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עמוד בית
Sat, 23.11.24

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June 2014
Hagit Peleg MD, Benjamin Koslowski MD, Nurit Hiller MD and Samuel N. Heyman MD
May 2014
Bonaguri Chiara PHD, Orsoni Jelka Gabriella MD, Russo Annalisa PHD, Rubino Pierangela MD, Bacciu Salvatore MD, Lippi Giuseppe MD Melegari Alessandra PHD, Zavota Laura MD, Ghirardini Stella AO and Mora Paolo MD

Background: Cogan’s syndrome (CS) is a rare autoimmune vasculitis characterized by ocular inflammation and sensorineural hearing loss. CS is divided into a “typical” form with non-syphilitic interstitial keratitis and audiovestibular symptoms, and an “atypical” form with ocular involvement affecting structures other than the cornea. Anti-Hsp70 antibodies were found at variable levels in patients presenting with various forms of autoimmune sensorineural hearing loss (ASNHL).

Objectives: To assess the correlation between anti-Hsp70 antibodies and specific ASNHL subgroups.

Methods: We divided 112 subjects into four groups: 14 subjects with typical CS, 24 with atypical CS, 55 with ASNHL, and 19 control subjects (healthy subjects and patients with systemic autoimmune diseases but no sensorineural hearing or audiovestibular alterations). Patients were tested for serological autoimmunity markers including anti-Hsp70.

Results: Positivity of the anti-Hsp70 antibody test was highest in the typical CS group (92.9%) and lowest in the control group (5.2%). The test was positive in 52.7% of patients in the ASNHL group and 16.6% in the atypical CS group. The paired comparison analysis between groups showed that sensitivity of anti-Hsp70 in the typical CS group was significantly higher, as compared to the other three study groups.

Conclusions: Anti-Hsp70 antibodies can be considered a serological marker of “typical” CS. “Atypical” CS is conceivably a sort of “melting pot” of different forms of autoimmune diseases still characterized by ocular inflammation and sensorineural hearing loss but whose antigenic characteristics need to be further defined.

April 2014
Tessa Chelouche MD
 Born in Czechoslovakia, psychiatrist Leo Eitinger (1912-1996) became internationally recognized for research on his fellow concentration camp inmates. He graduated as an MD in 1937, but being Jewish was prohibited from practicing as a doctor. When the Nazis moved into the area he was forced to flee to Norway, where in 1940 he was again deprived of his right to practice medicine. In 1942 he was arrested and deported to Auschwitz. There, as a physician inmate, he was able to help and in many cases save his fellow prisoners, not only with his medical skills but by falsifying prisoners' documents and hiding them from their Nazi captors. One of his patients was Elie Wiesel. Eitinger survived the camps but was forced to join a "death march." After the war he resumed medical practice in Norway, specializing in psychiatry. With his personal experience and knowledge of the suffering of camp survivors, he dedicated his life to studying the psychological effects of traumatic stress in different groups. Eitinger's academic contributions were crucial in the development of this area of research on the effects of excessive stress, laying the foundations for the definition of post-traumatic stress disorder and the post-concentration camp syndrome, thus facilitating recognition of the medical and psychological post-war conditions of the survivors and their resultant disability pensions. 

Ori Galante MD, Ella Abramovich MD, Anat Nevo-Shor MD and Yaniv Almog MD
March 2014
Aleksandra Djokovic, Ljudmila Stojanovich, Milica Kontic, Natasa Stanisavljevic, Slavica Radovanovic and Dragomir Marisavljevic
Background: Antiphospholipid syndrome (APS, also known as Hughes syndrome) may manifest itself as a primary or secondary disease, most commonly with systemic lupus erythemathosus (SLE) and various cardiac manifestations. 

Objectives: To report the first results from the Serbian National Cohort study, which was started in January 2000.

Methods: Our study included 374 patients: 260 primary APS patients and 114 SLE patients with secondary APS. Antiphospholipid antibody (aPL) analysis included detection of anticardiolipin antibodies (aCL) (immunoglobulin G and M), ß2-glycoprotein 1, and lupus anticoagulant. Echocardiography was performed in all patients, and data on myocardial infarction, unstable angina, chronic cardiomyopathy and acute heart failure were collected.

