[Visual acuity loss, the initial sympton of a spinal cord neoplasm]. / Disminución de agudeza visual, primer síntoma de un tumor medular.

CASE REPORT: A 46-year-old woman, who presented with right visual acuity loss, was found to have papilledema, and subsequently shown to have ventricular dilatation in a cerebral Magnetic Resonance Imaging (MRI) assessment. Elevated protein levels were found in the cerebrospinal fluid. Spinal MRI revealed the presence of a spinal cord neoplasm. After surgical removal of the tumor, which turned out to be a neurilemmoma, the patient's visual acuity was restored. DISCUSSION: The ocular presentation and the relationship between intracranial hypertension and spinal tumors are discussed. Likewise, the importance of considering the various causes of papilledema is emphasized.

Phenothiazine-induced cholestatic jaundice.

Proposed mechanisms, clinical features, prevalence, and treatment of phenothiazine-induced cholestatic jaundice are reviewed, and interactions between phenothiazines and other drugs that could theoretically alter the risk of cholestasis are described. Phenothiazine-induced jaundice is classified as a form of cholestatic hepatocanalicular hepatotoxicity and as an acute liver disease. Occasionally cholestatic jaundice may progress to chronic liver disease. The mechanism of hepatotoxicity is not completely understood but may involve a combination of physiochemical, immune, and direct toxic effects. Based on proposed mechanisms, concomitant use of drugs that alter microsomal hepatic enzyme function or have metabolic pathways that interfere with or overlap with those of the phenothiazines could be expected to potentiate or reduce the risk of cholestasis. The estimated prevalence of jaundice with chlorpromazine is 1-2%. The prevalence of jaundice with other phenothiazines is probably similar. The onset of jaundice usually occurs during the first one to four weeks of therapy. In most cases, discontinuation of the offending drug is the only treatment required. Jaundice usually resolves without sequelae two to eight weeks later. Pruritus can be relieved by topical corticosteroid or analgesic therapies or by oral antihistamines or bile acid sequestrants if topical therapy is ineffective. Whenever possible, reinstitution of neuroleptic therapy should be delayed until the reaction has resolved. Selection of a nonphenothiazine neuroleptic agent may be preferred. Phenothiazine-induced cholestatic jaundice occurs relatively infrequently and is usually self-limited; topical agents and oral antihistamines can alleviate the discomfort associated with the reaction.