Beta blockade in congestive cardiomyopathy.
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Biomedical subjects
Publications and source records attributed to M Brezis.
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The authors present a case of acute intermittent porphyria (AIP) in an almost fatal relapse with quadriplegia, bulbar paralysis and coma. Intravenous hematin produced an immediate arousal from coma and allowed a gradual resumption of bulbar and autonomic functions. Persistent tachycardia and hypertension necessitated huge doses of intravenous propranolol. Both hematin and propranolol administrations were followed by a remarkable decrease in urinary amino-levulinic acid and porphobilinogen excretion. Nevertheless, after the acute stage, the patient was left with a severe generalized muscle wasting. After 7 months of intensive physical therapy, complete recovery of all neuromuscular functions was achieved. The modern aspects of the management of AIP are presented; the efficacy and the limits of hematin and propranolol therapy are discussed.
Thrombocytosis has not yet been described in chronic eosinophilic pneumonia. A typical patient with chronic eosinophilic pneumonia is described. The patient's thrombocyte count was up to 900,000 per cu mm, which returned to normal under steroid therapy. Thrombocytosis may be associated with chronic inflammation and should not require further investigations such as lung biopsy, in an otherwise usual case of chronic eosinophilic pneumonia.
Two patients with myxedema coma and extreme hyponatremia associated with the syndrome of inappropriate secretion of antidiuretic hormone are described. Both recovered following i.v. hypertonic saline, furosemide and thyroxine. A review of 22 cases from the literature suggests that this therapeutic approach could improve the poor prognosis in this condition.
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A case is presented of a patient with 2 prosthetic valves and a mild chronic hemolytic anemia, in whom the hemolysis was suddenly aggravated by the occurrence of an acute gastrointestinal hemorrhage. This increased hemolysis was readily reversed by transfusion. It is postulated that the pathogenetic mechanism of this process was the increased direct crushing trauma and turbulence, both of which resulted from the tachycardia initiated by the gastrointestinal hemorrhage. The importance of avoiding or correcting tachycardia in patients with prosthetic valves is emphasized.
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Two patients with chronic mild to moderate renal failure presenting with unexplained hyperkalemia were studied, and found to have hyporeninemic hypoaldosteronism. Hyperkalemia, generally uncommon in nonoliguric stable renal failure, resulted from the combination of apparent insensitivity of the diseased kidney to aldosterone and variable degrees of impairment in the reninaldosterone axis. The clinical picture, the methods of establishing the diagnosis, the therapeutic alternatives and the possible pathogenetic mechanisms involved are described.
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BACKGROUND/AIMS: Contrast media (CM) induce a biphasic renal hemodynamic response, with late prominent cortical vasoconstriction and marked outer medullary vasodilation. The objective of the study was to explore a possible role for altered nitric oxide (NO) production or bioavailability in these hemodynamic responses. METHODS: We explored the impact of CM (sodium iothalamate) upon rat renal NO synthase (NOS) activity (citrulline recovery) and NO (using a NO electrode). RESULTS: The cortical NOS activity following CM was 11.5 +/- 1.0 versus 13.8 +/- 1.1 nmol/gww/min (gww = gram wet weight) in controls (p = 0.16, NS). In rats pretreated with the nonselective endothelin antagonist bosentan, CM reduced the cortical NOS activity to 8.5 +/- 1.2 nmol/gww/min (p < 0.005 vs. controls). Cortial NO readings declined over 30 min following CM by 13 +/- 8% (p < 0.05, Anova), in parallel with the decline in cortical blood flow. The outer medullary NOS activity was not affected by CM (5.2 +/- 1.5 vs. 5.5 +/- 1.3) nmol/gww/min in controls) or bosentan. Nevertheless, the outer medullary NO reading increased by 36 +/- 23% (p < 0.05), with a concomitant increase in regional blood flow. CONCLUSION: In the cortex, CM might reduce the NOS activity (an effect blunted by endothelin release). This may potentiate the effect of endothelin to induce regional vasoconstriction. In the outer medulla, the vasodilatory response to CM does not seem to be mediated by enhanced NOS activity and might reflect increased local NO bioavailability as the result of regional hypoxia.