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עמוד בית
Fri, 01.11.24

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August 2001
Altoon Dweck, MD, Ayala Abrahamov, MD, Irith Hadas-Halpern, MD, Ari Zimran, MD and Devorah Elstein, PhD
July 2001
Tsafra Ilan, MSc, Tamy Shohat, MD, Ana Tobar, MD, Nurit Magal, PhD, Michal Yahav, BSc, Gabrielle J. Halpern, MB, ChB, Gidi Rechavi, MD and Mordechai Shohat, MD

Background: Familial nephritis is a heterogeneous group of disorders caused by several genetic conditions such as Alport syndrome, glomerulonephritic syndromes, and unclas­sified nephritis without deafness or ocular defects.

Objectives: To describe a family of Iraqi Jewish origin, several of whose members suffer from non-syndromic renal failure without deafness or ocular defects and where transmis­sion is by autosomal dominant inheritance. We present the case histories of four family members and describe the molecular analysis performed in order to seek a possible linkage to one of the genes causing Alport or Alport-like syndromes.

Methods: We investigated all family members over the age of 18 for evidence of renal failure. We also extracted DNA and carried out molecular linkage analysis with polymorphic markers in each of the known loci involved in Alport and Alport­like syndromes.

Results: Histology of the renal biopsy specimens showed non-specific findings. Linkage was excluded for all the Alport and Alport-like syndrome loci.

Conclusions: The condition suffered by several members of this family seems to represent a unique autosomal dominant type of progressive hereditary nephritis, characterized by hypertension and progressive renal failure without significant hematuria or proteinuria. The main histological changes are non-specific in the early stage of the disease. Our study rules out all the currently known genes that cause Alport syndrome as being responsible for the basic defect in this type of nephritis.

Alberto Kurzbaum, MD, Claudia Simsolo, MD, Ludmilla Kvasha, MD and Arnon Blum, MD
June 2001
Elisheva Simchen, MD, MPH, Irit Naveh, RN, MSc, Yana Zitser-Gurevich, MD, MPH, Dalit Brown, MSc and Noya Galai, PhD

Objective: To explore the putative effect of cardiac rehabilitation programs on the health-related quality of life’ and ‘return to work’ in pre-retirement patients one year after coronary artery bypass grafting.

Methods: Of the 2085 patients aged 45-4 who survived one year after CABG and were Israeli residents, 145 (6.9%) had participated in rehabilitation programs. Of these, 124 (83%) who answered QOL questionnaires were individually matched with 248 controls by gender, age within 5 years. and the time the questionnaire was answered. All patients had full clinical follow-up including a pre-operative interview. The Short Form-36 QOL questionnaire as well  as a specific questionnaire were mailed to surviving patients one year after surgery. Study outcomes included the scores on eight scales and two summary components of the SF-36, as well as return to work’ and ‘satisfaction with medical services’ from the specific questionnaire. Analysis was done for matched samples.

Results: Cardiac rehabilitation participants had signifi­cantly higher SF-36 scores in general health, physical functioning, and social functioning. They had borderline significant higher scores in the physical summary component of the SF-36. The specific questionnaire revealed significantly better overall functioning, higher satisfaction with medical care. and higher rate of return to work. While participants in cardiac rehabilitation and their controls were similar in their socio­-demographic and clinical profiles, participating patients tended to be more physically active and more fully employed than their controls.

Conclusions: Rehabilitation participants had a self-per­ception of better HRQOL, most significantly in social function­ing. Our findings of more frequent return to work and higher satisfaction with medical care should induce a policy to encourage participation in cardiac rehabilitation programs after CABG.
 

Alex Kessler, MD, Ephraim Eviatar, MD, Judith Lapinsky, MD, Tifha Horne, MD, Nathan Shlamkovitch, MD and Shmuel Segal, MD
May 2001
Sydney Ben-Chetrit, Vidal Barchilon, MD, Ze’ev. Korzets, MD, BS, Joelle Bernheim, MD and Jacques Bernheim, MD
April 2001
Jamal Zidan, MD, Wolf Robenstein, MD, Amira Abzah, RN and Sigalit Tamam, RN

Background: Classic Kaposi's sarcoma is a rare tumor with an indolent behavior. Local therapy is not applicable in disseminated cutaneous disease. Patients with advanced disease are usually treated with systemic chemotherapy.

Objectives: To assess the effectiveness and toxicity of  single-agent vinblastine in the treatment of disseminated and recurrent Kaposi's sarcoma.

Methods: Ten patients with wide cutaneous spread of classic Kaposis sarcoma were treated with single-agent vinblastine, 6 mg/m2 intravenously once every 2 weeks. Vinblastine was continued for 2 months after achieving a maximal response.

Results: The male:female ratio was 2.3:1, and median age 64 years (range 50-79 years). The median number of involved nodules in the skin was 34. The overall response rate was 90%, 5 with complete response (50%) and 4 with partial response (40%). Complete responders had a longer duration of response than partial responders: 41.2 vs. 14.8 months. The median survival of all patients was 33 months. Side effects were minimal and tolerable.

Conclusions: Vinblastine is very effective in the treatment of extensive classic Kaposi's sarcoma, and results in a high response rate, long survival and disease-free survival with tolerable toxicity.

Dror Kraus Bmed, Sc, Igor Kaiserman, MD, Joseph Frucht-Pery, MD and Rami Rahamimoff, MD
Arnon Blum, MD, Yami Shapira, MD, Shay Yeganh, MD and Maya Rabinkov, MD
March 2001
Talia Weinstein, MD, Ran Tur-Kaspa, MD, Avry Chagnac, MD, Asher Korzets, MD, Yacov Ori, MD, Dina Zevin, MD, Michal Herman, MD and Uzi Gafter, MD PhD

Background: Hepatitis C virus is the major cause of acute and chronic hepatitis in patients with end-stage renal disease receiving replacement therapy.

