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At least 451 records · Page 25Linked to original sources
PubMed2001

Liver dysfunction in late pregnancy: cytomegalovirus-induced hepatitis or the HELLP syndrome?

A 27-year-old primiparous preeclamptic woman developed a skin rash in late pregnancy and was persistently febrile for 10 days after giving birth. Blood tests suggested that she developed the HELLP syndrome and had concomitant cytomegalovirus (CMV) infection. Hemolysis, slightly impaired liver function, and thrombocytopenia were explainable by either only the CMV infection or only the HELLP syndrome. A literature review of a limited number of such cases and our case suggests that laboratory data in patients with CMV infection can mimic those of the HELLP syndrome. Thus, it may be important to consider CMV infection as a possible cause of abnormal laboratory data similar to the HELLP syndrome.

Adult↗
PubMed2000

Liver dysfunction due to apoptosis in a patient with systemic lupus erythematosus.

We report on a 23-year-old Japanese female with a 13-year history of systemic lupus erythematosus (SLE), and two episodes of deterioration followed by treatment with high dose prednisolone. Although she had been recently treated with prednisolone (12.5 mg daily), her liver function became worse in July 1998. Results of a liver biopsy revealed multi-focal hepatic cell death in a severe fatty liver, without any inflammatory cell invasion. The biopsy also showed a positive TUNEL (Tdt-catalysed DNA nick end labelling) reaction indicating apoptosis. Her liver function recovered rapidly following steroid pulse therapy. Serum soluble Fas ligand (sFasL) was found to be elevated to a concentration of 0.395 ng/ml at the time of liver damage, but was less than 0.03 ng/ml before liver damage and after prednisolone treatment. The liver damage in this case appeared to be involved with apoptosis induced by sFasL. Although hepatitis associated with SLE is rare, apoptosis directly related to elevated sFasL levels might cause this complication.

Adult↗
PubMed1983

Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper-respiratory-tract infection.

In a one-year prospective study we assessed the incidence of Reye's syndrome in children presenting with the acute onset of vomiting after a prodromal upper-respiratory-tract infection or varicella, and with serum alanine or aspartate aminotransferase levels at least three times higher than normal, and a paucity of neurologic findings. Of 25 patients meeting the above criteria, 19 had liver biopsies yielding adequate tissue for diagnostic purposes. Biopsy specimens from 14 of these 19 patients (74 per cent) were diagnostic of Reye's syndrome, according to rigorous light-microscopical, histochemical, and ultrastructural criteria. None of the biopsy specimens contained evidence of other acute pathologic processes, including hepatitis. A wide spectrum of mitochondrial alterations existed at the ultrastructural level, ranging from mild to severe lesions that were indistinguishable from those seen in comatose patients with Reye's syndrome. Our findings suggest that the clinical complex of vomiting, hepatic dysfunction, and minimal neurologic impairment after varicella or an upper-respiratory-tract infection usually represents Reye's syndrome. This syndrome occurs more frequently than previously recognized.

Adolescent↗
PubMed2005

Effect of Asteracantha longifolia Nees. against CCl4 induced liver dysfunction in rat.

Significant recovery after treatment with the whole plant slurry of A.longifolia Nees. was observed in plasma AST, ALT and cholesterol levels in CCl4 induced hepatotoxic rats. This was amply supported by electron micrographs, which indicated normalization of cytoarchitecture of mitochondria and endoplasmic reticulum. The results suggest that the slurry of the plant is useful as a liver tonic.

Acanthaceae↗
PubMed1987

Vasopressin-resistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report.

A case of transient nephrogenic diabetes insipidus occurred in late pregnancy, the first associated with biopsy-proven hepatitis. Five previously reported cases occurred in pregnancy. All six patients demonstrated similar but transient signs, symptoms and laboratory abnormalities suggesting a syndrome peculiar to pregnancy. The characteristics of this syndrome are elevated liver function studies, decreased renal function, hyperuricemia and transient vasopressin-resistant diabetes insipidus.

Adult↗
PubMed1984

Cholestatic liver dysfunction after long-term phenytoin therapy.

Cholestatic jaundice developed in a 64-year-old woman who had received phenytoin sodium for more than 40 years. Discontinuation of phenytoin therapy resulted in resolution of the hepatic abnormalities, which recurred on rechallenge, strongly suggesting a causal relation to the drug. Phenytoin therapy was discontinued again, with complete resolution of the hepatic abnormalities. The liver biopsy specimen obtained during therapy showed cholestasis compatible with obstruction of the biliary tree, although an obstructive process was never demonstrated. The biochemical abnormalities and histologic features observed most likely represent an unusual response to phenytoin therapy.

Chemical and Drug Induced Liver Injury↗
PubMed2006

[Alcohol abuse case of severe liver dysfunction induced by acetaminophen poisoning which was diagnosed as non-hepatic toxicity on admission].

A 41-year-old female attempted suicide by taking 7.8g acetaminophen and was transferred to our hospital four hours after ingestion. The patient was diagnosed as non-hepatic toxicity (below the line set by the Rumack Matthew nomogram). Laboratory data showed an elevation in serum liver enzymes and coagulation defects at 3 days after ingestion, therefore, the patient was treated with plasma exchange and an oral administration of N-acetylcysteine (NAC). The elevation of liver enzymes was maximal at 4 days after ingestion, and the laboratory data became normalized at approximately 9 days after ingestion. In this case, habitual alcohol intake may have exacerbated the severe liver injury. We should consider an exacerbation of hepatotoxicity and administer NAC in any case having a history of habitual alcohol intake, even if the case was diagnosed as non-hepatic toxicity by the nomogram.

Acetaminophen↗