Klinische Wochenschrift
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Klinische Wochenschrift · Nov 1984
Case ReportsEtomidate: a selective adrenocortical 11 beta-hydroxylase inhibitor.
To investigate the adrenocortical suppression caused by the anesthetic etomidate, plasma levels of progesterone (P), 17-hydroxyprogesterone (17-OHP), 11-deoxycorticosterone (DOC), corticosterone (B), aldosterone (Aldo), 11-deoxycortisol (S), cortisol (F), and cortisone (E) were measured simultaneously before and after a short-term ACTH stimulation test in a 6.5-year-old boy whose convulsions could be kept under control only with constant etomidate infusions. During etomidate therapy, plasma levels of DOC and S were extremely elevated, the progestins P and 17-OHP were slightly elevated, whereas B and Aldo were in the lower normal range, and F and E were markedly decreased. A short-term ACTH stimulation test during etomidate infusion gave a blunted response of B, Aldo, F and E, whereas the level of DOC remained high and S even further increased. ⋯ In contrast, the ratios of DOC/P and S/17-OHP, which reflect 21-hydroxylase activity, were elevated and remained elevated after ACTH stimulation. After discontinuation of etomidate therapy, all the baseline steroid levels were somewhat elevated, but responded normally to ACTH. These results demonstrate that etomidate causes a specific and reversible blockade of the 11 beta-hydroxylation of adrenal steroid synthesis.
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Klinische Wochenschrift · Sep 1983
Glycosylated hemoglobin as a long-term parameter in appraising the severity of hemolytic disease.
Reduced levels of glycosylated hemoglobins (GHb) have been found to be closely related to red cell survival. We therefore studied the relation of this parameter to the clinical applicability in patients with hemolytic disease (n = 20). During a 5-week period we repeatedly measured severity of anemia, i.e., hemoglobin (Hb), packed red cell volume (VPRC), and red blood cell count (RBC), as well as reticulocytosis and parameters of red cell destruction such as serum concentration of lactic dehydrogenase (LDH) and bilirubin together with GHb. ⋯ A much closer correlation, however, was found between actual GHb levels and RBC determined 3-5 weeks previously (r = 0.72, P = 0.001), as well as Hb (r = 0.56, P = 0.015), VPRC (r = 0.57, P = 0.013), reticulocyte counts (r = -0.63, P = 0.006), LDH ( r = -0.53, P = 0.02), and serum bilirubin concentrations ( r = -0.55, P = 0.016). Ghb was also significantly decreased in patients with consistently low values of reticulocytes when red cell destruction was demonstrable. These results show that GHb is a measure of red cell destruction and restitution, and thus may be usefull for long-term monitoring of patients with hemolytic disease.
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Klinische Wochenschrift · Sep 1982
Mast cell receptors controlling histamine release: influences on the mode of action of drugs used in the treatment of adverse drug reactions.
In drug-induced allergic diseases of the immediate type (anaphylactic and anaphylactoid reactions), the primary target cells are tissue mast cells, which discharge their granular content upon interaction with different secretagogues (immunological releasers; histamine liberators) on specific plasma membrane receptors. Experiments are reviewed here which report that IgE-mediated histamine release from mast cells, and the secretion of histamine induced by non-immunological secretagogues (dextran; compound 48/80; acetylcholine) are blocked by beta-adrenoceptor and H2-receptor agonists, their inhibiting effect being surmountable by beta-adrenoceptor blocking drugs and by anti-H2-antihistamines. Specific radioligands ([3H]-dihydroalprenolol; [3H]-cimetidine) binding to rat mast cell membranes points to the possibility that inhibition of histamine release is brought about by the activation of mast cell beta-adrenoceptors and H2-receptors. Drugs used in therapy of anaphylactic or anaphylactoid reactions may act either on tissue receptors, competing with released mediators, or by inhibiting the release of allergic mediators from mast cells, on activation of specific receptors located in mast cell plasma membranes.
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Klinische Wochenschrift · Mar 1982
[The elimination of hydroxyethyl starch 200/0.5, dextran 40 and oxypolygelatine (author's transl)].
After withdrawal of 400 ml whole blood and subsequent infusion of 500 ml of a colloidal plasma substituent, the intravascular and renal colloid elimination was investigated in 40 test subjects. The individual colloidal solutions could no longer be demonstrated in the intravascular space after the following times: 10% hydroxyethyl starch 200/0.5 (anthrone method) after six weeks, 10% dextran 40 (anthrone method) after two weeks, 6% hydroxyethyl starch 200/0.5 (anthrone method) after four weeks and 5.5% oxypolygelatine (hydroxyproline method) after two days. Colloidal plasma substitutes are polydisperse solutions with various molecular weights and degree of hydroxyethylation and therefore, also have a large number of different elimination constants. ⋯ Oxypolygelatine was eliminated especially rapidly. Accordingly, the greatest renal clearance was found for oxypolygelatine, which showed a close relation to the molecular weight. On the other hand, a rapid elimination simultaneously is followed by a correspondingly lower volume effect.
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Obesity is a chronic, usually life-long condition. Therefore, the success of any treatment should be measured by the long-term weight loss. More patients lose weight than maintain the weight loss after the active phase of therapy has ended. ⋯ Both these procedures have definite risks. Rapid weight loss is induced by fasting but long-term follow-ups showed gradual regain of weight loss. Combinations of various techniques such as behavior modification, exercise, proper nutritional instruction and protein-sparing modified fast seem to have the best chance for long-term success.