Biomedical subjects

F Mullick

Publications and source records attributed to F Mullick.

4 recordsLinked to original sources

PubMed1991

Hypersensitivity myocarditis.

Autopsy tissue specimens of 69 cases of hypersensitivity myocarditis were studied to determine drug association, spectrum of histologic findings, distribution of infiltrates, and correlation between degree of infiltrates and cardiac symptoms. Hypersensitivity myocarditis was defined by the presence of eosinophils, a mixed lymphohistiocytic infiltrate along natural planes of separation, and an absence of fibrosis or granulation tissue in areas of infiltrate. Commonly implicated drugs were methyldopa, hydrochlorothiazide, ampicillin, furosemide, digoxin, tetracycline, aminophylline, phenytoin, benzodiazepines, and tricyclic antidepressants. Histiocytes composed the predominant cell type (in addition to eosinophils and lymphocytes). Lymphocytes were predominantly T cells in 12 cases studied immunohistochemically. Small foci of myocyte necrosis were present in 37 cases, and they correlated with the degree of infiltrate. A nonnecrotizing vasculitis was present in 28 cases. The right ventricle was involved in all but three cases. Cardiac arrhythmias or unexplained death occurred in 29 patients and did not correlate with the degree of myocardial infiltrate or presence of necrosis. Eosinophils were present in the livers of 30 of 58 patients, and their presence correlated with the degree of cardiac infiltration. A causative association between histologic findings and drugs is difficult to prove because of the common usage of many of the drugs implicated, multiple drug use, and the absence of clinical criteria of hypersensitivity. Symptoms do not appear related to the degree of infiltrate. In more than half the cases, infiltrates may be missed by endomyocardial biopsy due to focality of lesions.

Arrhythmias, Cardiac↗

PubMed1990

Pemoline-associated hepatic injury.

Among 100 cases of hepatic injury attributed to the administration of pemoline, 43 had sufficient accompanying information to permit analysis. All but two patients were less than 20 years old, and 80% were less than 12 years old. Males predominated the study. Injury appeared as early as 1 week or as late as greater than 1 year of taking the drug. The injury was uniformly hepatocellular as judged by the high values for aminotransferases and by death in massive necrosis in one patient. Mechanism was judged to be idiosyncratic, and the idiosyncrasy was probably metabolic rather than immunologic.

Adolescent↗

PubMed1990

Histopathologic analysis of suspected amiodarone hepatotoxicity.

This analysis of the morphology of suspected amiodarone (AD) liver disease is based on a study of liver specimens from 17 individuals. Changes similar to alcoholic liver injury were commonly seen. Steatosis, both macrovesicular and microvesicular, was the most frequent histopathologic feature. Ballooning of hepatocytes, Mallory bodies, and fibrosis were also common. Other changes included nuclear unrest, acidophilic bodies, foam cells, glycogenated nuclei, and portal inflammation. Characteristic lamellar lysosomal inclusion bodies representing phospholipidosis were found in two of 14 specimens studied ultrastructurally. These changes of pseudoalcoholic hepatitis and/or phospholipidosis were present in liver specimens from asymptomatic, anicteric patients with mild elevations in serum aminotransferase or alkaline phosphatase values with or without hepatomegaly, as well as in patients with clinically overt symptoms of hepatotoxicity. Phospholipidosis appears to be a generalized systemic effect of cationic amphophilic compounds, such as AD. The cytotoxic pseudoalcoholic changes appear to be an independent phenomenon in susceptible patients, whom we speculate may have been unable or less able to metabolize AD through normal pathways. The true incidence of hepatic injury from AD remains to be determined from prospective evaluations of pretreatment and follow-up liver biopsies.

Adolescent↗

PubMed1989

Amiodarone hepatotoxicity: prevalence and clinicopathologic correlations among 104 patients.

The prevalence of apparent amiodarone-related hepatic injury in 104 patients followed prospectively is compared to that reported in the literature. Asymptomatic elevation of serum aminotransferase levels was detected in approximately one-fourth of the patients, a figure similar to the average of reported cases. The frequency of extrahepatic organ toxicity was increased in patients with elevated levels. Symptomatic "hepatitis" developed in 3% of this series and in less than 1% of cases in the literature. Evidence of hepatic phospholipidosis and the development of pseudoalcoholic liver injury is most likely due to the biochemical effects of the drug and to possible metabolic idiosyncrasy, respectively. Serial blood enzyme measurements, as recommended by the manufacturer, may offer some protection against the development of more serious liver injury. However, levels of amiodarone may persist in various tissues for weeks to months following withdrawal, and stopping the drug does not guarantee the prompt reversal of any organ toxicity. Accordingly, the risks posed and benefits offered by amiodarone should be carefully weighed prior to discontinuing the drug, as the risk of sudden cardiac death may outweigh the hazards of ongoing hepatic, pulmonary or other toxicity.

Alanine Transaminase↗