Search

Objectives Tuberculosis (TB) is the most common opportunistic infection and cause of mortality among people living with HIV, and it is possible that it may also influence the evolution of the HIV infection. We assessed the differences between HIV-positive and -negative people infected with TB. Methods The present study is a cross-sectional retrospective study by electronic record revision. We included patients admitted to a tertiary hospital with a diagnosis of TB between 2011 and 2016, comparing those with HIV coinfection with non-HIV patients, according to demographic and clinical characteristics. Results This study included 591 patients, of whom 32% were HIV-coinfected. HIV-TB patients were younger, with a predominance of male gender. Considering TB risk factors, there was a higher prevalence of homelessness and intravenous drug use in the HIV group. In the non-HIV group, direct contact with other patients with TB and immunosuppression were more prevalent. Relative to TB characteristics, the HIV-coinfected group presents with a higher prevalence of disseminated disease and a higher occurrence of previous TB infection. Cancer was the most frequent cause of immunosuppression in the HIV group and the number testing positive for TB via microbiological culture was lower. Assessment of microbiological resistance and in-hospital mortality showed similar numbers in both groups. Conclusions There are few papers comparing clinical course of TB between HIV-infected and non-infected patients. Our study differs from others in the literature as we focused on a country with middling incidence of TB and further characterized the differences between HIV-infected and non-infected patients which can contribute to the management of these patients.

Background/purpose Despite effectiveness and favourable safety profile, antimalarials have the potential to cause irreversible macular retinopathy. Screening methods have evolved over the last decade and the optimal dose of hydroxychloroquine (HCQ) is now set at under 5 mg/kg real body weight. HCQ in Portugal comes only as a 400 mg pill and in 10 pills per package, which is neither friendly for optimising safe dosing nor for promoting compliance. This study aims to test the frequency of retinal hydroxychloroquine toxicity in a single-centre cohort. Methods Cross-sectional study conducted between January-2016 and May-2017, of a convenience sample of chronically compliant and well characterised patients. The screening strategy consisted of automated threshold visual fields and objective test: spectral-domain optical coherence tomography, fundus autofluorescence and multifocal electroretinogram. Toxicity was diagnosed on the basis of compatible visual fields defects together with at least one positive objective test. Univariate statistical analysis was performed using the Wilcoxon Mann-Whitney (WMW) and Chi-Square (CS) tests for non-parametric distributed data. Results Of the 62 patients screened, 32 (51%) had no prior ophthalmological examination. Median age was 46 years (y), IQR 37–60; range 27–83; 59 (95%) were female; the majority, 28 (45%) took HCQ due to SLE, 4 (6%) for Sjogren syndrome, 12 (19%) for UCTD, 11 (18%) for incomplete/cutaneous forms of lupus and 7 (11%) for other CTD. No patient had concomitant renal or liver disease. Median duration and cumulative dose were respectively 8 y (IQR 3–12; range 0.4–31) and 1168 g (IQR 584–2044; range 36–8760). Retinal toxicity was confirmed in 6 SLE and 1 non-SLE patient; in all HCQ was stopped (2/7 screen-naive; 1/7 on tamoxifen; 1/7 with visual loss). Toxicity correlated to disease (p=0,003) and HCQ therapy (p=0,002) duration, cumulative HCQ dose (p=0,001) and SLE (p=0,04). Table 1 dose adjustments were performed in 13 patients. Conclusion Using a standardised referral protocol for HCQ retinopathy screening led to cessation of therapy due to toxicity (11%) and adjustment of daily dosing (21%). This study highlights that regular adjustment of dose and retinal toxicity screening is mandatory in patients on prolonged HCQ therapy and reinforces lobbying for more flexible dosages. In addition, HCQ toxicity raises the need for alternative therapies in patients with CTD.

according to gender, age, seropositive RA, DAS28, mean disease duration, use of BMR, type and onset of primary malignancy. Results: Of the n= 155 pts with RA, n = 57 were receiving a biological agent. Of these n= 38 pts were female, with an average age of 55.37 years, a mean disease duration of 9.35 years andmean duration of BMR use of 3.6 years. The mean DAS28 was 5.9 and after BMR use 3.1. The n= 6 pts with neoplasia had an average age of 67.33 years (only n= 1 pt b65 years), a mean disease duration of 11.83 years; a mean duration of BMR use of 5.2 years (etanercept n= 3 pts, rituximab n= 2 pts and adalimumab n= 1 pt). The mean DAS28 was 5.3 and after BMR use 3.0. Neoplasia onset was previous to the use of a BMR in n= 2 pts (12 and 15 years), of which ovary n= 1 pt, breast and cervix n= 1 pt, there were no recurrences; in n= 4 pts the neoplasia occurred after the use of BMR (3, 4, 5 and 7 years), of which skin n= 2, breast n = 1 and prostate n= 1. None of the pts died, but n= 1 suspended BMR. Of the n= 108 pts under traditional DMARDs, n= 13 had the diagnosis of malignant diseasewith themean age of 61.54 years and n= 6 of themhad it before the diagnosis of RA. The remaining n= 7had the diagnosis of neoplasia a mean of 11.43 years after the diagnosis of RA. The types of primary neoplasia were gynecological n = 4, gastrointestinal tract n= 3, breast n = 2, leukemia n= 1, lung n= 1, kidney n= 1 and prostate n= 1. Conclusions: In our sample, the pts with malignancy were older, with a longer mean duration of a BMR use and similar DAS28 to all of the pts with RA. However, pts with RA without BMR have a lower age of onset and the distribution between the types of primary neoplasia is slightly different, which might be explained by the therapy's antiinflammatory effects in some malignancies vs. immunosuppression in others.