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Given the increased risk of infection after chemotherapy, hematological societies have proposed postponing chemotherapy, when feasible, during the COVID-19 pandemic [1], despite initial studies sho...

Isolated hypercalcaemia, leukocytosis or thrombocytosis is common in cancer patients, but the association of the first two is rarely described and the triple paraneoplastic syndrome is even more exceptional. Their concomitance portends a poor prognosis in solid tumor patients. We report the case of a 53-year old man with hypercalcaemia-leukocytosis-thrombocytosis paraneoplastic syndrome associated with a urothelial carcinoma which was fatal 4 months after diagnosis. Pathophysiology remains unclear but secretion of parathyroid hormone related protein (PTHrp) and cytokines such as granulocyte colony stimulating factor (G-CSF) as well as activation of thrombopoietin (TPO) receptor might be implicated. Although very rare, this paraneoplastic syndrome should be considered in solid tumor patients presenting with concomitant hypercalcaemia, leukocytosis and thrombocytosis, as it presages a poor prognosis with a rapid disease progression, and should be looked for and when present taken into account in the management of urothelial carcinoma, where no biological prognostic marker is available in clinical practice.

Background. Mediterranean spotted fever (MSF) is a tick-borne infection caused by Rickettsia conorii conorii mainly endemic in the Mediterranean Basin. Although usually considered as a benign disease, severe forms of MSF have been sporadically reported. Methods. We report on three patients who developed severe MSF complications after a stay in Morocco. Literature was reviewed to assess the frequency and pattern of MSF complications in the largest reported case series in endemic countries. Results. Each of our three patients diagnosed with MSF presented with a different complicated course: one with meningoencephalitis, one with lung embolism and one with septic shock and multi organ failure. In published series, rate of complications (defined as severe organ involvement) ranged from 1% to 20%. However, study designs and settings were highly variable and did not allow for relevant comparisons. Meningoencephalitis and shock with multi organ failure were the most frequently observed complications. Mortality of severe course was up to 20% in some series. Conclusion. Severe organ involvement is not infrequent in patients with Mediterranean spotted fever and fatal outcome is regularly reported. Because presentations of complicated course may be extremely diverse, a high index of suspicion is required in febrile patients with potential exposure, in particular if skin rash and/or eschar are found. Early appropriate antibiotherapy is crucial to improve outcome.

Aim: The aim of this study was to evaluate retrospectively the usefulness of [18F]fluorodeoxyglucose (FDG)-PET/computed tomography (CT) in patients affected by human immunodeficiency virus and suffering from fever of unknown origin (HIV-associated FUO). Material and methods: Ten patients (six males, four females, age 24-48 years) suffering from HIV-associated FUO were studied by FDG-PET/CT. Final diagnosis was established either by microbiological or histopathological analysis or by a more than 6-month follow-up. FDG-PET/CT was regarded as 'helpful for diagnosis' when the abnormal uptake pointed to the organ or location where the cause of fever was thereafter identified. Results: Nine out of 10 FDG-PET/CT were abnormal and the cause of fever was further demonstrated by other diagnostic procedures. An infectious process (tuberculosis) was diagnosed in six patients and a neoplasm in three (two lymphomas, one Kaposi's sarcoma). FDG-PET/CT directly suggested sites for biopsy in six patients (tuberculous lymphadenitis and neoplasm). The only patient with normal FDG-PET/CT suffered from drug-induced fever. Conclusion: FDG-PET/CT is a valuable tool in patients with HIV-associated FUO. FDG-PET/CT was categorized as 'helpful for diagnosis' in nine out of the 10 patients we studied. Adding the CT anatomical landmarks to the PET findings allowed an accurate and easy localization of the sites to be punctured in the six patients in whom histopathological diagnosis was needed. © 2009 Wolters Kluwer Health

The screening and treatment of latent tuberculosis (TB) infection reduces the risk of progression to active disease and is currently recommended for HIV-infected patients. The aim of this study is to evaluate, in a low TB incidence setting, the potential contribution of an interferon-gamma release assay in response to the mycobacterial latency antigen Heparin-Binding Haemagglutinin (HBHA-IGRA), to the detection of Mycobacterium tuberculosis infection in HIV-infected patients., SCOPUS: ar.j, info:eu-repo/semantics/published

Tuberculosis (TB) remains a leading cause of death, and the role of T-cell responses to control Mycobacterium tuberculosis infections is well recognized. Patients with latent TB infection develop strong IFN-gamma responses to the protective antigen heparin-binding hemagglutinin (HBHA), whereas patients with active TB do not.We investigated the mechanism of this difference and evaluated the possible involvement of regulatory T (Treg) cells and/or cytokines in the low HBHA T-cell responses of patients with active TB.The impact of anti-transforming growth factor (TGF)-beta and anti-IL-10 antibodies and of Treg cell depletion on the HBHA-induced IFN-gamma secretion was analyzed, and the Treg cell phenotype was characterized by flow cytometry.Although the addition of anti-TGF-beta or anti-IL-10 antibodies had no effect on the HBHA-induced IFN-gamma secretion in patients with active TB, depletion of CD4(+)CD25(high)FOXP3(+) T lymphocytes resulted in the induction by HBHA of IFN-gamma concentrations that reached levels similar to those obtained for latent TB infection. No effect was noted on the early-secreted antigen target-6 or candidin T-cell responses.Specific CD4(+)CD25(high)FOXP3(+) T cells depress the T-cell-mediated immune responses to the protective mycobacterial antigen HBHA during active TB in humans.