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עמוד בית
Mon, 15.04.24

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April 2004
A. Ya'ari, C.L. Jaffe and B-Z. Garty

Background: Visceral leishmaniasis was first reported in Israel (then Palestine) in 1929. In the 1960s and 1970s, it was endemic to northern Israel, but only partial data about the disease have been gathered since then.

Objective: To investigate the epidemiologic trends of visceral leishmaniasis in Israel from 1960 to 2000, and to delineate some clinical features of the infection.

Methods: Data were collected from hospital charts, scientific publications, and reports of the Ministry of Health and the Kuvin Center for the Study of Infectious and Tropical Diseases.

Results: During the last four decades, 87 cases of visceral leishmaniasis were diagnosed in Israel, 76 of them (87%) in children. All 54 patients diagnosed in the 1960s occurred in the northern part of the country. The rate of infection declined significantly in the 1970s (5 cases) and then increased slightly in the 1980s (11 cases) and 1990s (17 cases). More than 50% of the cases in the 1990s were in central Israel. Children accounted for 100% of cases in the 1960s but only 58% in the 1990s. The main clinical features of the patients diagnosed in the last decade were fever, weight loss, hepatosplenomegaly and pancytopenia. Three of the adults were co-infected with human immunodeficiency virus.

Discussion: The decline in the incidence of visceral leishmaniasis in the 1970s and the slight increase in the 1980s and 1990s can be attributed to changes in the animal reservoir and vectors, and in the immunity status of part of the population exposed to Leishmania.

Conclusions: Visceral leishmaniasis has reemerged in Israel. This mandates better control of the animal reservoir and vectors and increased awareness of this infection.

March 2004
R.M. Nagler and A. Nagler

Patients with graft-versus-host disease suffer from xerostomia, oral infections and mucosal pathologies. The continuous increase in the number of patients treated worldwide with bone marrow transplants, combined with improved survival statistics result in a concomitant increase in the number of GVHD[1] patients. the pathogenesis of GVHD is based on donor graft T lymphocytes that recognize antigenic disparities between donor and recipient, and on the disregulation of a broad panel of cytokines. Consequently, various tissues and organs, including the mucosa of the oral and gastrointestinal tract, are damaged via cytotoxicity caused by infiltrating T cells. Since the salivary glands are a known major target of GVHD and their secretions significantly contribute to preserving mucosal integrity, this mucosal insult is further enhanced by the reduced quantity and altered quality of saliva. GVHD occurs in 40–70% of patients treated by bone marrow and peripheral blood stem cell transplantation. limited studies suggest that a large percentage of GVHD patients are affected and that the induced salivary dysfunction occurs rapidly following transplantation, affecting both major and minor salivary glands and reflecting the severity of the disease. Moreover, profound sialochemical alterations may be diagnostic of GVHD. an additional reason for the vast amount of research is that GVHD, as an autoimmune-like disease, seems to be an appropriate model for studying a much more prevalent, well-known and studied autoimmune disease involving salivary glands, namely, sjögren’s syndrome. The present review describes the GVHD-related sialometric and sialochemical data available in the literature for both major and minor salivary glands in both human and rodent models, and discusses a possible mechanism.

[1] GVHD = Graft-Versus-Host Disease

January 2004
Y. Cohen and A. Nagler

In recent years, umbilical cord blood has emerged as an alternative source of hematopoietic progenitors (CD34+) for allogeneic stem cell transplantation, mainly in patients who lack an human leukocyte antigen-matched marrow donor. Since 1998, about 2,500 patients have received UCB[1] transplants for a variety of malignant and non-malignant diseases. The vast majority of recipients were children with an average weight of 20 kg, however more than 500 UCB transplantations have already been performed in adults. The “naive” nature of UCB lymphocytes may explain the lower incidence and severity of graft versus host disease encountered in UCBT[2] compared to the allogeneic transplant setting. Furthermore, UCB is rich in primitive CD16-CD56++ natural killer cells, which possess significant proliferative and cytotoxic capacities and can be expanded using interleukin-12 or 15, so as to mount a substantial graft versus leukemia effect. The major disadvantage of UCB is the low yield of stem cells, resulting in higher graft failure rates and slower time to engraftment compared to bone marrow transplantation. A rational approach thus involves ex vivo expansion of UCB-derived hematopoietic precursors.

[1] UCB = umbilical cord blood

[2] UCBT = UCB transplantations

November 2002
Arnon Blum, MD, Julia Sheiman, MD and Yonathan Hasin, MD
July 2002
Gidon Almogy, MD, Arnon Makori, MD, Oded Zamir, MD, Alon J. Pikarsky, MD and Avraham I. Rivkind, MD
Dorith Shaham, MD, Tamar Sella, MD, Arnon Makori, MD, Liat Appelbaum, MD, Avraham I. Rivkind, MD and Jacob Bar Ziv, MD
November 2001
Rahamim Avisar, MD, Aharon Arnon, MD, Erez Avisar, BSc and Dov Weinberger, MD

Background: The time to recurrence after surgical removal of primary pterygium (pterygium) and the association between the rate of recurrence and the postoperative interval remain unclear.

Objective: To determine the amount of follow-up time needed to identify recurrence in patients after surgical removal of pterygium.

Methods: We rviewed the files of 143 patients (143 eyes) with recurrent pterygium to determine the interval from surgery to recurrence.

Results: Almost all (91.6%) of the recurrences appeared by 360 days after surgery.

Conclusions: One year is the optimal follow-up time to identify recurrence of pterygium.

July 2001
Alberto Kurzbaum, MD, Claudia Simsolo, MD, Ludmilla Kvasha, MD and Arnon Blum, MD
April 2001
Arnon Blum, MD, Yami Shapira, MD, Shay Yeganh, MD and Maya Rabinkov, MD
September 2000
Arnon Broides MD, Shaul Sofer MD and Joseph Press MD

Background: The outcome of cardiopulmonary arrest in children is poor, with many survivors suffering from severe neurological defects. There are few data on the survival rate following cardiopulmonary arrest in children who arrived at the emergency room without a palpable pulse.

Objective: To determine the survival rate and epidemiology of cardiopulmonary arrest in children who arrived without a palpable pulse at a pediatric ER in southern Israel.

Methods: We retrospectively reviewed the medical records of all patients with cardiopulmonary arrest who arrived at the ER of the Soroka University Medical Center during the period January 1995 to June 1997.

Results: The study group included 35 patients. Resuscitation efforts were attempted on 20, but the remaining 15 showed signs of death and were not resuscitated. None of the patients survived, although one patient survived the resuscitation but succumbed a few hours later. The statistics show that more cardiopulmonary arrests occurred among Bedouins than among Jews (32 vs. 3, P0.0001).

Conclusions: The probability of survival from cardiopulmonary arrest in children who arrive at the emergency room without palpable pulse is extremely low. Bedouin children have a much higher risk of suffering from out-of-hospital cardiopulmonary arrest than Jewish children.

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