Objectives: The high mortality among HIV/tuberculosis (TB) coinfected patients in Eastern Europe is partly explained by the high prevalence of drug-resistant TB. It remains unclear whether outcomes of HIV/TB patients with rifampicin/isoniazid-susceptible TB in Eastern Europe differ from those in Western Europe or Latin America.Methods: One-year mortality of HIV-positive patients with rifampicin/isoniazidsusceptible TB in Eastern Europe, Western Europe, and Latin America was analysed and compared in a prospective observational cohort study. Factors associated with death were analysed using Cox regression modelsResults: Three hundred and forty-one patients were included (Eastern Europe 127, Western Europe 165, Latin America 49). Proportions of patients with disseminated TB (50, 58, 59%) and initiating rifampicin+isoniazid+pyrazinamide-based treatment (93, 94, 94%) were similar in Eastern Europe, Western Europe, and Latin America respectively, whereas receipt of antiretroviral therapy at baseline and after 12 months was lower in Eastern Europe (17, 39, 39%, and 69, 94, 89%). The 1-year probability of death was 16% (95% confidence interval 11-24%) in Eastern Europe, vs. 4% (2-9%) in Western Europe and 9% (3-21%) in Latin America; P< 0.0001. After adjustment for IDU, CD4(+) cell count and receipt of antiretroviral therapy, those residing in Eastern Europe were at nearly 3-fold increased risk of death compared with those in Western Europe/Latin America (aHR 2.79 (1.15-6.76); P=0.023).Conclusions: Despite comparable use of recommended anti-TB treatment, mortality of patients with rifampicin/isoniazid-susceptible TB remained higher in Eastern Europe when compared with Western Europe/Latin America. The high mortality in Eastern Europe was only partially explained by IDU, use of ART and CD4(+) cell count. These results call for improvement of care for TB/HIV patients in Eastern Europe. Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved.
BACKGROUND:We obtained estimates of the incidence of tuberculosis (TB) among patients receiving HAART and identified determinants of the incidence. METHODS:We analyzed the incidence of TB during the first 3 years after initiation of HAART among 17,142 treatment-naive, AIDS-free persons starting HAART who were enrolled in 12 cohorts from Europe and North America. We used univariable and multivariable Poisson regression models to identify factors associated with the incidence. RESULTS:During the first 3 years (36,906 person-years), 173 patients developed TB (incidence, 4.69 cases per 1000 person-years). In multivariable analysis, the incidence rate was lower for men who have sex with men, compared with injection drug users (relative rate, 2.46; 95% confidence interval [CI], 1.51-4.01), heterosexuals (relative rate, 2.42; 95% CI, 1.64-3.59), those with other suspected modes of transmission (relative rate, 1.66; 95% CI, 0.91-3.06), and those with a higher CD4+ count at the time of HAART initiation (relative rate per log2 cells/microL, 0.87; 95% CI, 0.84-0.91). During 28,846 person-years of follow-up after the first 6 months of HAART, 88 patients developed TB (incidence, 3.1 cases per 1000 person-years of follow-up). In multivariable analyses, a low baseline CD4+ count (relative rate per log2 cells/microL, 0.89; 95% CI, 0.83-0.96), 6-month CD4+ count (relative rate per log2 cells/microL, 0.90; 95% CI, 0.81-0.99), and a 6-month HIV RNA level >400 copies/mL (relative rate, 2.21; 95% CI, 1.33-3.67) were significantly associated with the risk of acquiring TB after 6 months of HAART. CONCLUSION:The level of immunodeficiency at which HAART is initiated and the response to HAART are important determinants of the risk of TB. However, this risk remains appreciable even among those with a good response to HAART, suggesting that other interventions may be needed to control the TB epidemic in the HIV-infected population.
3. Information on permissions/orders of reprints rheumatology and related fields. Silverman featuring research articles on clinical subjects from scientists working in is a monthly international serial edited by Earl D.
