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Biomedical subjects

J de Gans

Publications and source records attributed to J de Gans.

At least 19 recordsLinked to original sources
PubMed1992

Itraconazole compared with amphotericin B plus flucytosine in AIDS patients with cryptococcal meningitis.

OBJECTIVE: We conducted a comparison of itraconazole versus amphotericin B plus flucytosine in the initial treatment of cryptococcal meningitis in patients with AIDS and established the efficacy of itraconazole as maintenance treatment. DESIGN: The trial was a prospective, randomized, and non-blinded study. SETTING: The study was performed at an academic centre for AIDS, Amsterdam, The Netherlands. PATIENTS, PARTICIPANTS: Twenty-eight HIV-1-seropositive men with a presumptive diagnosis of cryptococcal meningitis, randomized between 5 February 1987 and 1 January 1990, were included for analysis. INTERVENTIONS: Oral itraconazole (200 mg twice daily), versus amphotericin B (0.3 mg/kg daily) intravenously plus oral flucytosine (150 mg/kg daily) was administered for 6 weeks followed by maintenance therapy with oral itraconazole (200 mg daily) to all patients. MAIN OUTCOME MEASURES: Outcome measures were a complete or partial response, recrudescence and relapse. RESULTS: A complete response was observed in five out of the 12 patients who completed 6 weeks of initial treatment with itraconazole versus all 10 patients who completed treatment with amphotericin B plus flucytosine (P = 0.009). A partial response was observed in seven out of the 14 patients assigned to itraconazole. During maintenance therapy, recrudescence (n = 6) or relapse (n = 1) occurred in seven out of the 12 patients initially assigned to itraconazole, whereas two relapses occurred among nine patients initially treated with amphotericin B plus flucytosine (P = 0.22); recurrence of clinical symptoms was significantly related to a positive cerebrospinal fluid culture at 6 weeks (P = 0.003). CONCLUSION: Itraconazole is less effective compared with amphotericin B plus flucytosine in achieving a complete response in initial therapy in AIDS patients with cryptococcal meningitis.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Disseminated actinomycosis due to Actinomyces meyeri and Actinobacillus actinomycetemcomitans.

A 44-year-old man presented with pulmonary lesions and neurological symptoms suggestive of lung carcinoma with cerebral metastases. He had non-specific chest X-ray findings since 6 years and he also suffered from relapsing purulent skin lesions which resolved spontaneously or by short courses of antibiotic treatment. When corticosteroids were given, multiple subcutaneous swellings developed that spontaneously ruptured. The pus contained Actinomyces meyeri and Actinobacillus actinomycetemcomitans. On operation, the intracerebral lesions appeared to be abscesses and the same bacteria were cultured as from the skin lesions. Bronchoscopical examination did not reveal a diagnosis. Amoxicillin was given for 12 months and the patient recovered.

Actinobacillus Infections↗
PubMed1992

Pyrimethamine alone as maintenance therapy for central nervous system toxoplasmosis in 38 patients with AIDS.

We retrospectively assessed the efficacy of maintenance therapy with pyrimethamine alone in 38 patients with AIDS and central nervous system (CNS) toxoplasmosis. The diagnosis was based on clinical presentation and compatible CT scan abnormalities with subsequent response to therapy. Survival analysis was performed by the product limit method of Kaplan-Meier. Fourteen patients received maintenance therapy with 25 mg pyrimethamine per day (group 1), and 24 patients were treated with 50 mg per day (group 2). The median survival from initiation of maintenance therapy until death or end of the study for the entire study population was 32 weeks. Median survival in group 1 was 28 weeks, as compared with 36 weeks in group 2 (p = 0.34). Relapses occurred in 12 patients, six in group 1 and six in group 2. There was no significant difference in failure-free survival between the two treatment groups (p = 0.09). One patient in group 1 and two patients in group 2 experienced severe toxicity, requiring discontinuation of therapy. All three patients relapsed and died. Two patients in group 2 who stopped treatment on their own initiative also had relapses. Thus, all five patients who discontinued therapy had relapses. Five of 13 patients in group 1 and two of 20 patients in group 2 relapsed during continuous therapy with pyrimethamine (p = 0.13); these seven patients responded to reintroduction of combination therapy (n = 6) or treatment with 50 mg pyrimethamine per day (n = 1). The results of our retrospective analysis suggest that maintenance therapy with oral pyrimethamine, 50 mg per day, in AIDS patients with CNS toxoplasmosis is effective.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Mental changes in patients with AIDS.

