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Hypercalcemia is a common pathological condition in clinical practice. The two most common causes are primary hyperparathyroidism and cancer. SIADH is often encountered in cancer cases and is the most common cause of hyponatremia. The aim of this study is to evaluate serum sodium levels in a cohort of patients with hypercalcemia and consider its predictive value in determining the origin of this hypercalcemia.We performed a retrospective study on a series of 15.284 blood tests among adult patients with hypercalcemia. After selection, the study population had 151 patients. We studied mainly serum sodium and etiology of hypercalcemia in our population.We observed a statistically significant association between the presence of hyponatremia and the neoplastic etiology of hypercalcemia. This association persisted after exclusion of patients under treatment with loop diuretics. Conversely, there was no association between hypernatremia and cancer-related hypercalcemia. Among 151 patients with hypercalcemia, 16 presented hyponatremia and 7 with hypernatremia. SIADH was the main cause of hyponatremia. We performed univariate and multivariate logistic regression showing the association between the presence of cancer and the presence of hyponatremia.Our study shows that there is an association between the presence of hyponatremia and neoplastic origin of hypercalcemia. Besides, the association described between hyponatremia and cancer is not faulted by the presence of hypercalcemia, a potential cause of acquired nephrogenic diabetes insipidus.L’hypercalcémie est une condition pathologique courante en pratique clinique. Les deux causes les plus fréquentes sont l’hyperparathyroïdie primaire et le cancer. Le syndrome de sécrétion inappropriée de l’hormone antidiurétique (SIADH) est souvent rencontré dans les cas de cancer, et constitue la cause la plus fréquente d’hyponatrémie. Le but de cette étude est d’évaluer la natrémie dans une cohorte de patients atteints d’hypercalcémie et d’apprécier sa valeur prédictive dans la détermination de l’origine de cette hypercalcémie. Matériel et méthode : Nous avons réalisé une étude rétrospective sur une série de 15.284 analyses sanguines chez des patients adultes hypercalcémiques. Après sélection, la population de l’étude comptait 151 patients. Nous avons étudié principalement la natrémie et l’étiologie de l’hypercalcémie au sein de notre population. Résultats : Nous avons observé une association statistiquement significative entre la présence d’une hyponatrémie et l’étiologie néoplasique de l’hypercalcémie. Cette association persistait après l’exclusion des patients sous traitement par diurétiques de l’anse. Par contre, il n’existait pas d’association entre l’hypernatrémie et l’origine cancéreuse de l’hypercalcémie. Sur 151 patients hypercalcémiques, 16 étaient hyponatrémiques et 7 étaient hypernatrémiques. Un SIADH représentait la cause principale des cas d’hyponatrémie. Nous avons réalisé une régression logistique uni- et multivariée montrant l’association entre l’existence d’un cancer et la présence d’une hyponatrémie.Notre étude montre qu’il existe une association entre la présence d’une hyponatrémie et l’étiologie néoplasique de l’hypercalcémie. Par ailleurs, l’association classiquement décrite entre hyponatrémie et cancer n’est pas prise en défaut par la présence d’une hypercalcémie, cause potentielle de diabète insipide néphrogénique acquis.

Intravascular large B-cell lymphoma is a rare entity characterized by the proliferation of neoplastic lymphocytes in the lumen of small blood vessels and high mortality. Diagnosis of intravascular lymphoma is often delayed or established postmortem. Here, we report the case of a 48-year-old woman presenting hemophagocytic syndrome, with pituitary gland and neurological involvement. Diagnosis of intravascular large B-cell lymphoma was made on perisplenic vessels, while liver and bone marrow biopsy was noncontributive. This case demonstrates the importance of thorough histopathologic investigations in the setting of high suspicion.

We report the case of a 74-year-old woman admitted to the emergency unit for resting dyspnea. Clinical presentation, cardiac MRI and echocardiography were consistent with cardiac tamponade requiring emergency pericardiocentesis. Cytologic examination of the pericardial fluid revealed the presence of CD68pos CD1aneg S100neg foamy histiocytes (Fig. 1). Additional investigations complied with the diagnosis of Erdheim-Chester histiocytosis. Treatment with αIFN was initiated but the patient developed severe neutropenia that contraindicated further administration. The detection of BRAFV600E mutation on histiocytes isolated from the pericardial liquid and CNS involvement (cerebral masses) prompted the administration of vemurafenib, a selective BRAFV600E kinase inhibitor. Four months after the initiation of low-dose vemurafenib, pericarditis almost resolved and cerebral masses decreased by 50% (Fig. 2). To our knowledge, analysis of pericardial fluid allowing the diagnosis of Erdheim-Chester disease and the detection of the BRAFV600E mutation has in fact been rarely described in the literature. This case report and the successful evolution under vemurafenib also support the use of BRAFV600E inhibitors in αIFN-intolerant patients with BRAFV600E mutation, particularly in case of heart and central nervous system involvement.

