Does acyclovir increase serum lithium levels?

A 42-year-old woman was admitted to the hospital to receive intravenous acyclovir for a herpes zoster infection. At the time she was taking lithium carbonate 450 mg twice/day. Six days after starting acyclovir she exhibited signs of lithium toxicity. When measured, the serum lithium level had increased 4-fold during acyclovir therapy. Both agents are excreted by the kidneys, raising the possibility that acyclovir at high serum concentrations may interfere with the renal excretion of lithium. A MEDLINE search did not identify any citation describing the possibility of an interaction between the drugs. This case suggests that acyclovir when given intravenously in doses of 10 mg/kg may result in increased serum lithium concentrations. Until additional data are available, if intravenous acyclovir is administered concurrently with lithium, we recommend closely monitoring patients for signs of lithium toxicity and measuring serum lithium levels every second or third day.

Opioid-induced muscle activity: implications for managing chronic pain.

OBJECTIVE: To increase awareness of opioid-induced involuntary muscle hyperactivity and to present management options. CASE SUMMARY: A ventilator-dependent 71-year-old man presented with pain caused by metastatic lung cancer. Transdermal fentanyl therapy was titrated to 200 micrograms/h. Two days later a continuous morphine infusion was initiated because of frequent administration of oral morphine solution for breakthrough pain. The patient became progressively less responsive and began exhibiting involuntary muscle hyperactivity thought to represent breakthrough pain. Despite the inability to assess pain control effectively in this unresponsive patient, the morphine infusion rate was increased from 22 to 717 mg/h within 7 days. No change in muscle hyperactivity was observed. DISCUSSION: Over the last decade involuntary muscle hyperactivity has been documented as an adverse effect of chronic opioid therapy. The literature describing the incidence of this toxicity, possible risk factors for its development, and recommendations for its management are discussed. CONCLUSIONS: The occurrence of muscle hyperactivity in an unresponsive patient receiving chronic opioid therapy may represent opioid toxicity. Recommendations for managing opioid-induced muscle hyperactivity include reduction of the opioid dosage and/or administration of clonazepam therapy.

Homoharringtonine-induced hyperglycemia.

Homoharringtonine (HHT) has been reported to induce hyperglycemia. This report describes a study conducted to characterize the effect of HHT on insulin production and action. Our data indicate that HHT-induced hyperglycemia results from the development of insulin resistance. A review of the literature suggests that patients receiving HHT continuous infusions of 5 mg/m2/d or greater and patients greater than 10 years of age may be at increased risk for the development of HHT-induced hyperglycemia. We recommend that patients with these risk factors, as well as diabetic patients and patients concurrently receiving asparaginase and/or prednisone, have their blood glucoses routinely monitored for hyperglycemia.

Excretion of hydroxyurea into milk.

This article documents that hydroxyurea (HUR) is excreted into human breast milk, and it reviews the literature describing similar evaluations for other antineoplastic agents.

Cytarabine-induced cerebellar syndrome: case report and literature review.

High-dose cytarabine (HDARAC) therapy is an effective regimen in treating refractory leukemias. A typical regimen is cytarabine 3 g/m2 iv over one to three hours q 12h for a total of 8 to 12 doses. This case report illustrates the neurotoxicity unique to HDARAC. The patient received two cycles of HDARAC over the course of a ten-week period. During the first treatment, dysarthria and ataxia were seen after completion of the patient's eighth and final dose of HDARAC. These symptoms resolved over a period of five days. Six weeks later a more severe syndrome of dysarthria and ataxia developed during a second cycle of treatment. These symptoms worsened over 24 hours despite discontinuation of therapy, then gradually decreased in severity but persisted until his death two months later. The neurotoxicity seen with HDARAC is dose-related and has occurred in up to 60 percent of treated patients. The incidence of cerebellar toxicity approaches 30 percent, with irreversible ataxia reported in up to 16.7 percent. Because the cerebellar toxicity may be worsened by continuation of therapy after initial onset of symptoms, prompt termination of HDARAC is recommended.

Impaired phenytoin bioavailability secondary to cisplatinum, vinblastine, and bleomycin.

A 24-year-old woman experienced grand mal seizures temporally related to cisplatin, vinblastine, and bleomycin (CVB) administration. A second episode of seizures occurred when the patient's phenytoin level was estimated to be in the range of 15 micrograms/ml. Her plasma phenytoin level at the time had dropped to 2 microgram/ml despite a recent dosage increase. To evaluate the cause of the subtherapeutic phenytoin levels, daily plasma phenytoin levels and 24-h urine collections were obtained during her next CVB cycle. Data revealed a mean phenytoin absorption of 32% (normal greater than 80%), establishing that phenytoin malabsorption occurred. The disruption of phenytoin absorption at a cellular level by CVB therapy is the proposed mechanism. Frequent monitoring of plasma phenytoin levels is recommended for patients receiving CVB.