OBJECTIVEAutommune diseases could constitute one emerging cause of morbidity in patients infected with human immunodeficiency virus (HIV) due to the chronicity of the infection and to the high level of B cell stimulation induced by HIV. We conducted a cross-sectional study investigating the clinical and biological signs of autoimmunity in HIV infected patients.METHODSWe studied the following plasma immunological variables: antinuclear antibodies (ANA) and antibodies to extractable nuclear antigens, antiphospholipids, anticardiolipins (aCL), antineutrophil cytoplasmic antibodies (ANCA), rheumatoid factor (RF), cryoglobulinemia, total complement, and C4 factor. HIV-RNA, CD4+ cell count, and serological status for hepatitis B (HBV) and C virus (HCV) were also studied. Clinical signs of autoimmune diseases were noted.RESULTSIn total, 97 patients were investigated (men 74%). Median age was 38 years (range 20-64). Median CD4+ count and HIV-RNA were 333/mm3 and 1662 copies/ml, respectively. Coinfection by HBV and HCV was present in 7% and 64% of the patients. In patients with HIV only, we detected cryoglobulinemia in 17% of patients, a positive RF in 19%, ANA > 1/100 in 21%, aCL in 51%, and ANCA > 1/20 in 17% (most of them type C by ELISA). There was a trend for a higher level of cryoglobulinemia and aCL in patients having CD4 lymphocyte counts > 350/mm3 than in others (25% vs 11%, p = 0.26, and 63% vs 42%, p = 0.23, respectively). Patients coinfected with HCV had a higher prevalence of cryoglobulinemia than HCV-free patients (42% vs 17%; p = 0.01). Prevalence of other immunological abnormalities was not different between patients with HIV only and HCV coinfected patients. Thirty patients expressed at least one clinical sign compatible with autoimmune disease. Patients with cryoglobulinemia more often had coinfection with HCV (OR 6.64, 95% CI 1.87-23.57) and IgM > 1.9 g/l (OR 6.16, 95% CI 2.15-17.67).CONCLUSIONHumoral immunological abnormalities are frequent in patients with HIV, but are rarely associated with severe clinical signs.
Although several reports of sarcoidosis have been reported in hepatitis C virus (HCV)-infected patients treated with interferon-alpha, this association has never been described in nontreated HCV patients. We report two cases of sarcoidosis associated with chronic hepatitis C infection. The patients developed multivisceral sarcoidosis (cutaneous, lungs, nodes) at two and at least six years after the presumed date of infection. One patient obtained remission of sarcoidosis with corticosteroid treatment but the other remained corticodependent. The levels of hepatic enzymes were not significantly modified throughout the course of corticosteroid therapy. In conclusion, these case reports suggest that HCV itself could induce a granulomatous reaction in chronic HCV-infected patients through the stimulation of the cellular immune system. It could be of interest to test for HCV infection all patients diagnosed with sarcoidosis and to watch over every treated or nontreated hepatitis C infected patient for the development of granulomatous lesions.
A symmetry-preserving approach to the continuum bound-state problem in quantum field theory is used to calculate the masses, leptonic decay constants and light-front distribution amplitudes of empirically accessible heavy-light mesons. The inverse moment of the B-meson distribution is particularly important in treatments of exclusive B-decays using effective field theory and the factorisation formalism; and its value is therefore computed: λB(ζ=2GeV)=0.54(3)GeV. As an example and in anticipation of precision measurements at new-generation B-factories, the branching fraction for the rare B→γ(Eγ)ℓνℓ radiative decay is also calculated, retaining 1/mB2 and 1/Eγ2 corrections to the differential decay width, with the result ΓB→γℓνℓ/ΓB=0.47(15) on Eγ>1.5GeV.
