Oral sex and recurrent vulvo-vaginal candidiasis.

(foscarnet) are effective in slowing the progress of CMV retinitis;23 however, neither is free from toxicity. Both drugs require life-long intravenous administration and ganciclovir may cause bone marrow suppression, while foscarnet may cause renal impairment.4 We have retrospectively reviewed our experience ofCMV retinitis over the period from January 1986 to August 1990 in order to examine survival trends, rates of relapse and complications of treatment. CMV retinitis was diagnosed on the basis of fundoscopic examination which showed perivascular haemorrhage, exudates and/or periphlebitis typical of CMV retinitis, in 46 patients (45 were homosexual men and one was a bisexual man). Mean age at diagnosis was 36.4 years. All patients received ganciclovir at an initial dose of 10 mg/kg/day for 1 days, followed by maintenance therapy of 5 mg/kg/day using a central venous Hickman catheter. A fall in haemoglobin to below 8 g/dl, total white blood cell count below 1 x 109/l, or platelet count below 20 x 109/1 was regarded as unacceptable toxicity. Foscarnet therapy was introduced either in the event of haematological toxicity to ganciclovir or failure of response to ganciclovir with evidence of progressive retinitis. Median survival following the diagnosis of CMV retinitis was 7 (range 1 to 29) months and did not change significantly over the study period. In two patients CMV retinitis was the presenting AIDS diagnosis; 44 patients had a previous AIDS defining diagnosis. Complications arising as a result oftreatment were common. Only 12 of the 46 cases studied reported no further deterioration in vision and experienced no complications of treatment. This subgroup had a median survival of five months. Overall, haematological toxicity occurred in 16 patients; in 11 haemoglobin levels fell below 8 g/dl, necessitating discontinuation of ganciclovir treatment, with or without transfusion; three patients developed thrombocytopenia, two as part of a pancytopenia and one as an isolated phenomenon requiring platelet transfusion. All these patients recovered adequate haematological function when ganciclovir was stopped. One patient suffered severe nausea and vomiting after the introduction ofganciclovir and elected to stop treatment. Problems related to venous access occurred in nine patients. Hickman line sepsis occurred in five, in two of these Staphyloccocus aureus was isolated as the causal organism and in two Staphyloccocus epidermidis; in one patient it was necessary to remove the central venous line and administer ganciclovir via a peripheral cannula. Axillary vein thrombosis occurred in four patients; three were successfully treated by anticoagulation, in one the line was removed. One Hickman line had to be resited due to intolerable discomfort at the original insertion site. Therapy was changed to foscarnet in nine cases; in four this was because of haematological toxicity and in five because of progressive retinitis. Four of these five patients also experienced toxicity from foscarnet. One patient developed acute renal failure three days after starting therapy, another experienced severe vomiting and hypokalaemia, one developed penile ulceration and one became hypercalcaemic, in all cases it was necessary to stop foscarnet treatment. In our cohort survival following a diagnosis ofCMV retinitis did not improve from 1986 to 1990, despite the introduction of zidovudine and primary and secondary prophylaxis against Pneumocystis carinii pneumonia. The median survival of seven months is consistent with data from other studies.5 Overall, less than one quarter of our patients were treated without complications or progressive disease. Since the completion of this study a number of changes in clinical practice have been introduced. It has now become standard practice to discontinue zidovudine therapy whilst patients are taking high dose ganciclovir, reducing the potential for drug induced myelotoxicity.6 The introduction of pre-prepared ganciclovir, with the dose individually tailored to the patient's requirements by the manufacturer removes the need for the patient to draw up his/her own drug and may reduce the risk of Hickman line sepsis. Finally CMV resistant to standard therapy and relapsing disease may now be treated with concomitant ganciclovir and foscarnet, although the success of this therapy is yet to be evaluated. JK EVANS A SCOULAR RF MILLER Departments of Genitourinary Medicine and Medicine, UCMSM, Middlesex Hospital, London WIN8AA, UK