ObjectivesTo describe the causes of death in HIV-infected patients in the era of highly active antiretroviral therapy (HAART). MethodA retrospective survey conducted in Bordeaux, France. Medical records of all deaths that had occurred in 1998 and 1999 amongst patients followed within the Aquitaine cohort were reviewed by the same physician. Immediate and underlying causes of death were described, taking into account the morbidity at the time of death. ResultsSixty-six deaths occurred in 1998, and 41 in 1999. Sixty-seven per cent of deceased patients were male. Median age at time of death was 43 years (range 25±71), median CD4 was 162 cells/mL (0±957); 28% of patients had a CD4 count > 200 cells/mL and 7% plasma viral load < 500 HIV-RNA copies/mL. Amongst morbidity present at the time of death, there were 23 bacterial infections, 16 non-Hodgkin's lymphomas, 16 cirrhoses, 15 non HIV-related malignancies, 13 central nervous system diseases and 10 myocardiopathies. The main immediate causes of death were: multiple organ failure (21%), coma (18%), septic shock (15%) and acute respiratory failure (14%). Underlying causes of death were AIDS-de®ning events (48%), non AIDS HIV-related infection (3%), hepatitis B-or C-associated cirrhosis (14%), non HIV-related malignancies (11%), cardiovascular events (10%), suicide and overdose (6%), treatment-related fatalities (4%), injury (2%) and unknown (2%). Patients dying from AIDS-related events were more often female, had a lower CD4 count, a higher level of HIV-RNA, a shorter history of HIV infection and were less often coinfected with hepatitis B and C viruses than those dying from other underlying causes.Conclusions AIDS-related events are no longer the major causes of death of HIV-infected patients in the era of HAART. This evolving mortality pattern justi®es an adaptation of both the epidemiological surveillance and the clinical monitoring of HIV-infected patients.
To determine the factors associated with clinical progression (AIDS events and death) in antiretroviral-naïve patients who have begun highly active antiretroviral therapy (HAART). MethodsHIV-infected patients naïve to antiretroviral therapy were included in a prospective hospital-based cohort who began HAART between June 1996 and December 2001. Progression was explained by baseline characteristics using Cox proportional hazards models. ResultsOverall, data for 709 patients were analysed. In multivariate analysis, factors associated with an increased risk of progression were CD4 count o50 cells/mL [hazard ratio (HR) 5 13.0 (95% confidence interval 3.8-44.3)] and between 50 and 199 cells/mL [HR 5 5.1 (1.6-16.3)], when compared with patients with CD4 count4350 cells/mL; AIDS events before HAART prescription [HR 5 2.1 (1.2-3.7)]; CD8 count o 400 cells/mL [HR 5 1.8 (1.1-3.0)]; and older age (HR 5 1.2 by 10 years (1.0-1.5)]. In a second model including CD4 percentage, factors associated with progression were CD4o10% [HR 5 6.3 (2.2-17.9)] and 10%oCD4 o15% [HR 5 4.2 (1.4-12.5)], when compared with patients with CD4420%; CD8 count; AIDS events before HAART prescription; and older age. In a third model including the CD4:CD8 ratio, factors associated with progression were CD4:CD8o15% [HR 5 8.2 (2.3-28.8)] and 15%oCD4:CD8o30% [HR 5 4.6 (1.3-16.0)], when compared with patients with CD4:CD8445%; AIDS events before HAART prescription; and older age. The Akaike information criteria for model analysis were 803, 805 and 815, respectively. ConclusionsConsideration of CD4 level in terms of CD4:CD8 ratio or CD4 percentage can be a good alternative to absolute CD4 count. Other prognostic factors such as older age, CD8 count o400 cells/mL and AIDS events also have to be considered in the decision to initiate HAART.
Neuropsychiatric forms of systemic lupus erythematosus (SLE) vary, most commonly consisting of seizures, psychiatric disturbances, or focal central nervous deficits. This is a new case of neuromyelitis optica or Devic's syndrome during the course of SLE. Few reports of this association exist in the literature. Our objective is to report this unique case of Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus. A 28-year-old woman had been diagnosed as having SLE with cutaneous and articular involvement in 1987 when she was 17 years old. She was treated with a synthetic antimalarial agent associated with corticosteroids. In 1994, during the fourth month of pregnancy, she had signs of transverse myelitis with a sensory level at T6 associated with an optic neuropathy suggesting a Devic's syndrome. The patient was managed by plasmapheresis sessions and intravenous corticosteroids. Transverse myelitis recurred postpartum and three years later at the same thoracic level. Management by bolus administration of a steroid and cyclophosphamide resulted in remission again. There have only been around a dozen reports in the literature of patients who had both Devic's neuromyelitis optica and SLE. Magnetic resonance imaging is contributive to diagnosis and therapeutic follow-up, showing spinal cord lesions with increased intensity on T2-weighted sequences. Although the clinical course of the present patient has been favourable so far, the prognosis of this neurologic disease is generally considered to be poor with elevated mortality.
In this retrospective study, the authors describe the clinical, histologic and laboratory features of 15 cases of chilblain or perniotic lupus. In winter, the patients (14 women, 1 man) develop chilblain-like lesions, chiefly in the toes (8 times) and fingers (11 times). Histologic features are identical to those of discoid lupus erythematosus. The damaged skin gives a positive fluorescent band test. Usually, these lesions occur in association with discoid lupus of the face. However, in 8 patients, they were the only cutaneous sign of lupus. This form of lupus can evolve to a systemic form, as was the case with 3 patients.
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