Rahamim Avisar MD, Nissim Loya MD, Yuval Yassur MD and Dov Weinberger MD
Background: Previous work has suggested an association between increasing size of pterygium and increasing degrees of induced corneal astigmatism.
Objectives: To assess the quantitative relation between pterygium size and induced corneal astigmatism using a computerized corneal analysis system (TMS II) and slit-lamp beam evaluation of pterygium size, and to conclude whether corneal astigmatism is an early indication for surgical intervention.
Methods: We evaluated 94 eyes of 94 patients with unilateral primary pterygium of different sizes, using TMS II and slit-lamp beam measurements of the size of the pterygium (in millimeters) from the limbus to assess parameters of pterygium size with induced corneal astigmatism. Best corrected visual Snellen acuity was performed.
Results: Primary pterygium induced with-the-rule astigmatism. Pterygium extending 16% of the corneal radius or 1.1 mm or less from the limbus produced increasing degrees of induced astigmatism of more than 1.0 diopter. Significant astigmatism was found in 16.16% of 24 eyes with pterygium of 0.2 up to 1.0 mm in size, in 45.45% of 22 eyes with pterygium of 1.1 up to 3.0 mm in size (P≤0.0004), and in 100% of 3 eyes with pterygium of 5.1 up to 6.7 mm in size (P=0.0005). We found that visual acuity was decreased when topographic astigmatism was increased.
Conclusions: When primary pterygium reaches more than 1.0 mm in size from the limbus it induces with-the-rule significant astigmatism (≥1.0 diopter). This significant astigmatism tends to increase with the increasing size of the lesion. Topographic astigmatism tends to be improved by successful removal of the pterygium. These findings suggest that early surgical intervention in the pterygium may be indicated when the lesion is more than 1.0 mm in size from the limbus.
Amos Katz MD, Adi Biron MD, Eli Ovsyshcher MD and Avi Porath MD MPH
Background: Previous studies have documented an increased incidence of cardiac mortality and sudden death during winter months.
Objectives: To evaluate seasonal variation in sudden death in a hot climate such as the desert region of southern Israel.
Methods: We analyzed the files of 243 consecutive patients treated for out-of-hospital sudden death by the Beer Sheva Mobile Intensive Care Unit during 1989-90. Daily, monthly and seasonal incidence of sudden death was correlated with meteorological data, including temperature, heat stress, relative humidity and barometric pressure.
Results: The seasonal distribution of sudden death was 23% in spring, 21% in summer, 25% in autumn and 31% in winter (not significant). In patients with known heart disease there were more episodes of sudden death in cold weather (<15.4°C) than hot (>34.2°C) (16 vs. 3, P<0.05). Resuscitation was less successful in cold compared with hot weather (28 vs. 11, P<0.05). Of patients older than 65 years, 11 sustained sudden death when heat stress was below 12.4°C compared to 2 patients when heat stress was above 27.5°C (P=0.05).
Conclusion: Despite the warm desert climate, there were more cases of sudden death in older patients and in those with known heart disease during the winter season and on particularly cold days.
Shoshana Merchav PhD, Ilana Tatarsky MD, Judith Chezar MD, Rivka Sharon MD, Hanna Rosenbaum MD and Yael Schechter MD
Background: The etiology of bone marrow failure, a prominent feature of paroxysmal nocturnal hemoglobulinuria, is presently unknown.
Objectives: To evaluate the possible influence of cellular immune mechanisms in the bone marrow failure of PNH.
Methods: We studied marrow erythroid colony formation in a patient with paroxysmal nocturnal hemoglobinuria without hypoplastic/aplastic marrow complications.
Results: In vitro assays revealed a pronounced inhibition of primitive erythroid (BFU-E) progenitor cell growth by marrow T lymphocytes. Removal of T cells prior to culture resulted in a 4.5-fold enhancement of BFU-E numbers. Reevaluation of in vitro erythropoiesis during steroid administration indicated a persistent, albeit less prominent, T cell inhibitory effect.
Conclusion: Our findings provide the first direct evidence for a cellular immune inhibitory phenomenon accompanying PNH.
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PNH= paroxysmal nocturnal hemoglobinuria
Iris Baumgartner, MD and Jeff M. Isner, MD
Amnon Zisman, MD, Allan J. Pantuck, MD and Arie Belldegrum, MD, FACS
Ella Ophir, MD and Moshe Oettinger, MD
Isabel Zvibel, PhD, Yaron Mintz, MD, Shlomo Brill, MD, Zamir Halpern, MD and Moshe Papa, MD
Shlomo Walfisch, MD, Lilinda Lupu, MD and David Czieger, MD, PhD, MD
Dvora Aharoni, MD, Irith Hadas-Halpern, MD, Deborah Elstein, PhD and Ari Zimran, MD