Metabolic acidosis drug related

Side effects are similar to the Nan- channel inhibitors, i.e. hyperkalaemia and metabolic acidosis. Side effects like gynacomastia and impotence are related to the steroid origin of the drug. It is contraindicated in patients with peptic ulceration. 

The most common and bothersome dose-related adverse effect of the oxazolidinediones is sedation. An unusual adverse effect is hemeralopia, a glare effect in which visual adaptation is impaired it is reversible upon withdrawal of the drug. Accumulation of dimethadione has been reported to cause a very mild metabolic acidosis. Trimethadione has been associated with many other toxic adverse effects, some of which are severe. These drugs should not be used during pregnancy. 

The primary adverse effect of intravenous cidofovir is a dose-dependent nephrotoxicity. Concurrent administration of other potentially nephrotoxic agents (eg, amphotericin B, aminoglycosides, nonsteroidal anti-inflammatory drugs, pentamidine, foscarnet) should be avoided. Prior administration of foscarnet may increase the risk of nephrotoxicity. Other potential side effects include uveitis, decreased intraocular pressure, and probenecid-related hypersensitivity reactions. Neutropenia and metabolic acidosis are rare. The drug caused mammary adenocarcinomas in rats and is embryotoxic. 

Acetazolamide toxicity was suspected, because of the temporal association between drug treatment and the onset of the neurological sjmptoms, together with metabolic acidosis. Gerstmann sjmdrome is usually due to an acute stroke. Although a brain CT scan was negative, such an event was likely in this patient, who had a history of cerebrovascular disease and multiple risk factors, and a causal relation to acetazolamide must be considered tenuous. 

Of about 50 patients with P-thalassemia who were treated with deferasirox, four (three children and one woman) developed Fanconi syndrome that was probably related to the drug [16 ]. The use of deferasirox (30 mg/kg/day in the children, 38 mg/ kg/day in the adult time to onset not specified) was followed by severe proximal renal tubular dysfunction characterized by hypokalemia, hypophosphatemia, glycosuria, and a metabolic acidosis. All recovered on withdrawal of deferasirox and electrolyte supplementation. The three children simultaneously had mild infections (gastrointestinal in two, respiratory in one) the woman had no other susceptibility factors for tubular dysfunction. 

Metformin has a half-life of 1.5-3 hours, is not bound to plasma proteins, is not metabolized, and is excreted by the kidneys as the active compound. As a consequence of metformin s blockade of gluconeogenesis, the drug may impair the hepatic metabolism of lactic acid. In patients with renal insufficiency, biguanides accumulate and thereby increase the risk of lactic acidosis, which appears to be a dose-related complication. 

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