Mental changes are common in patients with acquired immunodeficiency syndrome (AIDS). Neuropsychological data of 32 patients with AIDS and cognitive symptoms were reviewed. All patients were neurologically examined and ancillary investigations were performed. According to the neuropsychological data three groups could be distinguished: I) 4 patients with dementia and cortical deficits; II) 16 patients with subcortical dementia; III) 12 patients with subcortical cognitive deficits without global intellectual deterioration. AIDS Dementia Complex (ADC) was diagnosed in 12 patients and occurred in all three groups. The most frequent form of dementia in patients with AIDS is of a subcortical type. Impaired memory or reduced psychomotor speed, or both, are common in patients without global intellectual deterioration. ADC seems an unlikely diagnosis in patients with cortical dementia. Neuropsychological examination is important for diagnosing ADC but the diagnosis cannot be made without regarding the neurological findings and ancillary investigations.

AIDS Dementia Complex↗
PubMed1990

Therapy for cytomegalovirus polyradiculomyelitis in patients with AIDS: treatment with ganciclovir.

Six AIDS patients with progressive cytomegalovirus (CMV) polyradiculomyelitis were treated with ganciclovir in an open study. The diagnosis was based on the presence of a distinct clinical syndrome with progressive flaccid paraparesis, preserved proprioception and urinary retention with specific cerebrospinal fluid (CSF) findings. Ganciclovir therapy, 5-10 mg/kg per day, instituted 3-6.5 weeks after onset of symptoms, was ineffective in four patients with severe paraparesis. One patient developed CMV polyradiculomyelitis while receiving ganciclovir and further deteriorated during foscarnet therapy. One patient however, showing minor paresis of one leg, improved after institution of ganciclovir therapy 1 week after onset of symptoms. It is concluded that a presumptive diagnosis of CMV polyradiculomyelitis can be made on the basis of distinct clinical findings and CSF pleocytosis with predominance of polymorphonuclear leukocytes in patients with AIDS. Ganciclovir therapy does not appear to be beneficial for patients with advanced paresis in the doses used. Further investigations are needed in order to determine if early intervention with ganciclovir, when paresis is mild, or higher doses in advanced paresis, might be of some benefit.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Predominance of polymorphonuclear leukocytes in cerebrospinal fluid of AIDS patients with cytomegalovirus polyradiculomyelitis.

Cytomegalovirus (CMV) polyradiculomyelitis was diagnosed in 4 of 241 consecutive neurologically assessed human immunodeficiency virus type (HIV-1) seropositive patients. CMV-related neurologic disease was suspected on clinical grounds and was subsequently confirmed by CMV culture from cerebrospinal fluid (CSF) and/or CMV in situ hybridization on specific specimens. All four patients showed CSF pleocytosis with predominance of polymorphonuclear leukocytes (PMNs). Retrospective analysis of the results of CSF examination, performed in 143 of 241 patients with neurologic symptoms, showed pleocytosis in 58 of 143 patients. Predominance of PMNs was found in seven patients, including the four with CMV polyradiculomyelitis. It is concluded that in HIV-1 seropositive patients with a clinical diagnosis of polyradiculomyelitis, a predominance of PMNs in CSF could be an indication that the condition is CMV related. This should lead to early diagnosis and institution of specific antiviral therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Declining incidence of AIDS dementia complex after introduction of zidovudine treatment.

OBJECTIVE: To assess the incidence of the AIDS dementia complex and the presence of HIV I p24 antigen in cerebrospinal fluid in relation to zidovudine treatment. DESIGN: Retrospective study of a consecutive series of patients with AIDS from 1982 to 1988. SETTING: An academic centre for AIDS. PATIENTS: 196 Patients with AIDS and neurological symptoms examined from 1982 to 1988. INTERVENTIONS: Zidovudine treatment, which was introduced to The Netherlands on 1 May 1987 for patients with severe symptoms of HIV infection (Centers for Disease Control groups IVA, B, C, and D). MAIN OUTCOME MEASURES: Diagnosis of AIDS dementia complex and presence of HIV I p24 antigen in cerebrospinal fluid. RESULTS: The AIDS dementia complex was diagnosed in 40 of the 196 (20%) patients with AIDS. Thirty eight of 107 patients with AIDS (36%) not taking zidovudine developed the AIDS dementia complex compared with two of the 89 (2%) taking the drug (p less than 0.00001). The incidence of the AIDS dementia complex increased to 53% in the first half of 1987, after the introduction of zidovudine in May 1987, decreasing to 10% in the second half of 1987 and to 3% in 1988. Dementia was diagnosed before definition of the AIDS dementia complex (1986) according to DSM-III criteria and there was good agreement between diagnosis before and after 1986. Sixteen of 61 samples of cerebrospinal fluid (26%) from patients with AIDS (10 with the AIDS dementia complex) not taking zidovudine were positive for HIV I p24 antigen, whereas none of 37 cerebrospinal fluid samples from patients with AIDS (two with the AIDS dementia complex) taking zidovudine were positive. CONCLUSIONS: The incidence of AIDS dementia complex in patients with AIDS declined after the introduction of systematic treatment with zidovudine; the AIDS dementia complex might be prevented by inhibiting viral replication in the central nervous system.

