Israel Medical Association Journal

Background: While age at death is on the rise, the number of postmortem examinations is declining and is disproportionately low among the elderly population. Research on the subject of gender-associated pathology in the elderly is also scarce.

Objective: To seek eventual gender-related differences in autopsies of elderly patients.

Methods: We analyzed the data extracted from a published report on 93 PMEs[1] performed at a geriatric hospital during the past 20 years.

Results: Ninety-three autopsies, representing 1.2% of the 8,101 deaths during these 20 years, were performed. Forty-five of the deceased were women and 48 were men. The incidence of pulmonary embolism was significantly higher in women (28%) than in men (10%) (P< 0.02). There was no significant difference in the gender distribution of the other diagnoses.

Conclusion: Gender distribution of PME-based causes of death in elderly patients revealed a significant rate of pulmonary embolism in women. A thorough search of the medical literature revealed two previous studies with similar findings. Further research will determine whether pulmonary embolism is more frequent or whether it has a worse prognosis in frail elderly women.

Matrix metalloproteinases are a family of enzymes that degrade different components of extracellular matrix. They play an important role in normal physiologic processes of maintaining tissue integrity and remodeling, as in wound healing, processes of development, and regeneration. However, excessive expression of MMP[1] has been observed in many disease states, including rheumatoid arthritis and osteoarthritis, vascular remodeling in atherosclerosis and aortic aneurysm formation, neoplastic processes, macular degeneration and many others.

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Background: The ¹³C-urea breath test is the best non-invasive test to validate Helicobacter pylori eradication. Serology is unreliable for this purpose due to the slow and unpredictable decline in the antibodies titer.

Objectives: To characterize a specific group of patients who were treated for H. pylori and tested for successful eradication by ¹³C-UBT[1] in our central laboratory and to correlate the eradication success rate with specific drug combinations, and to evaluate other factors that may influence eradication success.

Methods: ¹³C-UBT for H. pylori was performed in the central laboratory of Clalit Health Services. The breath test was performed by dedicated nurses in 25 regional laboratories and the samples were analyzed by a mass spectrometer (Analytical Precision 2003, UK). The physician who ordered the test completed a questionnaire computing demographic data (age, gender, origin), indication, use of non-steroidal anti-inflammatory drugs or proton pump inhibitor, and combination of eradication therapy.

Results: Of the 1,986 patients tested to validate successful H. pylori eradication, 539 (27%) had a positive test (treatment failure group) and 1,447 (73%) had a negative test (successful treatment group). Male gender, older age and European-American origin predicted better eradication rates. Dyspeptic symptoms and chronic PPI[2] therapy predicted treatment failure. Combination therapy that included clarithromycin had a higher eradication rate than a combination containing metronidazole. The combination of omeprazole, amoxicillin and clarithromycin achieved an eradication rate of 81.3%, which was better than the combination of omeprazole, metronidazole and clarithromycin (77.2%) (not significant), or of omeprazole, amoxicillin and metronidazole (66.1%) (P < 0.01).

Conclusion: Gender, age, origin, dyspepsia and PPI therapy may predict H. pylori eradication results. Our findings also support an increase in metronidazole resistance of H. pylori strains in Israel, as described in other countries. We recommend combination therapy with omeprazole, amoxicillin and clarithromycin and avoidance of metronidazole as one of the first-line eradication drugs.

Background: Fractures of the stemum may be associated with major injuries to thoracic organs, with serious consequences.

Objective: To assess the hospital course of patients diagnosed with isolated sternal fracture.

Methods: We reviewed 55 medical records of patients who were admitted with isolated sternal fracture to the emergency department during the period from January 1990 through August 1999.

Results: Fifty-one patients were involved in motor vehicle accidents, and the remainder sustained the injury as a result of a fall. Lateral chest X-ray upon admission was diagnostic in the majority of these patients (n=53). Electrocardiography (n=52) was abnormal in four patients – old myocardial infarction (n=1), non-specific ST-T changes (n=3). Cardiac enzymes (creatine-kinase-MB, n=42) were pathologically elevated in five patients. Echocardiography, performed in patients with ECG[1] abnormalities and/or elevated myocardial enzymes (n=7), was normal in these patients as well as in another 18 patients. There were no intensive care unit admissions or arrhythmias during the hospital stay, which ranged from 6 hours to 6 days (mean 2.3 ± 1.3 days, median 2 days).

Conclusion: Our findings support the view that patients with isolated sternal fracture, who have no abnormality in ECG and cardiac enzymes during the early hours after injury, are expected to have a benign course and can be discharged home from the emergency room within the first 24 hours.

Background: Cigarette smoking is a well-known risk factor for the development of endothelial dysfunction and the progression of atherosclerosis. Oxidative stress and inflammation have recently been implicated in endothelial dysfunction.

Objectives: To assess the concomitant contribution of polymorphonuclear leukocytes to systemic oxidative stress and inflammation in cigarette smokers.

Methods: The study group comprised 41 chronic cigarette-smoking, otherwise healthy males aged 45.0 ± 11.5 (range 31–67 years) and 41 male non-smokers aged 42.6 ± 11.3 (range 31–65) who served as the control group. The potential generation of oxidative stress was assessed by measuring the rate of superoxide release from separated, phorbol 12-myristate 13-acetate-stimulated PMNL[1] and by plasma levels of reduced (GSH) and oxidized (GSSG) glutathione. Inflammation was estimated indirectly by: a) determining the in vitro survival of PMNL, reflecting cell necrosis; b) in vivo peripheral PMNL counts, reflecting cell recruitment; and c) plasma alkaline phosphatase levels, indicating PMNL activation and degranulation.

Results: PMA[2]-stimulated PMNL from cigarette smokers released superoxide at a faster rate than PMNL from the controls. Smokers had decreased plasma GSH[3] and elevated GSSG[4] levels. In vitro incubation of control and smokers' PMNL in sera of smokers caused necrosis, while control sera improved smoker PMNL survival. Smokers' PMNL counts, although in the normal range, were significantly higher than those of controls. Plasma ALP[5] levels in smokers were significantly higher than in controls and correlated positively with superoxide release and PMNL counts.

Conclusions: Our study shows that PMNL in smokers are primed in vivo, contributing concomitantly to systemic oxidative stress and inflammation that predispose smokers to endothelial dysfunction, and explains in part the accelerated atherosclerosis found in smokers.

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[1] PMNL = polymorphonuclear leukocytes

[2] PMA = phorbol 12-myristate 13-acetate

[3] GSH = reduced glutathione

[4] GSSG = oxidized glutathione

[5] ALP = alkaline phosphatase

The addition of methotrexate to treatment protocols in children with acute lymphoblastic leukemia has been found beneficial in preventing central nervous system relapse. However, MTX[1] itself may be associated with neurologic morbidities, the most significant of which is leukoencephalopathy. The present study describes the clinical spectrum of leukoencephalopathy, which ranges from a subclinical disease manifested only radiologically to a progressive, devastating encephalopathy. The interaction of MTX with other components of the treatment protocol is discussed, as is the effect of leucovorin. A summary is presented of the metabolic pathways that may be involved in the development of MTX toxicity. Researchers are still seeking a biochemical marker to aid in the determination of the amount of MTX that may be safely administered.

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