Adhesive capsulitis of the shoulder is reported to be a side-effect of protease inhibitor therapy in patients with HIV. The 18 patients with this type of frozen shoulder described in the literature were all receiving indinavir (Crixivan); a coincidence that corresponds to our daily practice, with several patients suffering from this incapacitating toxicity. We recently identified a patient presenting with the classical symptoms of iatrogenic adhesive capsulitis when being treated with the protease inhibitor nelfinavir (Viracept). A white man, 59 years old, was referred to our hospital for a positive HIV serology on a voluntary screening. Laboratory findings showed a CD4 lymphocyte count of 268 cells/mm3 and a plasma viral load (HIV RNA) of 100 000 copies/ml. Antiretroviral therapy was started using stavudine (Zerit), didanosine (Videx) and nelfinavir. Six weeks later the patient experienced progressive bilateral symmetrical shoulder pain and restricted shoulder motion. Clinical examination only noted a restricted range of motion of the glenohumeral joints, with an abduction of 60° and rotation of 20°. Classic radiography and magnetic resonance imaging of the shoulders were normal. No other conditions relating to secondary frozen shoulder could be identified (other medication, trauma, hyperthyroidism, diabetes or mediastinal disease). The diagnosis of adhesive capsulitis caused by nelfinavir was postulated and he received antalgic treatment with calcitonine and physiotherapy for passive mobilization of the shoulders. Although the antiretroviral therapy remained unchanged, clinical improvement showed a disappearance of the pain and complete recovery of shoulder function within 3 months. Our case report describes a classic presentation of frozen shoulder in HIV patients treated with protease inhibitors. The 18 cases so far reported in the literature [1–5] had an onset of symptoms after several months of treatment (2–36 months, mean 12.5). The complaints were often bilateral and complementary investigations were negative. Despite the continuation of antiretroviral treatment, the disappearance of the symptoms was observed in several months (1–20 months, mean 7) under symptomatic therapy. The incrimination of nelfinavir in adhesive capsulitis in our patient indicates that we are probably dealing with a pathogenic class-effect of protease inhibitors rather than a specific toxicity of the until now only implicated indinavir. Sten de Witte Fabrice Bonnet Mojgan Bonarek Paul Lamarque Philippe Morlat Marie-Catherine Receveur Jacques Beylot
A study evaluating alternative methods for long term operation of biomass production systems was recently completed at the Kennedy Space Center (KSC). The 418-day study evaluated repeated batch versus mixed-aged production of potato grown on either standard 12-strength Hoagland's nutrient solution or solutions including nutrients recycled from inedible plant material. The long term effects of closure and recycling on microbial dynamics were evaluated by monitoring the microbial communities associated with various habitats within the plant growth system (i.e., plant roots, nutrient solution, biofilms within the hydroponic systems, atmosphere, and atmospheric condensate). Plate count methods were used to enumerate and characterize microorganisms. Microscopic staining methods were used to estimate total cell densities. The primary finding was that the density and composition of microbial communities associated with controlled environmental plant growth systems are stable during long term operation. Continuous production resulted in slightly greater stability. Nutrient recycling, despite the addition of soluble organic material from the waste processing system, did not significantly increase microbial density in any of the habitats.
Introduction. – Les encéphalopathies associées à la thyroïdite de Hashimoto ont été décrites il y a plus de 30 ans. Elles sont rares mais leur existence est probablement sous-estimée.Exégèse. – Nous rapportons quatre observations de patients atteints de thyroïdite de Hashimoto compliquée de manifestations neuropsychiatriques. Il sˈagit de trois femmes et d’un homme âgés en moyenne de 68 ans ayant présenté des manifestations neuropsychiatriques variables : crises comitiales, confusion, hallucinations, myoclonies pour lesquelles les causes habituelles (infectieuses, tumorales, vasculaires, toxiques…) ont été éliminées. Les explorations neurologiques (électroencéphalogramme, tomodensitométrie cérébrale, imagerie par résonance magnétique) sont aspécifiques. Dans tous les cas, il existe une hyperprotéinorachie modérée sans pléiocytose. Les patients présentent tous une thyroïdite de Hashimoto avec anticorps antithyroperoxydase fortement positifs et une hypothyroïdie modérée. Malgré lˈopothérapie substitutive, les signes neurologiques persistent. Seule la corticothérapie permet une évolution neurologique favorable.Conclusion. – Entité rare, lˈencéphalopathie de Hashimoto doit être évoquée devant tout tableau neuropsychiatrie sans cause évidente. La pathogénie de ces troubles neuroencéphaliques reste imprécise mais très vraisemblablement dˈordre auto-immun en raison de leur forte corticosensibilité.Introduction. – Encephalopathy associated with Hashimoto’s thyroiditis has been recognized for more than 30 years and is probably underestimated.Exegesis. – We report four patients with Hashimoto’s thyroiditis who presented neurological or psychiatric features. There were three women and one man, with a mean age of 68 years. Neurological presentations were various: seizures, psychotic episodes, altered consciousness, hallucinations without usual aetiological diseases (infectious, metabolic, neoplasic, vascular, etc.). Neurological investigations (EEG, brain CT, magnetic resonance imaging) were unspecific. In all cases, a moderately high CSF protein level without pleocytosis was found. Patients presented slight hypothyroidism with high titers of antithyroperoxidase antibodies. Despite hormone therapy replacement, neurological features persisted. Outcome was favorable under steroid therapy.Conclusion. – Hashimoto’s encephalopathy must be considered in the face of neuropsychiatric manifestations without obvious etiology. Pathogenic mechanisms are not clear but probably involve autoimmune cerebral vasculitis because of the efficacy of steroids.