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עמוד בית
Mon, 26.02.24

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January 2011
Y. Landau, I. Berger, R. Marom, D. Mandel, L. Ben Sira, A. Fattal-Valevski, T. Peylan, L. Levi, S. Dolberg and H. Bassan

Background: Major advances in the treatment of perinatal asphyxial–hypoxic ischemic encephalopathy followed the translation of hypothermia animal studies into successful randomized controlled clinical trials that substantially influenced the current standard of care.

Objectives: To present our preliminary experience with the first cases of clinical application of therapeutic hypothermia for PA-HIE[1] in what we believe is the first report on non-experimental hypothermia for PA-HIE from Israel.

Methods: We reviewed the medical records, imaging scans, electroencephalograms and outcome data of the six identified asphyxiated newborns who were managed with hypothermia in our services in 2008–2009.

Results: All asphyxiated newborns required resuscitation and were encephalopathic. Systemic hypothermia (33.5ºC) was begun at a median age of 4.2 hours of life (range 2.5–6 hours) and continued for 3 days. All six infants showed a significantly depressed amplitude integrated electroencephalography background, and five had electrographic seizures. One infant died (16%) after 3.5 days. Major complications included fat necrosis and hypercalcemia (n=1), pneumothorax (n=1), and meconium aspiration syndrome (n=2). None of the infants developed major bleeding. Neurodevelopmental follow-up of the five surviving infants at median age 7.2 months (4.1–18.5 months) revealed developmental delays (Battelle screening), with their motor scores ranging from -1 to +1 standard deviation (Bayley scale). None developed feeding problems, oculomotor abnormalities, spasticity or seizures.

Conclusions: Our preliminary experience with this novel modality in a large Tel Aviv neonatal service is consistent with the clinical findings of published trials.






[1] PA-HIE = perinatal asphyxial–hypoxic ischemic encephalopathy


March 2010
O. Jarchowsky Dolberg, A. Elis and M. Lishner
March 2002
Alexander Kagan, MD, Nurit Haran, PhD, Ludmila Leschinsky, MD, PhD, Ruty Sarafian, RN, BA, Dan Aravot, MD, Jaffa Dolberg, RN, Ziv Ben-Ary, MD and Jason Rapoport, MB, BS, MRCP

Background: Leptin is a 16 kDa hormone synthesized by adipocytes and involved in body weight regulation.

Objectives: To determine serum leptin concentrations in heart, liver and kidney transplant recipients.

Methods: We investigated 57 patients: 18 male heart transplant recipients (age 25-69 years) at 1-66 months after transplantation, 6 female and 8 male liver transplant recipients (age 33-70) at 11-73 months after transplantation, and 10 female and 15 male kidney transplant recipients (age 20-61) at 3-138 months after transplantation. All recipients were receiving immunosuppressive therapy, including prednisone 0-20 mg/day, azathioprine 75-125 mg/day, cyclosporin 100-250 mg/day or tacrolimus 2-10 mg/day. The results were compared to those of 10 female and 10 male healthy controls. Morning serum concentrations of leptin were measured with a commercial radioimmunoassay (Linco Research Inc., USA), and serum insulin and cortisol levels were measured by radioimmunoassay.

Results: Patients (both men and women) after heart, liver and kidney transplantation exhibited significantly higher serum concentrations of leptin and leptin/body mass index ratios than controls. Serum leptin concentrations were significantly higher in women than in men and correlated very significantly with BMI[1] in all cases. The multivariate stepwise analyses showed that among parameters including BMI, gender, age, time after transplantation, prednisone dose, hematocrit, serum concentrations of glucose, albumin, creatinine, cortisol and insulin, only BMI, gender, cortisol and insulin were significant independent determinants of serum leptin levels in these patients.

Conclusions: This is the first report showing that, in addition to body mass index and gender, basal cortisol and insulin levels affect the hyperleptinemia in transplant patients. The clinical relevance of hyperleptinemia in these patients will require further investigation.






[1] BMI = body mass index



 
October 1999
Shaul Dollberg MD and Francis B. Mimouni MD
 Background and Objective: Very low birthweight infants (<1,500 g birthweight) often develop significant anemia that requires multiple blood transfusions, which carry a significant risk. Erythropoietin therapy is known to reduce the need for blood transfusions in preterm VLBW(1) infants. Analysis of cost had been reported in prospective studies with conflicting results. No studies comparing the cost-effectiveness of EPO(2) have been reported during routine use in preterm VLBW infants.

Methods: We compared the cost of treating anemia of prematurity in two consecutive 12-month periods: before and after the introduction of EPO therapy in our unit. The cost of blood bank charges as well as disposable items and the cost of EPO were compared.

Results: A significantly smaller number of infants required blood transfusions in the EPO group (2 of 25 vs. 9/21 before EPO was introduced). The cost of therapy for anemia of prematurity was significantly smaller in the EPO group (128±168 US$ per infant vs. 151±189 US$ per infant before the introduction of EPO).

Conclusion: We conclude that EPO is an efficient and cost-effective alternative to blood transfusions in VLBW infants.

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(1) VLBW = very low birthweight

(2) EPO = erythropoietin

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