565
Delusional bovine spongiform
encephalopathy S!R,—Dr Howard and Dr Castle (Aug 4, p 316) report a high level of concern among medical staff at the Maudsley Hospital about bovine spongiform encephalopathy (BSE). This concern affects our patients too, possibly in a less rational manner. An 80-year-old widow with a 12-year history of schizo-affective disorder relapsed with a florid paranoid psychosis followed by a depressive episode with agitation and somatic complaints. She spontaneously began to believe that she had acquired "mad cow disease" (MCD). Soon after eating a meal of minced beef, she complained of unsteady gait, blurred vision, and a dry mouth. In support of her belief she cited the fact that she was being treated at a psychiatric hospital (she was, however, not aware of Howard and Castle’s study). She would not accept reassurances that she did not have BSE or that her symptoms might be side-effects of drugs (dothiepen and flupenthixol). The belief that she had MCD was firmly held and she thought that she would die from it. She presented to the local casualty department and to a general practitioner complaining of the illness. One of the doctors she encountered assured her that the incubation period was four months. This did little to reduce her (or our) anxiety. As she recovered she continued to believe that she had MCD but affected an indifference to the diagnosis and no longer believed that she would die from it. This case illustrates the ease with which current concerns are incorporated into the content of delusions by some patients. It is perhaps ironic that the first case of delusional MCD should occur in a hospital where most surveyed doctors were so concerned that they ate less beef or had given it up altogether. It is interesting to speculate whether delusional MCD in patients might correlate with BSE anxiety in their doctors. However, this sole case probably does not have implications for menu planners in hospital canteens. The Maudsley Hospital, London SE5 8AZ, UK
SIMON LOVESTONE
Fluconazole-induced jaundice SIR,-Fluconazole has been used extensively for
patients
lymphocytes were 20/pl. Zidovudine was continued throughout the period of worsening jaundice and only withdrawn briefly after the bilirubin had started to fall. Fluconazole was stopped on Nov 21 and bilirubin and aspartate transaminase levels fell (figure). The patient began to feel
1990
in bilirubin (0), aspartate transaminase alkaline phosphatase (8).
Changes
(.),
and
better and started eating again. The presence of factor VIII inhibitor contraindicated liver biopsy. This patient had previously been diagnosed, on clinical grounds, as having chronic non-A, non-B hepatitis and was naturally immune to hepatitis B. Despite this evidence of pre-existing liver damage the temporal relation between stopping fluconazole and improvement in liver function leads us to the conclusion that fluconazole caused his jaundice. De Wit and colleagues! and Holmes and Clements2 have reported abnormal liver-function tests associated with fluconazole. Our experience in this case suggests the need for caution in the use of fluconazole, especially when a long course of therapy may be required or when the patient has pre-existing liver disease.
mucocutaneous
with HIV infection since its launch in January, 1989. Studies on the drug before it came onto the market had suggested that it causes little or no hepatotoxicity; if substantiated, this would be a major advantage over ketoconazole. A 41-year-old man with severe haemophilia and antibodies to factor VIII had a verv severe bleed in 1984 for which factor VIII concentrate and ’Feiba’ (Immuno, UK) were given. During this episode he had a brief febrile illness that may have indicated acute HIV infection; by November, 1984, he was seropositive for antibody to HIV. By May, 1988, he had no signs of HIV infection but in August of that year oral candidiasis developed and investigations revealed lymphopenia (T4 helper lymphocytes 330/u.I) and slightly abnormal liver function with a moderately raised aspartate transaminase. By November, 1988, he had further episodes of oral candidiasis and was put on oral zidovudine 1200 mg per day in divided doses. His T4 helper cell count was now 150/ul. A recurrence of the fungus infection, December, 1988, was treated with fluconazole 50 mg daily for 10 days. The next recurrence was in May, 1989, and again a 10-day course of fluconazole eradicated it. T4 helper lymphocytes had fallen to 80/ul. A further short course of fluconazole was required in June, 1989, and fluconazole was restarted on Sept 14, when candida was isolated from the throat and faeces. By Nov 18, while still taking fluconazole, he had become jaundiced, with nausea, anorexia, and itching. He had ankle oedema and a tender liver but no evidence of liver disease otherwise. Besides fluconazole 50 mg daily he was taking zidovudine, trimethoprim, and nystatin. His T44 helper candidiasis in
1989
Department of Haematology, Queen Elizabeth Hospital, Birmingham B15 2TH, UK
I. M. FRANKLIN E. ELIAS C. HIRSCH
1. De Wit F, Weerts D, Gooffens H, Clumeck N. Comparison of fluconazole and ketoconazole for oropharyngeal candidiasis in AIDS. Lancet 1989; i: 746-48. 2. Holmes J, Clements D. Jaundice in HIV positive haemophiliac. Lancet 1989; i: 1027.
