[Association of hyponatremia and eosinophilia: correlated idiopathic hypereosinophilic syndrome and SIADH or adrenal insufficiency with secondary eosinophilia]. / Associazione di iponatriemia ed eosinofilia: sindrome ipereosinofila idiopatica e SIADH correlata o insufficienza surrenalica con eosinofilia secondaria?

A 56 year old man was admitted cause he had increasing symptoms as weakness, lethargy, disorientation. The total eosinophil count was 3000/mm3, the serum sodium concentration was 120 mmol per litre. In spite of severe hyponatriemia, urinary sodium excretion was not suppressed and serum osmolality (240 mOsm/Kg was lower than urine osmolality (488 mOsm/Kg). SIADH and Idiopathic Hypereosinophilic Syndrome was diagnosed because we found systemic failure signs due to hypereosinophilia (hepatitis, gastritis, pulmonary hypertension, and encefalopathy). Cortisonic treatment was started with symptoms improving, natriemia, eosynophil count and hepatitis signs normalization. After treatment stopping, reappeared asymptomatic hypereosinophilia, than we choosed Idrossiurea but, non-standing hypereosinophilia disappeared, appeared signs of preexisting adrenal insufficiency, emphasized by stopping cortisone therapy. A RMN showed an hypofiseal adenoma. Many cases of SIADH and Hypereosinophilia hiding adrenocortical insufficiency are reported with severe and unusual hypereosinophilia.

Monoclonal anti-annexin V antibody inhibits trophoblast gonadotropin secretion and induces syncytiotrophoblast apoptosis.

The pathogenic role of anti-annexin V antibodies remains unclear. Anti-annexin V antibodies are frequently associated with higher incidences of intrauterine fetal loss, preeclampsia, and arterial and venous thrombosis. The present study investigated the in vitro ability of anti-annexin V antibody to bind human trophoblast cells, to affect trophoblast gonadotropin secretion and invasiveness, and to induce placental apoptosis. Cytotrophoblast cells were dispersed in Ringer bicarbonate buffer containing trypsin and DNase I, filtered, and layered over a Percoll gradient in Hanks balanced salt solution. In the case of monoclonal anti-annexin V antibody, the highest binding was found when the cells displayed the greatest amount of syncytium formation. Anti-annexin V antibody, but not its negative control, induced trophoblast apoptosis and significantly reduced trophoblast gonadotropin secretion. These findings suggest that recognition by anti-annexin V antibody of adhered annexin V on trophoblast cell structures might represent a potential pathogenic mechanism by which these antibodies can cause defective placentation.

Interleukin-3 and human trophoblast: in vitro explanations for the effect of interleukin in patients with antiphospholipid antibody syndrome.

OBJECTIVE: To examine the effect of interleukin (IL)-3 on in vitro trophoblast differentiation, hormone production, and invasiveness affected by antiphospholipid antibodies. DESIGN: Primary cytotrophoblast cell cultures. SETTING: Obstetrics and Gynecology Department of the Catholic University, Rome, Italy. PATIENT(S): Five normal pregnant women underwent uncomplicated vaginal delivery at 36 weeks of gestation. INTERVENTION(S): Immunoglobulin (Ig) G antibodies were isolated from the plasma of two patients with antiphospholipid syndrome and two normal control subjects with the use of protein-G Sepharose columns. Cytotrophoblast cells were dispersed in Ringer's bicarbonate buffer containing trypsin and DNAseI, filtered, and layered over a Percoll gradient in Hank's balanced salt solution. MAIN OUTCOME MEASURE(S): We investigated the effects of IL-3 and antiphospholipid antibodies on trophoblast cell invasiveness, differentiation, and hormone secretion. RESULT(S): IgG obtained from patients with antiphospholipid syndrome bound to trophoblast cells, with inhibitory effects on the cells' invasiveness, differentiation, and hCG secretion. IL-3 was able to restore in vitro placental functions. CONCLUSION(S): These results imply that IL-3 favorably affects human trophoblast implantation and development.

Antiphospholipid antibodies affect trophoblast gonadotropin secretion and invasiveness by binding directly and through adhered beta2-glycoprotein I.

OBJECTIVE: To investigate the in vitro ability of antiphospholipid antibodies (aPL) to bind human trophoblast cells and to affect gonadotropin secretion and invasiveness. METHODS: Antiphospholipid antibody IgG from women with recurrent miscarriages, beta2-glycoprotein I (beta2GPI)-independent IgG aPL human monoclonal antibody (mAb) (519), and IgM anti-beta2GPI human mAb (TMIG2) were investigated for their binding to trophoblasts cultured for various amounts of time, their ability to affect invasiveness of Matrigel-coated filters, and their release of human chorionic gonadotropin (hCG). RESULTS: Polyclonal IgG aPL, as well as mAb 519 and TMIG2, bound to trophoblasts, the highest binding being found when cells displayed the greatest amount of syncytium formation. TM1G2 binding was found to be betaGPI dependent. Both polyclonal and monoclonal aPL, but not the controls, significantly reduced hCG release and Matrigel invasiveness. CONCLUSION: These findings suggest that aPL recognition of both anionic PL and adhered beta2GPI on trophoblast cell structures might represent a potential pathogenetic mechanism for defective placentation in women with the antiphospholipid syndrome.

Low-molecular weight heparin restores in-vitro trophoblast invasiveness and differentiation in presence of immunoglobulin G fractions obtained from patients with antiphospholipid syndrome.

The present study was designed to investigate the effects of immunoglobulin G obtained from patients with antiphospholipid syndrome (APS) on in-vitro models of trophoblast invasiveness and differentiation. We tested the binding of affinity-purified immunoglobulin G to human primary trophoblast cells. These antibodies affected the invasiveness and differentiation of cytotrophoblast cells after binding to the cell surface. In addition, we determined whether the drugs used to treat APS might be able to restore the trophoblast functions. Low-molecular weight heparin, in a dose-dependent manner, significantly reduced the immunoglobulin G binding to trophoblast cells and restored in-vitro placental invasiveness and differentiation. No effect was observed in the presence of acetylsalicylic acid. These observations may help in understanding the role of these treatments in women with APS.

Use of medical resources and quality of life of patients with chronic heart failure: a prospective survey in a large Italian community hospital.

AIMS: To assess the prevalence, clinical characteristics, use of medical resources and quality of life in consecutive patients with chronic heart failure (CHF) hospitalized in a large community hospital during 3 months. METHODS AND RESULTS: The study group included 354 patients with CHF, admitted in the Departments of Internal Medicine (97%) and Cardiology. Median age was 78 years [72;85], 45% were males. CHF was the main diagnosis in 72%; 28% were in NYHA class III and 49% in class IV; 42% had atrial fibrillation. The median hospital stay was 8 days [5;14], in-hospital mortality 9% in those admitted for CHF and 19% in those admitted primarily for other diseases. Patients with CHF occupied 15% of the beds; 1330 ECGs, 389 chest X-rays, 112 echocardiograms and 10 coronary angiograms were performed. A quality of life questionnaire revealed that 82% had problems with mobility, 54% with self-care and 88% with everyday activity. Thirty-nine percent of patients had at least one hospitalization during the previous year. CONCLUSIONS: Ninety-seven percent of hospitalized patients with CHF are admitted in the Internal Medicine wards and occupy 15% of beds. The majority of the patients are 72 years or older, with severe heart failure. The frequency of rehospitalization(s) and mortality rate in this population remains high. Echocardiography is performed only in 27% of patients.