Hematological effects of corticosteroids

Zinc intoxication may cause anemia by blocking the absorption of copper from the stomach and duodenum . [2] Zinc also upregulates the expression of chelator metallothionein in enterocytes , which are the majority of cells in the intestinal epithelium. [2] Since copper has a higher affinity for metallothionein than zinc, the copper will remain bound inside the enterocyte, which will be later eliminated through the lumen . [2] This mechanism is exploited therapeutically to achieve negative balance in Wilson’s disease , which involves an excess of copper. [2]

The most frequent adverse reactions to Efudex occur locally and are often related to an extension of the pharmacological activity of the drug. These include burning, crusting, allergic contact dermatitis , pruritus , scarring, rash, soreness, and ulceration . Ulcerations, other local reactions, cases of miscarriage and a birth defect ( ventricular septal defect ) have been reported when Efudex was applied to mucous membrane areas. Leukocytosis is the most frequent hematological side effect. Although a causal relationship is remote, other adverse reactions which have been reported infrequently are:

Riluzole is administered orally. Riluzole is highly bound to plasma protein (about 96%), mainly to albumin and lipoproteins. Hepatic metabolism is extensive, producing 6 major and a number of minor metabolites. The cytochrome P450 enzyme system is involved in hydroxylation and glucuronidation. The main isozyme involved in hydroxylation is CYP1A2. Approximately 90% of a dose is excreted in the urine; however, only 2% is excreted as unchanged drug. Elimination in the feces accounts for 5% of a dose. Riluzole is largely excreted as its glucuronide metabolites (85%). The elimination half-life is 12 hours.
Affected cytochrome P450 isoenzymes and drug transporters: CYP1A2
Riluzole is primarily metabolized by CYP1A2.

Hematological effects of corticosteroids

hematological effects of corticosteroids


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