Cyclophosphamide for chronic relapsing thrombotic thrombocytopenic purpura SIR,-Dr Lenz and colleagues (June 30, p 1593) describe a case of chronic relapsing thrombotic thrombocytopenic purpura (TTP) which responded to splenectomy. We report a 26-year-old woman whose disease remitted with cyclophosphamide. She presented in 1982 with a spontaneous abortion and was found to be anaemic and thrombocytopenic; steroids were administered. In October, 1985, gum bleeding developed and she became confused. Her haemoglobin was 10-8 g/dl and platelet count 17 000/ul. She had pronounced red-cell fragmentation and creatinine clearance was 82-5 ml/min. TTP was diagnosed and remission was induced with repeated infusions of fresh-frozen plasma. Over the next 38 months she had eight acute relapses characterised by paraesthesiae and pain in her fingers, bruising, thrombocytopenia (mean platelet count at relapse onset 40 000/ul, range 14 000-85 000), and microangiopathic anaemia. Therapy, including repeated plasmapheresis (all eight relapses), vincristine (six), high-dose methylprednisolone (two), and intravenous immunoglobulin (one), resulted in normal platelet counts every time, the mean duration of thrombocytopenia being 16 days. However, the remissions were shortlived (87 days on average, range 19-183) and she became allergic to fresh-frozen plasma. Aspirin and dipyridamole failed to prevent the relapses. In December, 1988, the
Delusional bovine spongiform
encephalopathy S!R,—Dr Howard and Dr Castle (Aug 4, p 316) report a high level of concern among medical staff at the Maudsley Hospital about bovine spongiform encephalopathy (BSE). This concern affects our patients too, possibly in a less rational manner. An 80-year-old widow with a 12-year history of schizo-affective disorder relapsed with a florid paranoid psychosis followed by a depressive episode with agitation and somatic complaints. She spontaneously began to believe that she had acquired "mad cow disease" (MCD). Soon after eating a meal of minced beef, she complained of unsteady gait, blurred vision, and a dry mouth. In support of her belief she cited the fact that she was being treated at a psychiatric hospital (she was, however, not aware of Howard and Castle’s study). She would not accept reassurances that she did not have BSE or that her symptoms might be side-effects of drugs (dothiepen and flupenthixol). The belief that she had MCD was firmly held and she thought that she would die from it. She presented to the local casualty department and to a general practitioner complaining of the illness. One of the doctors she encountered assured her that the incubation period was four months. This did little to reduce her (or our) anxiety. As she recovered she continued to believe that she had MCD but affected an indifference to the diagnosis and no longer believed that she would die from it. This case illustrates the ease with which current concerns are incorporated into the content of delusions by some patients. It is perhaps ironic that the first case of delusional MCD should occur in a hospital where most surveyed doctors were so concerned that they ate less beef or had given it up altogether. It is interesting to speculate whether delusional MCD in patients might correlate with BSE anxiety in their doctors. However, this sole case probably does not have implications for menu planners in hospital canteens. The Maudsley Hospital, London SE5 8AZ, UK
SIMON LOVESTONE
Fluconazole-induced jaundice SIR,-Fluconazole has been used extensively for
patients
lymphocytes were 20/pl. Zidovudine was continued throughout the period of worsening jaundice and only withdrawn briefly after the bilirubin had started to fall. Fluconazole was stopped on Nov 21 and bilirubin and aspartate transaminase levels fell (figure). The patient began to feel
1990
in bilirubin (0), aspartate transaminase alkaline phosphatase (8).