Results: There were 30.7% secondary APS patients and 9.2% primary APS patients with pseudo-infective endocarditis (P = 0.0001). Cardiac manifestations were observed in 28.7% of patients who had more than one type of antibody (category I), in 24.1% with category IIa, in 23.1% with category IIb, and in 27.8% with category IIc (P = 0.78). Age was confirmed as a significant factor for cardiac manifestations in APS patients (52.3 and 43.3 years, respectively, P = 0.001). aCL IgG and IgM positivity was related to valvular changes in all APS patients and high levels of those antibodies increased the risk of these manifestations.

Conclusions: Patients with secondary APS had a higher prevalence of valvular lesions, and some aPL types and high levels of aPL were risk factors for specific cardiac manifestations in APS patients.

January 2014
December 2013
Arie Drugan, Irena Ulanovsky, Yechiel Burke, Shraga Blazer and Amir Weissman
 Background: Reduction of fetal number has been offered in high order multiple gestations but is still controversial in triplets. Since recent advances in neonatal and obstetric care have greatly improved outcome, the benefits of multifetal pregnancy reduction (MFPR) may no longer exist in triplet gestations.

Objectives: To evaluate if fetal reduction of triplets to twins improves outcome.

Methods: We analyzed the outcome of 80 triplet gestations cared for at Rambam Health Care Campus in the last decade; 34 families decided to continue the pregnancy as triplets and 46 opted for MFPR to twins.

Results: The mean gestational age at delivery was 32.3 weeks for triplets and 35.6 weeks for twins after MFPR. Severe prematurity (delivery before 32 gestational weeks) was experienced in 37.5% of triplets and in 7% of twins. Consequently, the rate of severe neonatal morbidity (respiratory distress syndrome, bronchopulmonary dysplasia, intraventricular hemorrhage) and of neonatal death was significantly higher in unreduced triplets, as was the length of hospitalization in the neonatal intensive care unit (31.4 vs. 15.7, respectively). Overall, the likelihood of a family with triplets to take home all three neonates was 80%; the likelihood to take home three healthy babies was 71.5%.

Conclusions: MFPR reduces the risk of severe prematurity and the neonatal morbidity of triplets. A secondary benefit is the reduction of cost of care per survivor. Our results indicate that MFPR should be offered in triplet gestations.

November 2013
O. Havakuk, M. Entin-Meer, J. Ben-Shoshan, P. Goryainov, S. Maysel-Auslender, E.l Joffe and G. Keren
 Background: Vitamin D has been shown to induce beneficial effects on cardiovascular and renal morbidity by regulating inflammation and tissue fibrosis.

Objectives: To evaluate the effect of vitamin D analogues on cardiac function and fibrosis in an animal model of cardiorenal syndrome.

Methods: Unilateral nephrectomy was performed and myocardial infarction induced in rats. Rats were treated with vitamin D receptor activator (VDRA, paricalcitol, 40 ng/250 g x 3/week) versus a vehicle. A third group of animals, which served as the control, underwent sham surgery and received no treatment. After 4 weeks of treatment, cardiac function and fibrosis were assessed by trans-thoracic echo and histology, respectively. As a parameter of systemic inflammation, previously shown to be altered in acute coronary syndrome, T regulatory (Treg) cell levels were measured by flow cytometry. Renal dysfunction was documented by standard laboratory tests.

Results: After 4 weeks of treatment, no significant improvement in cardiac function parameters was noted following VDRA administration. VDRA treatment did not significantly alter Treg cell systemic levels. Consistently, despite a trend toward less extent of myocardial fibrosis, we found no clear beneficial effects of VDRA on myocardial tissue inflammation and remodeling.

Conclusions: Vitamin D treatment showed no beneficial effects on cardiac function parameters and fibrosis in an animal model of cardiorenal syndrome. 

M. P. Cruz-Domínguez, O. Vera-Lastra, A. Deras-Quiñones, F. Jandete-Rivera, P. Grajeda-Lopez, D. Montes-Cortes, G. Medina and L. J. Jara
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