Background The multi-morbid burden and use of systemic immunosuppressants in people with psoriasis may confer greater risk of adverse COVID-19 outcomes but data are limited. Objective Characterize the course of COVID-19 in psoriasis and identify factors associated with hospitalization. Methods Clinicians reported psoriasis patients with confirmed/suspected COVID-19 via an international registry, PsoProtect. Multiple logistic regression assessed the association between clinical/demographic characteristics and hospitalization. A separate patient-facing registry characterized risk-mitigating behaviours. Results Of 374 clinician-reported patients from 25 countries, 71% were receiving a biologic, 18% a non-biologic and 10% no systemic treatment for psoriasis. 348 (93%) fully recovered from COVID-19, 77 (21%) were hospitalized and nine (2%) died. Increased hospitalization risk was associated with older age (multivariable-adjusted OR 1.59 per 10 years, 95% CI 1.19-2.13), male sex (OR 2.51, 95% CI 1.23-5.12), non-white ethnicity (OR 3.15, 95% CI 1.24-8.03) and comorbid chronic lung disease (OR 3.87, 95% CI 1.52-9.83). Hospitalization was more frequent in patients using non-biologic systemic therapy than biologics (OR 2.84, 95% CI 1.31-6.18). No significant differences were found between biologic classes. Independent patient-reported data (n=1,626 across 48 countries) suggested lower levels of social isolation in individuals receiving non-biologic systemic therapy compared to biologics (OR 0.68, 95% CI 0.50-0.94). Conclusion In this international moderate-severe psoriasis case series, biologics use was associated with lower risk of COVID-19-related hospitalization than non-biologic systemic therapies, however further investigation is warranted due to potential selection bias and unmeasured confounding. Established risk factors (being older, male, non-white ethnicity, comorbidities) were associated with higher hospitalization rates. Clinical Implications We identify risk factors for COVID-19-related hospitalization in psoriasis patients, including older age, male sex, non-white ethnicity and comorbidities. Use of biologics was associated with lower hospitalization risk than non-biologic systemic therapies.

BackgroundDuring the last few years, investigators have debated the role that infectious agents may have in sarcoidosis pathogenesis. With the emergence of new molecular biology techniques, several studies have been conducted; therefore, we performed a meta-analysis in order to better explain this possible association.MethodsThis review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement from the Cochrane collaboration guidelines. Four different databases (Medline, Scopus, Web of Science, and Cochrane Collaboration) were searched for all original articles published from 1980 to 2015. The present meta-analysis included case–control studies that reported the presence of microorganisms in samples of patients with sarcoidosis using culture methods or molecular biology techniques. We used a random effects or a fixed-effect model to calculate the odds ratio (OR) and 95% confidence intervals (CI). Sensitivity and subgroup analyses were performed in order to explore the heterogeneity among studies.ResultsFifty-eight studies qualified for the purpose of this analysis. The present meta-analysis, the first, to our knowledge, in evaluation of all infectious agents proposed to be associated with sarcoidosis and involving more than 6000 patients in several countries, suggests an etiological link between Propionibacterium acnes and sarcoidosis, with an OR of 18.80 (95% CI 12.62, 28.01). We also found a significant association between sarcoidosis and mycobacteria, with an OR of 6.8 (95% CI 3.73, 12.39). Borrelia (OR 4.82; 95% CI 0.98, 23.81), HHV-8 (OR 1.47; 95% CI 0.02, 110.06) as well as Rickettsia helvetica, Chlamydia pneumoniae, Epstein-barr virus and Retrovirus, although suggested by previous investigations, were not associated with sarcoidosis.ConclusionThis meta-analysis suggests that some infectious agents can be associated with sarcoidosis. What seems clear is that more than one infectious agent might be implicated in the pathogenesis of sarcoidosis; probably the patient’s geographical location might dictate which microorganisms are more involved. Future investigations and more clinical trials are need to bring these evidences to a more global level.Electronic supplementary materialThe online version of this article (doi:10.1186/s12890-016-0332-z) contains supplementary material, which is available to authorized users.

