Trois cas graves de rickettsiose humaine à R. conori sans transmission entomologique avérée

Bertoye A., Royer J., Vincent P., Joubert L., Guillermet F. N., Garin J. P. Trois cas graves de Rickettsiose humaine à R. Conori, sans transmission entomologique avérée. In: Bulletin de l'Académie Vétérinaire de France tome 123 n°6, 1970. pp. 247-256

Contrarian clade confirms the ubiquity of spatial origination patterns in the production of latitudinal diversity gradients

The latitudinal diversity gradient (LDG), wherein the number of species and higher taxa peaks in the tropics and decreases toward the poles, is the best-documented large-scale diversity pattern on Earth, but hypotheses explaining the standard LDG must also account for rare “contrarian” taxa that show diversity maxima outside of the tropics. For marine bivalves, one of the few groups that provide spatially explicit temporal data on a global scale, we show that a major contrarian group, the Anomalodesmata, unexpectedly exhibits the same large-scale dynamics as related clades having normal LDGs in two key respects. First, maxima in standing genus diversity and genus origination rates coincide spatially. Second, the strength of a clade's present-day LDG is significantly related to the proportion of its living genera that originated in the tropics during the late Cenozoic, with the contrarian gradient strength at both species and genus level predicted quantitatively by the values for the other clades. Geologic age distributions indicate that the anomalous LDG results from origination that is damped in the tropics rather than heightened in the temperate zones. The pervasive role of spatial origination patterns in shaping LDGs, regardless of the position of their diversity maxima, corroborates hypotheses based on clades showing standard gradients and underscores the insights that contrarian groups can provide into general principles of diversity dynamics

Safety of Inulin and Sinistrin: Combining Several Sources for Pharmacovigilance Purposes

Introduction: Inulin and its analog sinistrin are fructose polymers used in the food and pharmaceutical industries. In 2018, The French National Agency for the Safety of Medicines and Health Products (ANSM) decided to withdraw products containing sinistrin and inulin due to several reports of serious hypersensitivity reactions, including a fatal outcome.Objective: To assess the safety of inulin and sinistrin use in France.Methods: We searched multiple sources to identify adverse reactions (ARs) to inulin or sinistrin: first, classical pharmacovigilance databases including the French Pharmacovigilance (FPVD) and the WHO Database (VigiBase); second, data from a clinical trial, MultiGFR; third, data regarding current use in an hospital. All potential ARs to inulin or sinistrin were analyzed with a focus on hypersensitivity reactions and relationships to batches of sinistrin.Results: From 1991 to 2018, 134 ARs to inulin or sinistrin were registered in the FPVD or VigiBase. Sixty-three cases (47%) were classified as serious, and 129 cases (96%) were hypersensitivity reactions. We found an association between a batch of sinistrin and the occurrence of hypersensitivity reactions. During the MultiGFR clinical trial, 7 patients (7/163 participants) had an Adverse reaction; of these, 4 were hypersensitivity reactions including one case of grade 4 anaphylactic shock. In the hospital, no ARs were observed. In the literature, ARs to inulin and sinistrin are very rarely reported and mostly benign.Conclusion: Most ARs to inulin and sinistrin are hypersensitivity reactions that appear to be associated with sinistrin batches.</jats:p

Performance of ion chromatography to measure picomole amounts of magnesium in nanolitre samples

International audienc

Safety of Inulin and Sinistrin: Combining Several Sources for Pharmacovigilance Purposes

International audienceIntroduction: Inulin and its analog sinistrin are fructose polymers used in the food and pharmaceutical industries. In 2018, The French National Agency for the Safety of Medicines and Health Products (ANSM) decided to withdraw products containing sinistrin and inulin due to several reports of serious hypersensitivity reactions, including a fatal outcome.Objective: To assess the safety of inulin and sinistrin use in France.Methods: We searched multiple sources to identify adverse reactions (ARs) to inulin or sinistrin: first, classical pharmacovigilance databases including the French Pharmacovigilance (FPVD) and the WHO Database (VigiBase); second, data from a clinical trial, MultiGFR; third, data regarding current use in an hospital. All potential ARs to inulin or sinistrin were analyzed with a focus on hypersensitivity reactions and relationships to batches of sinistrin.Results: From 1991 to 2018, 134 ARs to inulin or sinistrin were registered in the FPVD or VigiBase. Sixty-three cases (47%) were classified as serious, and 129 cases (96%) were hypersensitivity reactions. We found an association between a batch of sinistrin and the occurrence of hypersensitivity reactions. During the MultiGFR clinical trial, 7 patients (7/163 participants) had an Adverse reaction; of these, 4 were hypersensitivity reactions including one case of grade 4 anaphylactic shock. In the hospital, no ARs were observed. In the literature, ARs to inulin and sinistrin are very rarely reported and mostly benign.Conclusion: Most ARs to inulin and sinistrin are hypersensitivity reactions that appear to be associated with sinistrin batches

Hypomagnesemia, Hypocalcemia, and Tubulointerstitial Nephropathy Caused by Claudin-16 Autoantibodies.

Chronic hypomagnesemia is commonly due to diarrhea, alcoholism, and drugs. More rarely, it is caused by genetic defects in the effectors of renal magnesium reabsorption. In an adult patient with acquired severe hypomagnesemia, hypocalcemia, tubulointerstitial nephropathy, and rapidly progressing kidney injury, similarities between the patient's presentation and features of genetic disorders of renal magnesium transport prompted us to investigate whether the patient had an acquired autoimmune cause of renal magnesium wasting. To determine if the patient's condition might be explained by autoantibodies directed against claudin-16 or claudin-19, transmembrane paracellular proteins involved in renal magnesium absorption, we conducted experiments with claudin knockout mice and transfected mouse kidney cells expressing human claudin-16 or claudin-19. We also examined effects on renal magnesium handling in rats given intravenous injections of IgG purified from sera from the patient or controls. Experiments with the knockout mice and in vitro transfected cells demonstrated that hypomagnesemia in the patient was causally linked to autoantibodies directed against claudin-16, which controls paracellular magnesium reabsorption in the thick ascending limb of Henle's loop. Intravenous injection of IgG purified from the patient's serum induced a marked urinary waste of magnesium in rats. Immunosuppressive treatment combining plasma exchange and rituximab was associated with improvement in the patient's GFR, but hypomagnesemia persisted. The patient was subsequently diagnosed with a renal carcinoma that expressed a high level of claudin-16 mRNA. Pathogenic claudin-16 autoantibodies represent a novel autoimmune cause of specific renal tubular transport disturbances and tubulointerstitial nephropathy. Screening for autoantibodies targeting claudin-16, and potentially other magnesium transporters or channels in the kidney, may be warranted in patients with acquired unexplained hypomagnesemia