A double-blind placebo-controlled crossover trial of intravenous magnesium sulfate for foscarnet-induced ionized hypocalcemia and hypomagnesemia in patients with AIDS and cytomegalovirus infection.

Foscarnet (trisodium phosphonoformate hexahydrate) is an antiviral agent used to treat cytomegalovirus disease in immunocompromised patients. One common side effect is acute ionized hypocalcemia and hypomagnesemia following intravenous administration. Foscarnet-induced ionized hypomagnesemia might contribute to ionized hypocalcemia by impairing excretion of preformed parathyroid hormone (PTH) or by producing target organ resistance. Prevention of ionized hypomagnesemia following foscarnet administration could blunt the development of ionized hypocalcemia. To determine whether intravenous magnesium ameliorates the decline in ionized calcium and/or magnesium following foscarnet infusions, MgSO(4) at doses of 1, 2, and 3 g was administered in a double-blind, placebo-controlled, randomized, crossover trial to 12 patients with AIDS and cytomegalovirus disease. Overall, increasing doses of MgSO(4) reduced or eliminated foscarnet-induced acute ionized hypomagnesemia. Supplementation, however, had no discernible effect on foscarnet-induced ionized hypocalcemia despite significant increases in serum PTH levels. No dose-related, clinically significant adverse events were found, suggesting that intravenous supplementation with up to 3 g of MgSO(4) was safe in this chronically ill population. Since parenteral MgSO(4) did not alter foscarnet-induced ionized hypocalcemia or symptoms associated with foscarnet, routine intravenous supplementation for patients with normal serum magnesium levels is not recommended during treatment with foscarnet.

Apophysomyces elegans infection in a renal transplant recipient.

A 50-year-old cadaveric renal transplant recipient on immunosuppressive therapy is described with post-traumatic cutaneous infection caused by Apophysomyces elegans. He showed no evidence of hematogenous dissemination and recovered fully after therapy with extensive local debridement and amphotericin B lipid complex. An apparent drug-drug interaction between amphotericin B lipid complex and cyclosporine was encountered. The course of A elegans infection in transplant recipients may be similar to that described in immunocompetent hosts. A elegans infection should be considered in evaluation of post-traumatic cutaneous infection not readily responsive to antibacterial therapy.

Paranasal sinus infection due to atypical mycobacteria in two patients with AIDS.

Atypical mycobacteria, which are common opportunistic pathogens in patients with AIDS, have not been previously implicated in the pathogenesis of paranasal sinus infections; we describe two such patients. Clinical and radiographic evidence of bilateral maxillary and ethmoid sinusitis was observed for one patient; his infection proved resistant to therapy with conventional antimicrobials and decongestants. Endoscopic ethmoid sinus biopsy yielded a specimen containing acid-fast bacilli (AFB) that were later identified as Mycobacterium kansasii. Antimycobacterial therapy had not resulted in amelioration of the sinusitis > 2 months later, at which time he died of cerebral toxoplasmosis. The second patient presented with a tender right frontotemporal soft-tissue mass; a computed tomogram disclosed that it extended through the frontal bone to the frontal sinus. Inflamed tissue debrided from the sinus contained AFB; cultures first yielded M. kansasii and later Mycobacterium avium complex. Bacteremia due to both organisms was also demonstrated. Infection progressed despite therapy.

Mupirocin resistance in methicillin-resistant Staphylococcus aureus from a veterans hospital.

679 clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) which occurred from 1986 and 1992 were retrospectively tested to determine the frequency of mupirocin resistance. With disk agar diffusion screening, 26 of 679 MRSA had zones of inhibition of < 18 mm using a 5 micrograms mupirocin disk. Minimal inhibitory concentrations (MICs) by agar dilution on the 26 suspect MRSA revealed that 9 were resistant. Of these 9, 1 had a MIC of 6.25, 4 of 12.5, 1 of 25, 1 of 500 and 2 of > 1,000 micrograms/ml. Although the overall incidence of mupirocin resistance was low in our hospital, 5 of the 9 resistant isolates occurred in 1992 and may signal a much more serious threat in the future.