Objectives: To define the prevalence of HCV RNA in a population of patients on dialysis in Israel, to determine the relative risk of acquiring HCV infection while treated by hemodialysis or chronic ambulatory peritoneal dialysis, and to define the HCV genotypes in this population.

Methods: During 1995 we studied 162 dialysis patients. Information was obtained regarding the mode of dialysis, years of treatment, number of blood transfusions, and results of serological testing for HCV, hepatitis B virus, and human immunodeficiency virus. Anti-HCV antibodies were tested by a third-generation microparticle enzyme immunoassay. HCV RNA was determined by polymerase chain reaction. HCV genotyping was performed by a hybridization assay.

Results: HCV RNA was detected in 18% of the HD group and 7% of the CAPD group. The number of HCV RNA-positive patients was significantly higher in the HD than the CAPD group (P < 0.05). HCV RNA-positive HD patients were treated longer than the HCV RNA-negative patients (P < 0.02).

Conclusions: Third-generation immunoassay proved to be highly sensitive (94%) and specific (91%) in identifying HCV RNA positivity. Several HCV subtypes were detected, lb being the most frequent. Identification and isolation of infected HCV patients may minimize its spread in dialysis units and prevent cross-infection.

Imad R. Makhoul, MD DSc, Osnat Zmora, MD, Ada Tamir, DSc, Eli Shahar, MD and Polo Sujov, MD

Background: Congenital subependymal pseudocysts are incidental findings that are found in 05-5.2% of neonates during postmortem examination or head ultrasonography. In our institution we detected 10 neonates with CSEPC.

Objective: To investigate associated etiological factors, morphologic characteristics and outcome of CSEPC.

Methods: We performed a meta-analysis of the literature on CSEPC (1967-98), including our 10 cases.

Results: A total of 256 cases of CSEPC were analyzed. Ultrasound diagnosed 77.6% of CSEPC 48.8% were bilateral and 53.4% were located in the caudothalamic groove or head of caudate nucleus. Altogether, 93.5% resolved during 1-12 months of ultrasonographic follow-up. Compared to the general neonatal population, the following features were more prevalent in the CSEPC population: prematurity, maternal vaginal bleeding, preeclamptic toxemia, intrauterine growth restriction, asphyxia, fetal cytomegalovirus and rubella infec­tions, congenital malformations, chromosomal aberrations, infant mortality, and neurodevelopmental handicap. The risk for neurodevelopmental handicap was significantly higher when CSEPC were associated with fetal infections, IUGR, malformations and chromosomal aberrations, or persistence of CSEPC during follow-up. CSEPC infants without any of these four conditions had a low risk for neurodevelopmental handi­cap.

Conclusions: CSEPC are morphologic features of various underlying conditions encountered in the fetus. Association of CSEPC with IUGR, fetal infections, malformations and chromosomal aberrations or persistence of CSEPC indicates a higher risk for future neurodevelopmental handicaps, probably because of the deleterious effects on the fetal brain that are inherent in these conditions. A favorable outcome is expected in the absence of these risk factors.
 

Elizabeth Fireman, MD, Mordechai R. Kramer, MD, Nathan Kaufman, MD, Joachin Muller-Quernheim, MD and Yehuda Lerman, MD, MPH
February 2001
Ma C. Gutierrez-Ruiz, PhD, Luis E. Gomez Quiroz, MSc, Elizabeth Hernandez, MSc, Leticia Bucio, PhD, Veronica Souza, MSc, Luis Llorente, PhD and David Kershenobich, PhD

Background: Inflammatory mediators, including cytokines and reactive oxygen species. are associated with the pathology of chronic liver disease. Hepatocytes are generally considered as targets but not producers of these important mediators.

Objectives: To investigate whether cells of hepatocellular lineage are a potential source of various cytokines we estimated the expression and secretion of tumor necrosis factor alpha, transforming growth factor beta 1 and interleukins I beta, 6 and 8 in the culture of well-differentiated human HepG2 cells treated for 24 hours with ethanol, acetaldehyde and lipopolysaccharide. Lipid peroxidation damage, glutathione content and glutathione perox­idase, catalase and superoxide dismutase activity were also determined.

Methods: HepG2 cells were treated for 24 hours with ethanol (50 mM), acetaldehyde (175 ìM) and LPS (1 ìg/ml). TNF-á, TGF­-â, L-1â, IL-6 and IL-8 mRNA were determined by reverse transcriptase polymerase chain reaction and secretion by en­zyme-linked immunoassay. Lipid peroxidation damage, glutathione content and antioxidant enzyme activities were determined spectrophotometrically.

Results: Exposure to ethanol for 24 hours induced the expression of TNF-á and TGF- â1. secretion of IL-1â and TGF-â1 and decreased catalase activity. Acetaldehyde markedly increased TNF-á and IL-8 expression, stimulated IL-1â and IL-8 secretion, increased lipid peroxidation damage and decreased catalase activity, while LPS exposure induced the expression of TNF-á. TGF- â1, IL-6 and IL-8, the secretion of TGF-â1, IL-1â, IL-6 and IL-8, and a decrease in catalase activity. No change in GSH, GSHPx or SOD was found in any experimental condition.

Conclusions: The present studies confirm and extend the notion that hepatocytes respond to ethanol, acetaldehyde and LPS-producing cytokines. Oxidative stress produced by the toxic injury plays an important role in this response through up­regulation of inflammatory cytokines.

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