Daniel Chemtob, MD, MPH, DEA, Leon Epstein, MD, MPH, Paul E. Slater, MD, MPH and Daniel Weiler-Ravell, MD
Background: Sensing an inadequacy of tuberculosis control due to an influx of TB associated with immigration, we analyzed TB treatment outcome in Israel by population groups.
Objectives: To provide an epidemiological basis necessary for any new national TB control policy, and to bring it to the attention of the medical profession in Israel and abroad since its results led to a change in Israel’s TB control policy.
Methods: We reviewed all TB cases notified during the period 1990 to September 1992. New cases” (820 cases, 93.5%) and “re-treatment cases” (57 cases, 6.5%) were analyzed according to three mutually exclusive groups: “successful outcome,” “death” and “potentially unsatisfactory outcome” (according to WHO/IUATLD definitions).
Results: Of 820 “new cases,” 26.6% had a satisfactory outcome,” 68.5% had a “potentially unsatisfactory outcome” and 4.9% died compared to 47.4%, 45.6% and 7% among 57 “re-treatment cases,” respectively. Using logistic regression analysis, outcome was associated with the district health office (P<0.0001), the TB experience” of the notifying clinic (P<0.0001), and the form of TB (P=0.02). No significant relationships were obtained for population groups, gender and age, interval between arrival in Israel and TB notification, and bacteriological results.
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.
Mehrdad Herbert, MD, Michael Segal, MD, Gratiana Hermann, MD and Judith Sandbank, MD
by Rasmi Megadle, MD, Paltiel Weiner, MD, Alexander Sotzkover, MD, Miri Mizrahi-Reuveni, MD and Noa Berar Yanay, MD