Adequate protein folding is necessary for normal cell function and a tightly regulated process that requires proper intracellular ionic strength. In many cell types, imbalance between protein synthesis and degradation can induce endoplasmic reticulum (ER) stress, which if sustained, can in turn lead to cell death. In nematodes, osmotic stress induces massive protein aggregation coupled with unfolded protein response and ER stress. In clinical practice, patients sustaining rapid correction of chronic hyponatremia are at risk of osmotic demyelination syndrome. The intense osmotic stress sustained by brain cells is believed to be the major risk factor for demyelination resulting from astrocyte death, which leads to microglial activation, blood-brain barrier opening, and later, myelin damage. Here, using a rat model of osmotic demyelination, we showed that rapid correction of chronic hyponatremia induces severe alterations in proteostasis characterized by diffuse protein aggregation and ubiquitination. Abrupt correction of hyponatremia resulted in vigorous activation of both the unfolded protein response and ER stress accompanied by increased autophagic activity and apoptosis. Immunofluorescence revealed that most of these processes occurred in astrocytes within regions previously shown to be demyelinated in later stages of this syndrome. These results identify osmotic stress as a potent protein aggregation stimuli in mammalian brain and further suggest that osmotic demyelination might be a consequence of proteostasis failure on severe osmotic stress., SCOPUS: ar.j, info:eu-repo/semantics/published

Introduction Il existe de multiples medicaments susceptibles de causer une hyperprolactinemie. Cette elevation ne depasse generalement pas 100 ng/mL sauf pour certains neuroleptiques, comme la risperidone, ou cette elevation peut atteindre 200 ng/mL. Au-dela de cette valeur, le diagnostic de prolactinome est le plus probable. Observations Une patiente de 48 ans est admise pour mise au point d’une inappetence associee a des nausees, une perte de poids et une fatigue extreme. L’examen clinique revele un IMC a 17,6 kg/m2 et une legere hypertension arterielle. La patiente ne presente ni gynecomastie, ni galactorrhee. Son traitement a domicile consiste en amitriptyline, L-thyroxine, pantoprazole, pilule œstro-progestative en continu (Yasmin), zolpidem, et domperidone ou metoclopramide en alternance depuis plusieurs semaines. Une gastroscopie montre une oesophagite associee a une hernie hiatale. Le scanner abdominal est sans particularite. La biologie montre une hyperprolactinemie severe (694 ng/mL). Une IRM hypophysaire decrit un microadenome de 5 mm de plus grand axe. Un rythme hormonal de 24 h realise apres l’arret de sa pilule œstro-progestative et des anti-nauseeux montre une nette diminution des taux de prolactine (49 a 71 ng/mL). L’arret ulterieur de l’amitriptyline n’entraine qu’une diminution marginale de la prolactinemie (49 a 56 ng/mL). Discussion Le cas de cette patiente decrit une hyperprolactinemie d’origine medicamenteuse inhabituellement severe (pres de 700 ng/mL), associee principalement a la prise d’anti-nauseeux. Il est en outre probable qu’un microprolactinome et/ou l’anxiodepression severe presentee par la patiente aient aggrave l’elevation observee, comme en temoigne l’hyperprolactinemie moderee persistante malgre l’arret des medicaments incrimines.

Oral urea has been used in the past to treat various diseases like gastric ulcers, liver metastases, sickle cell disease, heart failure, brain oedema, glaucoma, Meniere disease, etc. We have demonstrated for years, the efficacy of urea to treat euvolemic (SIADH) or hypervolemic hyponatremia. We briefly describe the indications of urea use in symptomatic and paucisymptomatic hyponatremic patients. Urea is a non-toxic, cheap product, and protects against osmotic demyelinating syndrome (ODS) in experimental studies. Prospective studies showing the benefit to treat mild chronic hyponatremia due to SIADH and comparing water restriction, urea, high ceiling diuretics, and antivasopressin antagonist antagonist should be done., SCOPUS: ar.j, info:eu-repo/semantics/published