[Hyponatremic-hypertensive syndrome successfully treated by endovascular therapy: A case report]. / Syndrome hyponatrémie hypertension artérielle efficacement traité par angioplastie à propos d'un cas.

INTRODUCTION: Hyponatremic-hypertensive syndrome (HHS) is characterized by hypertension and hyponatremia. CASE PRESENTATION: We report a case of HHS in a 73-year-old woman, revealed by a hyponatremia leading to status epilepticus, without initial hypertension due to hypovolemia. She was successfully treated by endovascular therapy without any long-term supplementation or anti-hypertensive medication. CONCLUSION: Physiopathology hypothesis of HHS implicate pressure natriuresis, in this case, hypertension is not initially found and we discuss other hyponatremia mechanisms.

Lactobacillus bacteremia: Pathogen or prognostic marker?

OBJECTIVE: Lactobacillus bacteremia is a rare event and its epidemiology is poorly known. Whether Lactobacillus bacteremia is a contaminant, a risk factor, or a risk marker of death remains an open question. PATIENTS AND METHODS: We conducted a retrospective study of patients presenting with Lactobacillus bacteremia (LB), between January 2005 and December 2014, at the Grenoble University Hospital. RESULTS: LB was observed in 38 patients (0.34% of all positive blood cultures). Cancer (40%), immunosuppression (37%), and use of central venous devices (29%) were frequently associated with LB. We observed a significant increase with time in the number of Lactobacillus positive blood cultures among all blood cultures performed (P=0.04). LBs were divided into two clinical-biological presentations: secondary bacteremia with a known portal of entry (n=30) and isolated bacteremia (n=8). Case fatality was 31% at D28, 55.2% at 1 year in the secondary bacteremia group, and 12.5% (both at D28 and 1 year) in the isolated bacteremia group. Secondary bacteremia with a known portal of entry was significantly associated with case fatality after adjustment for age, co-infection, cancer, immunosuppression, diabetes, and sex (OR 14.9 [1.04-216] P=0.047) for fatality at one year, but not for D28 fatality (P=0.14). CONCLUSION: Lactobacillus bacteremia may be an important marker of disease severity rather than a pathogen, suggesting comorbidities. It should not be considered a contaminant, but should lead physicians to screen for associated infections and underlying diseases.

[Cohort of renal infarction during 2years at Grenoble teaching hospital]. / Série d'infarctus rénaux au CHU de Grenoble sur 2ans.

BACKGROUND: Renal infarctions are rare events, clinical symptoms are various and diagnosis may be difficult, leading to diagnosis delay with kidney dysfunction risk. METHODS: During 24 months (March 2013-February 2015), all patients admitted in nephrology, cardiology, or internal medicine for renal infarction were recorded. Cardiovascular risk, clinic-biologic and radiologic data were recorded. A prospective follow-up at 6 months was offered for each patient. RESULTS: Eleven patients were admitted from emergency unit and 1 from general practitioner. Clinic symptoms are various: abdominal pain, headache, hypertension, and stroke. Diagnosis was not initially evocated, and was given by CT scan with 3 days median delay. Etiologies were composed of 5 dissections, 4 embolisms (atrial fibrillation), 1 cannabinoid arteritis, 1 thrombosis on atheroma, 1 thrombosis on postradiotherapy stenosis. Initial treatment was anticoagulation alone for 7 patients, with antiplatelet agent for 1 patient, anticoagulation followed by antiplatelet agent for 2 patients, and antiplatelet agent alone for 2 patients. We observed LDH elevation (4 cases on 5 available data) at admission; inflammatory syndrome, hypokalemia, and hypertension at 48-72h of symptoms. At 6months follow-up, one patient had altered glomerular filtration rate, and one patient had recidivism. CONCLUSION: Delay of diagnosis is a real problem for renal infarction, and need to be evocated every flank pain. LDH elevation may help clinician to suggest renal infarction and lead to CT scan. Association of delayed inflammatory syndrome, hypertension and hypokalemia after flank pain strongly suggest renal infarction.

Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma.

Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALK+ ALCL) is characterized by constitutive activation of the Janus kinase (JAK)3/signal transducers and activators of transcription 3 (STAT3) signaling pathway. SHP1, a tyrosine phosphatase that negatively regulates JAK/STAT, is frequently absent in ALK+ ALCL owing to gene methylation. To test the hypothesis that loss of SHP1 contributes to JAK3/STAT3 activation in ALK+ ALCL cells, we induced SHP1 expression using 5-aza-2'-deoxycytidine (5-AZA), an inhibitor of DNA methyltransferase, in ALK+ ALCL cell lines, and correlated with changes in the JAK3/STAT3 pathway. 5-AZA gradually restored SHP1 expression in Karpas 299 and SU-DHL-1 cells over 5 days. The initially low level of SHP1 expression did not result in significant changes to the expression or tyrosine phosphorylation of JAK3 and STAT3. However, higher levels of SHP1 seen subsequently correlated with substantial decreases in JAK3 and pJAK3, followed by pSTAT3 (but not STAT3). Importantly, the decrease in JAK3 was abrogated by MG132, a proteasome inhibitor. 5-AZA induced no significant increase in apoptosis but it sensitized ALCL cells to doxorubicin-induced apoptosis. Our findings support the concept that loss of SHP1 contributes to the constitutive activation of JAK3/STAT3 in ALK+ ALCL cells. SHP1 appears to downregulate JAK3 by two mechanisms: tyrosine dephosphorylation and increased degradation via the proteasome pathway.