Changes
(.),
and
better and started eating again. The presence of factor VIII inhibitor contraindicated liver biopsy. This patient had previously been diagnosed, on clinical grounds, as having chronic non-A, non-B hepatitis and was naturally immune to hepatitis B. Despite this evidence of pre-existing liver damage the temporal relation between stopping fluconazole and improvement in liver function leads us to the conclusion that fluconazole caused his jaundice. De Wit and colleagues! and Holmes and Clements2 have reported abnormal liver-function tests associated with fluconazole. Our experience in this case suggests the need for caution in the use of fluconazole, especially when a long course of therapy may be required or when the patient has pre-existing liver disease.
mucocutaneous
with HIV infection since its launch in January, 1989. Studies on the drug before it came onto the market had suggested that it causes little or no hepatotoxicity; if substantiated, this would be a major advantage over ketoconazole. A 41-year-old man with severe haemophilia and antibodies to factor VIII had a verv severe bleed in 1984 for which factor VIII concentrate and ’Feiba’ (Immuno, UK) were given. During this episode he had a brief febrile illness that may have indicated acute HIV infection; by November, 1984, he was seropositive for antibody to HIV. By May, 1988, he had no signs of HIV infection but in August of that year oral candidiasis developed and investigations revealed lymphopenia (T4 helper lymphocytes 330/u.I) and slightly abnormal liver function with a moderately raised aspartate transaminase. By November, 1988, he had further episodes of oral candidiasis and was put on oral zidovudine 1200 mg per day in divided doses. His T4 helper cell count was now 150/ul. A recurrence of the fungus infection, December, 1988, was treated with fluconazole 50 mg daily for 10 days. The next recurrence was in May, 1989, and again a 10-day course of fluconazole eradicated it. T4 helper lymphocytes had fallen to 80/ul. A further short course of fluconazole was required in June, 1989, and fluconazole was restarted on Sept 14, when candida was isolated from the throat and faeces. By Nov 18, while still taking fluconazole, he had become jaundiced, with nausea, anorexia, and itching. He had ankle oedema and a tender liver but no evidence of liver disease otherwise. Besides fluconazole 50 mg daily he was taking zidovudine, trimethoprim, and nystatin. His T44 helper candidiasis in
1989
Department of Haematology, Queen Elizabeth Hospital, Birmingham B15 2TH, UK
I. M. FRANKLIN E. ELIAS C. HIRSCH
1. De Wit F, Weerts D, Gooffens H, Clumeck N. Comparison of fluconazole and ketoconazole for oropharyngeal candidiasis in AIDS. Lancet 1989; i: 746-48. 2. Holmes J, Clements D. Jaundice in HIV positive haemophiliac. Lancet 1989; i: 1027.
Cyclophosphamide for chronic relapsing thrombotic thrombocytopenic purpura SIR,-Dr Lenz and colleagues (June 30, p 1593) describe a case of chronic relapsing thrombotic thrombocytopenic purpura (TTP) which responded to splenectomy. We report a 26-year-old woman whose disease remitted with cyclophosphamide. She presented in 1982 with a spontaneous abortion and was found to be anaemic and thrombocytopenic; steroids were administered. In October, 1985, gum bleeding developed and she became confused. Her haemoglobin was 10-8 g/dl and platelet count 17 000/ul. She had pronounced red-cell fragmentation and creatinine clearance was 82-5 ml/min. TTP was diagnosed and remission was induced with repeated infusions of fresh-frozen plasma. Over the next 38 months she had eight acute relapses characterised by paraesthesiae and pain in her fingers, bruising, thrombocytopenia (mean platelet count at relapse onset 40 000/ul, range 14 000-85 000), and microangiopathic anaemia. Therapy, including repeated plasmapheresis (all eight relapses), vincristine (six), high-dose methylprednisolone (two), and intravenous immunoglobulin (one), resulted in normal platelet counts every time, the mean duration of thrombocytopenia being 16 days. However, the remissions were shortlived (87 days on average, range 19-183) and she became allergic to fresh-frozen plasma. Aspirin and dipyridamole failed to prevent the relapses. In December, 1988, the
