Biomedical subjects
Publications and source records attributed to G Hennen.
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Antisera directed against the beta subunit of human Luteinizing Hormone (h. LH) and Chorionic Gonadotropin (HCG) were made totally specific to either gonadotropin by adsorbing cross-reacting antibodies. Simple absorption in solution or immunosorption on solid phase were employed. Pituitary functions were examined during pregnancy and until three weeks following delivery h.LH and HCG were assayed before and after injection of Luteinizing Hormone Releasing Hormone (LH-RH). Similiarly TSH was assayed in a homologous TSH beta subunit system before and after injection Thyrotropin Releasing Hormone (TRH). No pituitary release of LH was observed after LH-RH in our experimental conditions while TRH induced a surge of pituitary TSH in the blood.
A brief review of the cancers derived from the follicular thyroid epithelium and parafollicular cells (medullar cancer) is made. The contribution of clinical biology to the diagnosis has little significance in the case of thyroid cancer. On the other hand, the quantitative analysis of thyroglobulin is very important for the detection of recurrence in the course of the follow-up of a patient who has been treated by complete thyroidectomy. The biological markers of medullar cancer are most specific. The observation of pathological secretion of thyrocalcitonin is determining for the diagnosis of medullary carcinoma. It must lead to a parathyroid and medulloadrenal exploration as well as to systematic investigation of family history. These steps are essential for the diagnosis of the syndromes of multiple endocrine neoplasias types 2a and 2b.
In many instances amiodarone-induced hyperthyroidism has been reported as mild, thyroid functions returning to normal after discontinuation of the drug. Nevertheless, life-threatening amiodarone-induced thyrotoxicosis has also been described. Conventional treatments such as with antithyroid drugs (Thionamide) and corticosteroids are essentially ineffective or fail to stop the dramatic course of the thyroid crisis. This limited efficacy of medical therapy, particularly in patients with previously--neglected or unknown--thyroid disease, prompted us to intervene surgically. We report a series of six patients who underwent total or nearly total thyroidectomy as first line therapy for four of them. Surgery resulted in rapid resolution of thyrotoxicosis with an uneventful postoperative course. This approach has the advantage of immediate and safe efficacy, low risk of relapse and finally, appears to be the only antithyroid treatment that permits continued therapy with amiodarone.
Pituitary reserves in TSH, during pregnancy and post-partum, were studied by TRH tests. TSH levels in sera were determined by two sensitive and specific radio-immunological systems. In all casses (42 tests) after intravenous injection of 200 mug of TRH a positive response in TSH was observed. Basal TSH levels (1.52 +/- 0,28 muU MRCA/ml), peak values and duration of the response after TRH were similar to those observed in a control group of non pregnant-women.
The objective of this study was to determine the effects of pituitary hormones (luteinizing hormone [LH], follicle-stimulating hormone [FSH], growth hormone [GH], and prolactin [PRL]) on interstitial cell proliferation and differentiation in the testis of immature hypophysectomized rats. Macrophages, Leydig cells, precursor mesenchymal cells, endothelial lymphatic cells, and myoid cells were studied. Our experimental approach was aimed at determining whether changes in a cellular subpopulation observed after pituitary hormone treatments were the result of division of existing cells in the population, of differentiation of interstitial precursor cells, or both. In this context, it must be stressed that our data reflected the effects of hormones to prevent the decline of cells due to hypophysectomy rather than their recovery. Macrophage proliferation was taken into account because macrophages closely resemble Leydig cells and are known to proliferate after hormonal treatment. A double-labeling procedure (acid phosphatase and anti-bromodeoxyuridine [anti-BUdR]) revealed that LH, FSH, and PRL increased the number of testicular macrophages 105-, 104-, and 103-fold, respectively, in hypophysectomized rats compared to hypophysectomized control animals. BUdR incorporation in testicular macrophages was greater after PRL treatment than after LH and FSH supplementation. In contrast, we were unable to demonstrate any effect of rat GH on the macrophage population. Light microscopic analysis of plastic embedded sections of treated rat testis revealed that LH increased the numbers of Leydig, precursor mesenchymal, and myoid cells 6-, 4-, and 1.3-fold, respectively. LH also stimulated BUdR incorporation into all interstitial cell types. PRL administration increased both the number of Leydig and precursor mesenchymal cells (each 3-fold) but decreased the number of endothelial lymphatic cells (1.5-fold) when compared to the control animals. In contrast, FSH did not increase the number and proliferation of Leydig cells but exerted a slight proliferative effect on the other interstitial cell populations. In GH-treated rats, the number of precursor mesenchymal cells increased two fold above the control rats. GH also exerted slight proliferative effects on both precursor mesenchymal and myoid cells. Immunohistochemical studies of steroidogenic enzymes in the testicular interstitium of treated rats demonstrated the presence of steroidogenic enzymes, not only in Leydig and precursor mesenchymal cells, but also in some (1%-2%) endothelial lymphatic cells and myoid cells. This may indicate that both of these cell types are also constitutively equipped to perform steroidogenesis or that they are precursor cells undergoing differentiation. Taken together, changes in the number of Leydig cells in our animal model appeared more likely to be dependent on the transformation of precursor cells than on division of preexisting mature Leydig cells.