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L Siekmann

Publications and source records attributed to L Siekmann.

49 records · Page 3Linked to original sources
PubMed1974

Chemical and biochemical studies on 18-hydroxyoestrone.

1. 18-Hydroxyoestrone was reduced by NaBH(4) in methanol, giving 18-hydroxyoestradiol-17alpha and 18-hydroxyoestradiol-17beta in the ratio 3:7. 2. Treatment of 18-hydroxyoestrone with a strong alkali yielded 18-noroestrone; however, the 18-hydroxyoestradiols did not undergo transformation to their respective 18-nor derivatives. 3. All the 18-hydroxylated oestrogens were stable under acid conditions. They formed Kober chromogens: the chromogenicity of 18-hydroxyoestrone was only one-third that of the 18-hydroxyoestradiols and oestriol. 4. Paper-, thin-layer- and gas-liquid-chromatographic systems for the characterization of these compounds are described. 5. An examination of the mass spectra revealed peaks characteristic of the substituted carbon atoms. Definite assignment of the 17alpha- and 17beta-hydroxyl groups of the epimeric 18-hydroxyoestrogens was possible by characteristic fragmentation of the free steroids. Further, the configuration of 18-hydroxyoestradiol-17beta was confirmed by the formation of the dimethylsildioxy derivative of the 3-methylether of the steroid. 6. Both rat and rabbit liver slices reduced 18-hydroxyoestrone to 18-hydroxyoestradiol-17beta and some other labile, polar metabolites with properties similar to 2-hydroxylated oestrogens. No formation of 18-hydroxyoestradiol-17alpha in vitro was observed. 7. The results are discussed with respect to the possible influence of the 18-hydroxyl group on reactions at C-17, as well as the reactions of 18-hydroxylated oestrogens with strong acid (Kober reactions) and alkali.

Animals↗
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Adrenocortical insufficiency in Rhodesian sleeping sickness is not attributable to suramin.

Suramin, a polysulphonated naphthylurea used in the treatment of human African trypanosomiasis (HAT), is known to cause adrenocortical insufficiency in doses exceeding the quantity used for treatment of HAT. We have previously reported that Trypanosoma brucei rhodesinese infection causes a combined central and peripheral adrenal insufficiency. To evaluate whether suramin therapy acts as an additional adrenotoxic factor, we assessed adrenocortical function in 72 patients suffering from HAT at different times during treatment with either suramin or melarsoprol by a rapid adrenocorticotropic hormone test. We found a significantly diminished peak cortisol response to stimulation in the acutely ill patients (P = 0.001), indicating impaired adrenocortical function, as well as a high incidence of partial adrenocortical insufficiency (27%). During and after trypanocidal therapy the incidence of partial adrenal insufficiency gradually declined (to 25% and 18% respectively). Stimulated peak cortisol levels did not differ significantly between patients receiving suramin and those given melarsoprol. No correlation was found between serum suramin concentration and the cortisol response to stimulation (r = 0.09, P = 0.47). Thus we conclude that suramin in trypanocidal doses neither causes nor worsens the adrenocortical dysfunction observed in Rhodesian HAT.

Addison Disease↗