[The 60th birthday of Prof. François Reubi].
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Biomedical subjects
Publications and source records attributed to P Cottier.
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Accidental hypothermia, in contrast to medical hibernation, corresponds to a sudden, unforeseen lowering of the body temperature below 35 degrees C. This may occur endogenously in association with various diseases. On the other hand, it may be due to the exogenous influences of very low environmental temperatures. An impressive observation of accidental hypothermia is described and the pathophysiological findings in accidental hypothermia are reviewed.
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To investigate the role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome two patients with hypercorticism were infused with 20 mg saralasin (1-sar-8-ala-angiotensin II) over a period of 30 minutes under constant blood pressue control. In addition, one patient with primary aldosteronism, an established form of mineralocorticoid hypertension, served as control. Neither in the two patients with Cushing's syndrome nor in the patient with primary aldosteronism could a blood pressure lowering effect of saralasin be observed. In the two patients with hypercoritcism both renin activity and plasma aldosterone increased during saralasin infusion. The patient with primary aldosteronism only showed a weak increase in plasma aldosterone concentration.
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Current pathogenetic concepts regarding renal hypertension are reviewed. Alterations of the renin-angiotensin-aldosterone system (RAA) on the one hand, and disturbances of NaCl and water metabolism on the other, represent the dominant factors in renal hypertension. The present view of the reactions within the RAA system and of its activators, inhibitors or antagonists is described schematically. The angiotensin II-antagonist 1-sar-8-ala-angiotensin II (Saralasin), when infused in a patient with angiotensinogenic hypertension, induces normalization of the blood pressure during the course of the infusion. The Saralasin infusion test may be of assistance in detecting cases with angiotensinogenic hypertension. The pressor(s) and the extracellular fluid volume appear to be the decisive pathogenetic factors in renal hypertension. As long as the functioning renal mass is sufficient to excrete water and salt normally or in excess, as is the case when the renal perfusion pressure in hypertension is elevated, the pressor is the dominating factor besides other, so far hypothetical mechanism such as the neurogenic. A critical reduction of the renal mass will enhance fluid and salt retention. Thus, an increase in extracellular fluid volume and blood volume will emerge as a major factor inducing hypertension. As a consequence of the volume gain and salt retention, renin secretion may slow down. The possibility is mentioned that the absence or ineffectiveness of renal depressor substances (prostaglandins) may be involved in renal hypertension. Finally, two hypotheses are presented which may explain the finding of LARAGH et al., who grouped their essential hypertensives into 'high, normal and low renin hypertensives'.
The present clinical aspects of Paget's osteodystrophy are reviewed. The nosological definition, localiztion, natural course and signs are described and the recent description of "rheumatoid manifestations" in Paget's disease by FRANCK et al. is mentioned. The same authors revealed a positive correlation between the grade of extenstion of Paget's disease in the whole skeleton and the concentration values for alkaline phosphatase and uric acid in the serum. Among the complications of Paget's disease the orthopedic, neurological, haemodynamic, oncologic, hematological and dermatological are reviewed X-ray of the involved skeleton, which in most cases is diagnostic, may be supported by isotope scanning with 18F or 87mSr and bone biopsy for establishment of diagnosis. Current drug therapy is confined to diphosphonate and calcitonin. The antibiotic mithramycin, which is cytotoxic, reduces bone turnover and may improve the course in Paget's disease. However, toxic side effects on kidney, liver and hemopoiesis do not allow its further therapeutic use in this disease. A case is described which demonstrates that a spontaneous or traumatic fracture in the area of osteodystrophy exhibits almost the same potential for conso lidation as normal bone tissue following both conservative and osteosynthetic treatment of the fracture. In a further instance corrective osteotomy with osteosynthesis (plate) because of serious varisation and antecurvature of the femur due to Paget's disease were performed sucessfully without assisting drug therapy. A third patient displayed extensive osteodystrophy of the whole pelvic skeleton, which was discovered by X-ray as rehabilitation following CVA failed to progress due to severe bilateral reduction of hip joint function. In view of the age and general status of the patient and the absence of pain, no medication or surgical therapy was performed in this case.
The review discusses the pathophysiology of the renal mechanisms of blood-pressure control. The physiology of the renin-angiotensin system is described and the mineralo-corticoid function has also been considered. The implications of alterations of these systems in various nephropathies are briefly summarized (renal artery stenosis, infarction, Page's syndrome, acute glomerulonephritis, essential hypertension a.o.).