[Recurrent subileus--chronic hemorrhagic anemia--status following small bowel resection].
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Biomedical subjects
Publications and source records attributed to R Gonzenbach.
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Automated routine platelet counting in 18,602 patients revealed thrombocytosis (platelet count above 400,000/mm3) in 9% (n = 1602) of cases. In 32% of the patients with thrombocytosis an acute or chronic inflammatory process was found, 9% had a malignant tumor and 9% anemia. 6% were alcoholics and 6% had a myeloproliferative syndrome. Chronic gastrointestinal disease was found in 4% and postoperative thrombocytosis in 3% of cases. 32% of the thrombocytosis cases could not be classified under any of the known causes of this disorder. In 51% of the cases the platelet count ranged from 400,000 to 450,000/mm3. Primary thrombocythemia often produced clinical symptoms, whereas secondary thrombocytosis almost always was asymptomatic.
In 14 patients with essential hypertension, left ventricular function was assessed echocardiographically before and after 4 and 8 weeks of treatment with the betablocking agent atenolol. Atenolol was given orally in a dose of 100 mg/day. After 4 weeks of treatment systolic blood pressure decreased from 160 to 138 mm Hg(p less than 0.001) and diastolic pressure from 105 to 91 mm Hg(p less than 0.001). Heart rate decreased from 76 to 64 beats/min (p less than 0.05). Systolic shortening of the left ventricular transverse diameter declined from 41 to 36% (p less than 0.01), though in no instance did it fall below the lower limit of normality (30%). After 8 weeks of betablocking therapy, blood pressure and heart rate remained essentially unchanged. Systolic shortening increased slightly but insignificantly to 38%. The left ventricular enddiastolic diameter did not change throughout the study. It is concluded that longterm betablocking therapy is associated with a significant reduction of left ventricular function which improves in the later stage of treatment. Since the diminution of left ventricular function is slight, the induction of left heart decompensation is unlikely, at any rate in patients with initially normal left ventricular function.
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