AIDS Dementia Complex↗
PubMed1989

Human immunodeficiency virus type 1 antigen in cerebrospinal fluid. Correlation with clinical neurologic status.

Human immunodeficiency virus type-1 (HIV-1) antigen was assayed in paired serum/cerebrospinal fluid (CSF) specimen from 85 adults and 58 children with acquired immunodeficiency syndrome and was compared with clinical neurological status. A quantitative comparison of HIV-1 antigen levels in matched serum and CSF specimens indicated that HIV-1 antigen expression in these compartments is independent and is correlated with acquired immunodeficiency syndrome dementia complex in adults and progressive encephalopathy in children. In a longitudinal study (n = 47), 16 patients tested positive for HIV-1 antigen in the CSF before (n = 2) or coincident (n = 14) with neurological deterioration. Six patients who tested positive for HIV-1 antigen in the CSF remained neurologically normal for a median duration of follow-up of 11 months. Six of 25 patients who tested negative for HIV-1 antigen in the CSF, subsequently showed neurological deterioration. These data indicate that HIV-1 antigen expression in the CSF is not useful in predicting neurological deterioration.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Effect of zidovudine on serum human immunodeficiency virus antigen levels in symptom-free subjects.

18 men with longstanding human immunodeficiency virus (HIV) antigenaemia but no symptoms received zidovudine in low-dose regimens (250 mg 6-hourly, 500 mg 6-hourly, or 500 mg 12-hourly) with or without acyclovir. Serum HIV antigen rose in only 1 patient and declined significantly in 13 (to below cut-off values in 9). In the 1 subject from whom HIV antigen positive cerebrospinal fluid was obtained, the fluid was antigen negative after 12 weeks of treatment. Acyclovir treatment alone or in addition did not seem to influence serum antigen levels. In 7 untreated men serum antigen levels rose or remained stable during follow-up. CD4+ cell counts increased in 14/18 treated subjects and 1/7 untreated subjects. No disease progression was observed in either group. Regression of enlarged lymph nodes was seen in the zidovudine-treated subjects. Adverse reactions to the study drugs were infrequent and mild. Anaemia caused symptoms in 2, but serious leucopenia or neutropenia was not observed.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Transmission of HIV and AIDS by plasmapheresis for Guillain-Barré syndrome.

A 58-year-old patient suffering from Guillain-Barré syndrome was successfully treated with plasma exchange therapy. Two- and half year later she developed AIDS. The only risk factor of this patient was plasmapheresis and it appeared, retrospectively, that one of the plasma donor samples contained antibodies to HIV. Knowing the exact moment of infection of our patient we documented the transfer of HIV antibodies from donor to patient, a HIV antigen peak two weeks after transmission (reflecting the initial virus replication in the patient) and subsequently the occurrence of patients' HIV antibodies and the reoccurrence of HIV antigen at the moment AIDS was diagnosed.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Decline of HIV antigen levels in cerebrospinal fluid during treatment with low-dose zidovudine.

Six HIV-antigenaemic patients with AIDS or AIDS-related complex were studied to assess the effect of treatment with low-dose zidovudine (250 mg) in 6-hourly doses on HIV antigen (HIV-Ag) levels in cerebrospinal fluid (CSF). HIV-Ag was detected in CSF of three patients before treatment. These patients became CSF HIV-Ag-negative within 8 weeks of treatment. One initially CSF HIV-Ag-negative patient became strongly CSF HIV-Ag-positive during interruption of zidovudine treatment; CSF HIV-Ag disappeared again after treatment was restarted. None of our patients showed a significant neurological improvement during the study. These results show that low-dose zidovudine can suppress viral expression in CSF. Whether suppression of viral replication can prevent future HIV-related neurological disease remains to be investigated.

Acquired Immunodeficiency Syndrome↗