Acta medica Scandinavica最新文献

The gain in the diagnostic power of the routine preoperative bilateral renal vein renin investigation by the inclusion of an acute stimulation of renin release was studied in 25 hypertensive patients with fibromuscular (FMD) and 44 with arteriosclerotic (AS) renovascular disease. Nine FMD and 17 AS patients had renal vein renin ratios greater than or equal to 1.50 under unstimulated conditions. Of these 26 patients, 8 in each group improved after surgical treatment. Among the 14 FMD and 24 AS patients with ratios less than 1.50, another 9 FMD and 7 AS patients improved after operation. After acute stimulation of renin release, no less than 18 FMD and 26 AS patients had a unilateral renin secretion from the diseased kidney and of these, 14 FMD and 14 AS patients were successfully treated with operation of the stenosis. Thus the stimulation was necessary for correct preoperative diagnosis in 38% of 32 successfully operated patients, and at the same time the predictive value of a negative test increased from 0.58 to 0.80. It is concluded that acute stimulation of renin release greatly improves the diagnostic power of the renal vein renin investigation in renovascular hypertension.

Eighteen patients with clinical signs suggesting severe mitral regurgitation secondary to ischaemic heart disease were assessed by echocardiography. Non-ischaemic diseases needing specific therapy were revealed in six patients. In the other 12 patients echocardiography demonstrated myocardial lesions explaining the mitral regurgitation. Apart from the distinction between non-ischaemic conditions and lesions induced by ischaemia, echocardiography seems to be helpful in the demonstration of severe yet operable mitral valve regurgitation due to a small ischaemic lesion. Such cases are opposed to functional mitral regurgitation caused by extensive myocardial injury as demonstrated by two-dimensional echocardiography and reflected by a minimum mitral valve/septum separation of more than 2 1/2 cm on the M-mode echocardiogram. These conditions make symptomatic improvement by mitral valve surgery unlikely and carry an extremely high operative mortality. A more precise definition by heart catheterization is required when serious clinical heart failure is not explained by the echocardiographic finding of severe global myocardial impairment.

Two patients, 15 and 20 years old, were admitted after an overdose of theophylline in a slow-release preparation. The gradual occurrence of clinical symptoms reflected the slow gastrointestinal absorption of the drug, and therefore active treatment was not started until 10 and 12 hours after intake, respectively. Peak s-concentrations were 275 and 1295 mumol/l, respectively. One patient was treated with hemoperfusion only, whereas the more severely intoxicated patient was treated with combined hemoperfusion and hemodialysis. Only about 0.2 g theophylline was eliminated by hemodialysis in this patient compared to a calculated amount of 6.9 g by hemoperfusion. Severely theophylline-intoxicated patients should be treated with supportive therapy and hemoperfusion.

Three patients suffering from systemic scleroderma and Raynaud's phenomenon in the digits as well as the tongue are reported. Following exposure to cold, a vasospasm was observed in the digits and the tongue accompanied by severe dysarthria. These striking oral symptoms had been overlooked for years in the medical ward. It is recommended to question all patients with Raynaud's phenomenon about visceral manifestations during the digital attacks.

Several reports have suggested that iron deficiency might explain "sports anemia" especially in long distance runners. The present study was made to further study the iron metabolism in runners as the proposed cause of "sports anemia" is abstruse considering the good iron nutrition in these athletes. Based on a screening of 43 elite male runners, using bone marrow hemosiderin, serum ferritin and transferrin saturation, two groups of subjects were selected for a very extensive study on iron metabolism. In group 1 (n = 5) iron depletion was suggested in at least one of the screening studies. In group 2 (n = 7) at least one test strongly indicated good iron repletion. This experimental design was chosen to obtain two groups with similar body composition and exercise load but different iron metabolism. The studies comprised determinations of red cell and plasma volumes, plasma iron turnover and red cell incorporation of radioiron, red cell indices, plasma iron and transferrin, red cell protoporphyrin, serum ferritin, serum haptoglobin, urinary iron losses, iron absorption, bone marrow hemosiderin, dietary intake of energy and nutrients and a Desferal test. Pooling the results together it was obvious that none of the subjects were truly iron-deficient. A few occasional findings suggesting low iron stores cannot be satisfactorily explained and indicate that further studies are needed.

A hematological comparison was performed between 43 middle and long distance male runners and 119 male controls. The hematocrit, serum iron, transferrin saturation and serum ferritin values were significantly lower in the athletes. The amount of bone marrow hemosiderin was also lower in the athletes than in a group of non-athletic men of the same age. Even if these values were clearly lower than in the controls, they were not low enough to indicate iron deficiency. The observations that sideroblast counts in bone marrow smears were normal and that both red cell indices and red cell protoporphyrin were normal strongly support the conclusion that lack of iron had not limitated erythropoiesis or the formation of an optimal red cell mass. Low serum haptoglobin values in most athletes indicated an increased intravascular hemolysis. As the hemoglobin-haptoglobin complex formed is taken up by hepatocytes, this implies that there is a shift in the red cell catabolism in these athletes from the reticuloendothelial system to the hepatocytes. This shift may explain the paradoxical findings of low serum ferritin concentrations and reduced contents of bone marrow hemosiderin. This is consistent with the observed normal erythropoiesis. It was concluded that runners "anemia" is no true anemia and not caused by iron deficiency. "Sports anemia" is thus no indication for routine iron supplementation.

A 20-year-old man developed pneumonia and glomerulonephritis concomitantly with significantly rising Mycoplasma pneumoniae complement-fixing antibody titres. Renal biopsy showed mesangiocapillary glomerulonephritis type II (dense deposit disease). Attempts to demonstrate mycoplasmal antigen in the glomeruli failed. This is the third of five previously reported cases of glomerulonephritis associated with Mycoplasma pneumoniae and exhibiting dense deposit disease.

The effects of glipizide on the absorption of glucose and d-xylose were studied in six type II diabetics on diet treatment alone. Glipizide was given intravenously (12 micrograms/kg at 0 min) or orally (5 mg at -30 min). Oral glucose (15 g) and xylose (25 g) loads were given at zero time. Glipizide stimulated insulin secretion and reduced glucose and xylose levels significantly with both routes of administration. The suppression of xylose levels lasted longer after oral than after intravenous administration of the drug. It is suggested that part of the influence of glipizide on postprandial glucose levels may represent interference with absorptive mechanisms.

The indications for plasmapheresis in the different hyperviscosity syndromes are discussed on the basis of data on relative serum viscosity at 13 and 37 degrees C. Beside monoclonal macroglobulinemia there are conditions with a high content of polyclonal IgM and also of IgG and IgA where hyperviscosity is a dominant symptom. The importance of what may be called macroglobulinemia polyclonalis spuria is stated and a number of patients belonging to this type are discussed. Polyclonal increase in IgG, even at high levels, usually does not cause severe hyperviscosity. Case histories of patients with rheumatoid disease and marked hyperviscosity constitute one group. Another is formed by diseases leading to the development of immune complexes. Such complexes are usually caused by binding of polyclonal IgG to monoclonal IgM, but other combinations are also known. A number of clinical examples of these different disease conditions, some probably indicating intense plasmapheresis, are analyzed. The limited value of plasmapheresis alone without cytostatic treatment is stressed as regards hyperviscosity. Another indication is removal of noxious protein components.