{"title":"溶血性尿毒综合征并发播散性神经外隐球菌病。","authors":"A L Pozniak, S B Lucas, R F Miller","doi":"10.1136/sti.73.5.410","DOIUrl":null,"url":null,"abstract":"Case report (Dr R F Miller) A 33 year unemployed white man was admitted to hospital in January 1994 complaining of a 1 week history of diarrhoea, passing up to 30 stools per day. The stool consisted of watery yellow fluid without blood or mucus. He reported associated anorexia with intermittent nausea and vomiting together with left lower quadrant colicky abdominal pain and sweats but no fever. The patient had been seen in a local casualty department 4 days previously at which time he had reported 3 days of diarrhoea. At that time he reported that he was HIV antibody positive and examination had revealed no abnormalities. Investigations revealed normal urea and electrolytes, a haemoglobin of 10.4 g/dl, a total white blood count of 6.8 x 109/l, and a platelet count of 68 x 109/l. This latter finding was ascribed to the effects of HIV infection. The patient was treated symptomatically and discharged. On admission to hospital in January 1994 the patient reported that 72 months previously he had developed night sweats, gingivitis, and oral candidiasis. He had been admitted to another hospital in April 1988 with a chest infection and, in May of that year following a party, he had been admitted to the Middlesex Hospital with diarrhoea and vomiting. He subsequently reported that he had passed malaena stools and, in addition, stated that he had been found to be HIV positive in October 1987; this positive result was performed on a sample of serum stored from 1982. The investigation had been carried out at another hospital. On that admission in 1988 examination (including rectal examination) was unremarkable. Sigmoidoscopy and biopsy were normal and the patient was noted to have an inappropriate effect with a rather dramatic story. Investigations revealed a normal full blood count. During the admission the patient was counselled and underwent HIV testing: the results were positive. The diagnosis at that time was one of Munchausen's/malingering. Subsequently, the patient had experienced chronic diarrhoea and had attended many different clinics. In the year before his admission with diarrhoea Cryptosporidium parvum had been isolated repeatedly in the stool. Six months before admission the patient had experienced recurrent episodes of perianal herpes simplex virus infection and began aciclovir suppression. Two months before admission his CD4 count had fallen from 290 x 106/1 to 110 x 106/1. The patient had declined antiretroviral therapy but had begun co-trimoxazole as primary prophylaxis against Pneumocystis carinii pneumonia. At this stage the patient also reported that in 1987 he had cytomegalovirus (CMV) colitis and hepatitis which were treated with foscarnet. This episode had occurred at another hospital. Contact with that hospital revealed no patient of that name. On further inquiry the patient reported a family history of haemophilia, he was unable to say of what sort. His social history revealed that he was unemployed but had worked in several different jobs. His homosexual life style was his risk factor for HIV infection. He had no travel history of note. On examination in January 1994 he was pyrexial with a temperature of 38.2°C. He had shotty lymphadenopathy in the right inguinal region. In the abdomen there was generalised tenderness but no organomegaly or masses: rectal examination was unremarkable. The rest of the examination was normal; he was normotensive. Initial investigations included a CMV DEAFF test which was positive in urine and negative in blood. Culture of urine, blood, and stool were negative for bacteria, fungi, protozoa, and acid and alcohol fast bacilli (AAFB). Sigmoidoscopy revealed a mildly inflamed mucosa but biopsy was normal. Urea and electrolytes were repeated. The patient refused to stay in hospital but returned to the ward the following day having sustained a soft tissue injury to his right thumb. This had happened as he had fallen at home. Having been seen and assessed he left the ward once more and again returned the following day; at that time he was verbally aggressive to nursing and medical staff. He made a self diagnosis of HIV myelopathy and he based this diagnosis on the fact that he was unable to walk downstairs. He was noted to have uncontrollable spasms of his arms and legs but declined investigations of these symptoms. Four days after his original admission he once more returned to the ward at which time he was apyrexial and his diarrhoea had ceased. On re-examination the abdomen was still diffusely mildly tender and the rest of the examination was normal. In particular there were no neurological abnormalities, no rash, and no signs of spontaneous bleeding. Investigations revealed that the haemoglobin was now 6.5 g/dl, the platelet count had fallen to 74 x 109/l, and the serum Academic Unit, Department of Genitourinary Medicine, King's College School of Medicine and Dentistry, London SE5 9RS A L Pozniak","PeriodicalId":12621,"journal":{"name":"Genitourinary Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1997-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/sti.73.5.410","citationCount":"0","resultStr":"{\"title\":\"Haemolytic uraemic syndrome complicated by disseminated extraneural cryptococcosis.