Search PubMed⌕ Search

Biomedical subjects

B H Stricker

Publications and source records attributed to B H Stricker.

At least 199 records · Page 11Linked to original sources
PubMed1987

Optic neuropathy and amiodarone therapy.

Optic neuropathy has been diagnosed in several amiodarone-treated patients, including the 13 patients described in this report. The clinical severity of this drug-related optic neuropathy is milder than that characteristically described in anterior ischemic optic neuropathy. The incidence of occurrence was significantly higher than that found in an age-matched general population sample. Whether this result was due solely to amiodarone therapy, to the underlying poor health of these patients, or to a combination of these two factors is uncertain. The findings in this study prompt us to recommend that all patients who receive amiodarone undergo complete ophthalmologic examinations, including careful evaluation of the ocular fundus regularly during such therapy. Appearance of optic neuropathy is probably a relative indication for discontinuing the use of the drug, in the hopes of avoiding bilateral involvement or perhaps recovering vision. The risks of complications of amiodarone treatment must be weighed against the benefit of therapy in patients whose lives are threatened by cardiac arrhythmias. On the basis of this study, the benefits of treatment seem to outweigh the small risk of optic neuropathy. No randomized study has been undertaken to determine the true incidence of complications associated with this medication and at this time could not be justified.

Aged↗
PubMed1987

Pirprofen-associated hepatic injury.

Four cases of hepatic injury attributed to the use of pirprofen (Rengasil) were reported to the Monitoring Centres for Adverse Reactions of Belgium, The Netherlands and the German Medical Association. One man and three women developed severe hepatic injury between 3 1/2 and 6 1/2 months after starting treatment with 400-1200 mg pirprofen daily. Histology showed acute hepatocellular damage, often with bridging necrosis. Two patients died. The other two patients made an incomplete recovery. It is possible that this severe type of hepatic injury is due to a metabolic idiosyncrasy to pirprofen, as this reaction seems to be rare and unpredictable but is not associated with immunoallergic signs.

Adult↗
PubMed1986

Fever induced by labetalol.

Fever caused by beta-adrenoceptor blocking agents is rare. We describe fever in two patients who had been treated with labetalol. In both patients, two challenge periods were rapidly followed by a relapse, whereas on each occasion there was normalization of temperature after discontinuation of the drug therapy. This reaction is rare and unpredictable. Because there was a clear sensitization period of three to four weeks, dose independency, and an accelerated reaction to rechallenge, this adverse effect seems to be caused by an immunoallergic reaction.

Aged↗
PubMed1986

Ketoconazole-associated hepatic injury. A clinicopathological study of 55 cases.

Fifty-five cases of ketoconazole-associated hepatic injury, reported to the Netherlands Centre for Monitoring of Adverse Reactions to Drugs, were analysed in detail. In 50 cases a causal relationship was considered likely, i.e. 'probable' (27 cases) or 'possible' (23 cases). Eighty-four % of individuals were women. Forty-six % of patients were over 50 years of age which suggests that, considering the lower prescription rate in this age group, the elderly are more vulnerable to ketoconazole. In 60% of all cases hepatic injury appeared within the first 6 weeks of therapy but in the group of 'probable'-cases the onset was mostly later. Jaundice was present in 44% of all cases but in 63% of the group of 'probable'-cases. Eosinophilia (10%), fever (6%) and rash (2%) were uncommon. Biochemically the pattern was hepatocellular in 54%, cholestatic in 16% and mixed cholestatic-hepatocellular in 30%. Histology (14 cases) showed a predominantly hepatocellular pattern in 57% with extensive centrilobular necrosis and mild to moderate bridging. In 43% cholestasis predominated. None of the cases had a fatal course. The incidence of symptomatic hepatic injury may be estimated at approximately 1:2000 but is probably higher. The mechanism of ketoconazole-induced hepatic injury seems to be based on metabolic idiosyncrasy although it is not excluded that in some patients an immunoallergic mechanism is causative.

Biopsy↗
PubMed1986

Glafenine-associated hepatic injury. Analysis of 38 cases and review of the literature.

Glafenine was associated with hepatic injury in 38 cases. The causal relationship was assessed on the basis of the temporal relationship with drug use, course and exclusion of other causes. In 27 cases a causal relationship was considered likely, i.e. 'probable' (12 cases) or 'possible' (15 cases), whereas in 11 cases it was either unlikely or unclassifiable. In both the 'probable' and 'possible' groups 60-70% of individuals were women. Jaundice was present in three-quarters of cases in both groups. Eosinophilia was more frequent in the group of 'probable' cases, and this group had the highest case-fatality rate (42%). Onset varied from 2 days (after a rechallenge) to 8 months, but most cases appeared between 2 weeks and 4 months after starting therapy. Histology in 22 cases showed a predominantly hepatocellular pattern, varying from spotty panlobular necrosis, centrilobular and (sub)massive necrosis (acute pattern) to fibrosis and cirrhosis (chronic pattern). The chemical structure of glafenine and the clinicopathological pattern it induces resemble that of cinchophen. The incidence is unknown. Either metabolic idiosyncrasy or an immunoallergic mechanism seems to be responsible.

Adult↗
PubMed1985

Thrombocytopenia and leucopenia with mianserin-dependent antibodies.

By indirect immunofluorescence specific mianserin-dependent antibodies were detected against platelets but not against granulocytes in the serum of a patient with thrombocytopenic purpura and mild leucopenia. A complement-mediated cytotoxicity assay demonstrated 70% lysis of granulocytes but no lysis of platelets, only when mianserin was added to the medium. We suggest that, at least in some patients, mianserin may cause blood disorders by an immunologically-mediated mechanism.

Aged↗