMID:[Two forms of alkaline phosphatase and 5'-nucleotidase in the serum of persons with jaundice of different origin]. 101 37

Fifteen patients with cholestatic disorders were treated for 1 to 5 months with phenobarbital. Primary biliary cirrhosis was diagnosed in seven, sclerosing cholangitis in two, intrahepatic biliary hypoplasia in three, and cholestatic hepatitis in three. Except for the patients with cholestatic hepatitis, in whom marked cholestasis was virtually the only abnormality in liver biopsy specimens, serum bilirubin and bile acid concentrations were diminished during therapy, the hepatic clearance of sulfobromophthalein and 131-I-rose bengal was variably enhanced, and there was relief from pruritus. Serum cholesterol concentrations and other measures of hepatic function were not significantly changed during therapy except for serum alkaline phosphatase activity, which rose in twelve patients. Parallel changes occurred in 5'-nucleotidase, suggesting a hepatic origin for the alkaline phosphatase activity. These studies indicate that phenobarbital therapy is associated with improvement in organic anion clearance in some patients with cholestatic disorders and may be beneficial to such patients.
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PMID:Phenobarbital effects in cholestatic liver diseases. 111 64

7 cases of pruritus in pregnancy are reported and their laboratory findings compared with a group of normal pregnant women; then pruritus is reviewed with respect to diagnosis, pathogenesis, therapy, and prognosis. The 7 women developed pruritus in 28-38 weeks of typically the 2nd pregnancy, although during oral contraception in 1 woman. The frequency was about 2/1000 pregnancies. Lab findings suggestive of cholestasis included normal prothrombin, elevated transaminaes, alkaline phosphatase, total bilirubin, total cholesterol, and slowed BSP clearance. None of these women had any history of hepatitis, medication, or positive Australia antigen. It is important in diagnosis to rule out infections, toxic or iatrogenic hepatitis, and especially herpes gestationis, which is teratogenic. Pruritus of pregnancy is identical to that seen during oral contraception, i.e., it is a less severe form of cholestatsis than jaundice. It can be treated with cholestyramine, or will regress spontaneously after delivery, but may cause prematurity.
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PMID:[Significance of pruritus during pregnancy. Relations with the hepatic disorders of gestation]. 113 31


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