\",\"authors\":\"A L Pozniak, S B Lucas, R F Miller\",\"doi\":\"10.1136/sti.73.5.410\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Case report (Dr R F Miller) A 33 year unemployed white man was admitted to hospital in January 1994 complaining of a 1 week history of diarrhoea, passing up to 30 stools per day. The stool consisted of watery yellow fluid without blood or mucus. He reported associated anorexia with intermittent nausea and vomiting together with left lower quadrant colicky abdominal pain and sweats but no fever. The patient had been seen in a local casualty department 4 days previously at which time he had reported 3 days of diarrhoea. At that time he reported that he was HIV antibody positive and examination had revealed no abnormalities. Investigations revealed normal urea and electrolytes, a haemoglobin of 10.4 g/dl, a total white blood count of 6.8 x 109/l, and a platelet count of 68 x 109/l. This latter finding was ascribed to the effects of HIV infection. The patient was treated symptomatically and discharged. On admission to hospital in January 1994 the patient reported that 72 months previously he had developed night sweats, gingivitis, and oral candidiasis. He had been admitted to another hospital in April 1988 with a chest infection and, in May of that year following a party, he had been admitted to the Middlesex Hospital with diarrhoea and vomiting. He subsequently reported that he had passed malaena stools and, in addition, stated that he had been found to be HIV positive in October 1987; this positive result was performed on a sample of serum stored from 1982. The investigation had been carried out at another hospital. On that admission in 1988 examination (including rectal examination) was unremarkable. Sigmoidoscopy and biopsy were normal and the patient was noted to have an inappropriate effect with a rather dramatic story. Investigations revealed a normal full blood count. During the admission the patient was counselled and underwent HIV testing: the results were positive. The diagnosis at that time was one of Munchausen's/malingering. Subsequently, the patient had experienced chronic diarrhoea and had attended many different clinics. In the year before his admission with diarrhoea Cryptosporidium parvum had been isolated repeatedly in the stool. Six months before admission the patient had experienced recurrent episodes of perianal herpes simplex virus infection and began aciclovir suppression. Two months before admission his CD4 count had fallen from 290 x 106/1 to 110 x 106/1. The patient had declined antiretroviral therapy but had begun co-trimoxazole as primary prophylaxis against Pneumocystis carinii pneumonia. At this stage the patient also reported that in 1987 he had cytomegalovirus (CMV) colitis and hepatitis which were treated with foscarnet. This episode had occurred at another hospital. Contact with that hospital revealed no patient of that name. On further inquiry the patient reported a family history of haemophilia, he was unable to say of what sort. His social history revealed that he was unemployed but had worked in several different jobs. His homosexual life style was his risk factor for HIV infection. He had no travel history of note. On examination in January 1994 he was pyrexial with a temperature of 38.2°C. He had shotty lymphadenopathy in the right inguinal region. In the abdomen there was generalised tenderness but no organomegaly or masses: rectal examination was unremarkable. The rest of the examination was normal; he was normotensive. Initial investigations included a CMV DEAFF test which was positive in urine and negative in blood. Culture of urine, blood, and stool were negative for bacteria, fungi, protozoa, and acid and alcohol fast bacilli (AAFB). Sigmoidoscopy revealed a mildly inflamed mucosa but biopsy was normal. Urea and electrolytes were repeated. The patient refused to stay in hospital but returned to the ward the following day having sustained a soft tissue injury to his right thumb. This had happened as he had fallen at home. Having been seen and assessed he left the ward once more and again returned the following day; at that time he was verbally aggressive to nursing and medical staff. He made a self diagnosis of HIV myelopathy and he based this diagnosis on the fact that he was unable to walk downstairs. He was noted to have uncontrollable spasms of his arms and legs but declined investigations of these symptoms. Four days after his original admission he once more returned to the ward at which time he was apyrexial and his diarrhoea had ceased. On re-examination the abdomen was still diffusely mildly tender and the rest of the examination was normal. In particular there were no neurological abnormalities, no rash, and no signs of spontaneous bleeding. Investigations revealed that the haemoglobin was now 6.5 g/dl, the platelet count had fallen to 74 x 109/l, and the serum Academic Unit, Department of Genitourinary Medicine, King's College School of Medicine and Dentistry, London SE5 9RS A L Pozniak\",\"PeriodicalId\":12621,\"journal\":{\"name\":\"Genitourinary Medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1136/sti.73.5.410\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Genitourinary Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1136/sti.73.5.410\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genitourinary Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1136/sti.73.5.410","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Haemolytic uraemic syndrome complicated by disseminated extraneural cryptococcosis.