Abstract. We performed serological and pathological studies on 495 patients with Chagas' disease from different areas of Bolivia. Eighty-nine Trypanosoma cruzi strains, isolated by xenodiagnosis, were characterized by 12 isoenzyme loci and were related to the presence of cardiac changes and enteric disease with megacolon. There was a high heterogeneity of human zymodemes, presenting evidence of 2 predominant zymodemes genetically dissimilar from each other and ubiquitous in Bolivia. The frequencies of these predominant zymodemes among strains from patients were compared to strains from triatomine bugs previously studied. We observed mixtures of different zymodemes within the same patient, a phenomenon seen previously in Bolivian patients. There was no apparent difference of pathogenicity between the 2 more frequent zymodemes isolated from humans.Trypanosoma cruzi, the agent of Chagas' disease, is associated with 2 main clinical forms, cardiac and intestinal. These clinical forms are not equally distributed within the geographical range of the disease, and it has been proposed that T. cruzi zymodeme distribution could explain this fact.' We present here pathological, serological, and parasitological studies, involving 495 patients from Bolivia, showing the diversity of the clinical forms and the distributions of these clinical forms and T. cruzi zymodemes isolated from human. The relationships are presented and discussed. MATERIALS AND METHODS PatientsTwo groups were examined at different times and under different conditions. Group I, consisting of 364 patients, was from the villages of Chiwisivi (Department La Paz) at 2,800 meters above sea level (mas), Salinas (Department Santa-Cruz) at 800 mas, and Camiri (Department Santa-Cruz) at 800 mas ( Table 1) The second group was composed of 13 1 patients, all exhibiting a positive serology (serodiagnosis as noted above). They originated from different endemic regions of Bolivia, although 108 had been living in La Paz (3,600 mas) for at least 5 years (average time spent in La Paz: 10 years). The endemic areas where the patients had spent their childhoods or the first endemic area where they had spent > 1 year were considered the geographical origins of infection ( Table 2). The following tests were conducted ECG, x-ray of the right anterior side of the esophagus, and x-ray of colon after barium washing (4 x-ray fìlms. Group II patients were then classified as follows:Asymptomatic-positive serology, normal ECG, normal esophagus and colon.Cardiopathy-positive serology, ECG with 52 1

BackgroundTumor necrosis factor alpha (TNF-α) blockers are recognized as a risk factor for reactivation of granulomatous infections. Leishmaniasis has been associated with the use of these drugs, although few cases have been reported.MethodologyWe performed a retrospective observational study including patients with confirmed leishmaniasis acquired in the Mediterranean basin that were under TNF-α blockers therapy at the moment of the diagnosis. Patients diagnosed in our hospital from 2008 to 2018 were included. Moreover, a systematic review of the literature was performed and cases fulfilling the inclusion criteria were also included.Principal findingsForty-nine patients were analyzed including nine cases from our series. Twenty-seven (55.1%) cases were male and median age was 55 years. Twenty-five (51%) patients were under infliximab treatment, 20 (40.8%) were receiving adalimumab, 2 (4.1%) etanercept, one (2%) golimumab and one (2%) a non-specified TNF-α blocker. Regarding clinical presentation, 28 (57.1%) presented as cutaneous leishmaniasis (CL), 16 (32.6%) as visceral leishmaniasis (VL) and 5 (10.2%) as mucocutaneous leishmaniasis (MCL). All VL and MCL patients were treated with systemic therapies. Among CL patients, 13 (46.4%) were treated with a systemic drug (11 received L-AmB, one intramuscular antimonials and one miltefosine) while 14 (50%) patients were given local treatment (13 received intralesional pentavalent antimonials, and one excisional surgery). TNF-α blockers were interrupted in 32 patients (65.3%). After treatment 5 patients (10.2%) relapsed. Four patients with a CL (3 initially treated with local therapy maintaining TNF-α blockers and one treated with miltefosine) and one patient with VL treated with L-AmB maintaining TNF-α blockers.ConclusionsThis data supports the assumption that the blockage of TNF-α modifies clinical expression of leishmaniasis in endemic population modulating the expression of the disease leading to atypical presentations. According to the cases reported, the best treatment strategy would be a systemic drug and the discontinuation of the TNF-α blockers therapy until clinical resolution.

A clinical, histopathological and microbiological correlation is essential to corroborate this diagnosis. Solitary lesions are easily treated with surgery, but larger or multiple lesions may require long medical treatments combined with surgery and modification of immunosuppressive medication. The list of dematiaceous fungi implicated in cutaneous infections is expanding, in line with the availability of more sophisticated identification methods and the increasing number of immunosuppressed patients.