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Lovastatin, a drug that lowers blood cholesterol levels, is associated with muscle damage in some cases. However, excessive exercise itself can cause some of the same symptoms; in patients who take lovastatin and who also exercise, the effects could be more pronounced. To evaluate this, 10 healthy men were studied after they took either lovastatin or a placebo (inactive) pill for a month according to a cross-over design in which each subject served as his own control. The subjects underwent physical examination and blood testing before the study began; their levels of cholesterol and creatine kinase (CK), a measure of muscle damage, were noted. After completing their medication, they returned for cholesterol measurements and one hour of exercise on a downhill treadmill. Blood samples were obtained at regular intervals during the hour for determination of CK levels. Results showed that the cholesterol level did not change after one month's ingestion of placebo, but that it fell by an average of 58 milligrams per deciliter after lovastatin. After lovastatin, blood CK levels increased from 114 units per liter to an average maximum of 168 units per liter; after placebo treatment, they rose from 101 units per liter to an average peak of 147 units per liter. Lovastatin did not lead to a significantly greater increase in CK concentrations than the placebo drug. Reports in the medical literature concerning muscle damage associated with lovastatin have been based primarily on patients who took other potent medication, as well. This study allowed the lovastatin to be evaluated as an independent risk factor for such damage. (Consumer Summary produced by Reliance Medical Information, Inc.)

Phenytoin Absorption in Volunteers Receiving Selected Enteral Feedings The first documentation of poor absorption of oral phenytoin in patients receiving continuous enteral tube feedings was by Bauer in 1982. [1] [...]

ALTHOUGH a number of standard textbooks and reference sources indicate that psychosis can occur during procainamide hydrochloride administration, we found few cases of documentation. To our knowledge, the following case report is the first detailed description of such a psychosis.Report of a CaseA 45-year-old man was admitted to the medical intensive care unit after a routine ECG showed unifocal premature ventricular contractions (PVCs) of 16 to 22/min, with occasional periods of bigeminy. He gave no history of cardiac symptoms or illness. Hospital records verified intermittent psychotic behavior during a ten-year period, which was thought to reflect a manic-depressive illness.On admission, his medications consisted of lithium carbonate, 300 mg four times a day (serum lithium level, 0.55 mEq/liter); haloperidol, 2 mg twice daily; and trihexphenidyl hydrochloride, 5 mg daily. Evaluation by a cardiologist failed to show any obvious cause for the arrhythmia. Lithium therapy was discontinued without any

• Phenytoin, administered by suspension into a feeding tube through which continuous enteral feedings are being given, is very poorly absorbed. There appears to be very little information regarding this potentially serious problem in the general medical literature. Commonly used doses of phenytoin (300 to 500 mg/d) may result in almost undetectable serum levels. Therapeutic phenytoin levels may be obtained if a very large dose of the drug is given. Our patient required 1800 mg daily In two divided doses to get a serum phenytoin level of 9 μg/mL. Commonly used enteral feedings were being delivered by way of a continuous infusion pump. We found one enteral feeding product that did not severely impair the absorption of phenytoin. The mechanism by which enteral feedings Impair phenytoin absorption is unknown.(Arch Intern Med 1987;147:1821)

We appreciate Dr Menken's comments and the opportunity to respond. We were not suggesting that this patient's behavior was due to a functional psychosis but only that his mental status examination was consistent with such a state. By this we meant that schizo-affective disorders are occasionally similar and that disorientation and impairment of memory, information, and ability to calculate were never such that would be inconsistent with manicdepressive illness or schizophrenia. Alterations in motor activity, sleep patterns, attention span, affect, social restraint, and judgment were present but were nonspecific findings and did not help clarify the diagnosis. We believe that this episode of aberrant behavior was drug induced (organic) but that delirium was absent. Because organic mental disorders can occur without evidence of delirium, they can imitate a variety of psychiatric syndromes. Perhaps the best known example of this is reserpine-induced depression. We described this patient as having

TO THE EDITOR. —We agree with Labadie and Hamilton1 that successful treatment of coccidioidal meningitis requires doses of amphotericin that exceed doses previously recommended. Since doses given less frequently than daily may not be fungistatic,2 we have attempted to treat patients every day with 1 mg of amphotericin B. In our experience, required dosages often exceed 80 mg. However, a significant obstacle to adequate therapy has been poor patient compliance because of the severe headaches and vomiting caused by intracisternal administration of amphotericin B.The use of a subcutaneous reservoir with access to the cisterna magna has facilitated therapy, in spite of the need for frequent reservoir revisions and complicating infections.2 This route of administration is more comfortable and results in fewer significant neurologic complications than does direct cisternal puncture. We abandoned lumbar intrathecal injections because of the almost universal appearance of permanent neurologic injury to the