Case report (Dr R F Miller) A 33 year unemployed white man was admitted to hospital in January 1994 complaining of a 1 week history of diarrhoea, passing up to 30 stools per day. The stool consisted of watery yellow fluid without blood or mucus. He reported associated anorexia with intermittent nausea and vomiting together with left lower quadrant colicky abdominal pain and sweats but no fever. The patient had been seen in a local casualty department 4 days previously at which time he had reported 3 days of diarrhoea. At that time he reported that he was HIV antibody positive and examination had revealed no abnormalities. Investigations revealed normal urea and electrolytes, a haemoglobin of 10.4 g/dl, a total white blood count of 6.8 x 109/l, and a platelet count of 68 x 109/l. This latter finding was ascribed to the effects of HIV infection. The patient was treated symptomatically and discharged. On admission to hospital in January 1994 the patient reported that 72 months previously he had developed night sweats, gingivitis, and oral candidiasis. He had been admitted to another hospital in April 1988 with a chest infection and, in May of that year following a party, he had been admitted to the Middlesex Hospital with diarrhoea and vomiting. He subsequently reported that he had passed malaena stools and, in addition, stated that he had been found to be HIV positive in October 1987; this positive result was performed on a sample of serum stored from 1982. The investigation had been carried out at another hospital. On that admission in 1988 examination (including rectal examination) was unremarkable. Sigmoidoscopy and biopsy were normal and the patient was noted to have an inappropriate effect with a rather dramatic story. Investigations revealed a normal full blood count. During the admission the patient was counselled and underwent HIV testing: the results were positive. The diagnosis at that time was one of Munchausen's/malingering. Subsequently, the patient had experienced chronic diarrhoea and had attended many different clinics. In the year before his admission with diarrhoea Cryptosporidium parvum had been isolated repeatedly in the stool. Six months before admission the patient had experienced recurrent episodes of perianal herpes simplex virus infection and began aciclovir suppression. Two months before admission his CD4 count had fallen from 290 x 106/1 to 110 x 106/1. The patient had declined antiretroviral therapy but had begun co-trimoxazole as primary prophylaxis against Pneumocystis carinii pneumonia. At this stage the patient also reported that in 1987 he had cytomegalovirus (CMV) colitis and hepatitis which were treated with foscarnet. This episode had occurred at another hospital. Contact with that hospital revealed no patient of that name. On further inquiry the patient reported a family history of haemophilia, he was unable to say of what sort. His social history revealed that he was unemployed but had worked in several different jobs. His homosexual life style was his risk factor for HIV infection. He had no travel history of note. On examination in January 1994 he was pyrexial with a temperature of 38.2°C. He had shotty lymphadenopathy in the right inguinal region. In the abdomen there was generalised tenderness but no organomegaly or masses: rectal examination was unremarkable. The rest of the examination was normal; he was normotensive. Initial investigations included a CMV DEAFF test which was positive in urine and negative in blood. Culture of urine, blood, and stool were negative for bacteria, fungi, protozoa, and acid and alcohol fast bacilli (AAFB). Sigmoidoscopy revealed a mildly inflamed mucosa but biopsy was normal. Urea and electrolytes were repeated. The patient refused to stay in hospital but returned to the ward the following day having sustained a soft tissue injury to his right thumb. This had happened as he had fallen at home. Having been seen and assessed he left the ward once more and again returned the following day; at that time he was verbally aggressive to nursing and medical staff. He made a self diagnosis of HIV myelopathy and he based this diagnosis on the fact that he was unable to walk downstairs. He was noted to have uncontrollable spasms of his arms and legs but declined investigations of these symptoms. Four days after his original admission he once more returned to the ward at which time he was apyrexial and his diarrhoea had ceased. On re-examination the abdomen was still diffusely mildly tender and the rest of the examination was normal. In particular there were no neurological abnormalities, no rash, and no signs of spontaneous bleeding. Investigations revealed that the haemoglobin was now 6.5 g/dl, the platelet count had fallen to 74 x 109/l, and the serum Academic Unit, Department of Genitourinary Medicine, King's College School of Medicine and Dentistry, London SE5 9RS A L Pozniak