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Biomedical subjects

A Gompel

Publications and source records attributed to A Gompel.

63 records · Page 4Linked to original sources
PubMed1983

Pre- and posttransplant glomerulonephritis in a case of sarcoidosis.

A 39-year-old woman with documented sarcoidosis and membranous glomerulonephritis (GN) with renal failure received a kidney from her identical twin. A few months after transplantation a proliferative GN appeared with hematuria, proteinuria and progressive renal failure over 2 years. Indeed the occurrence of GN in patients with sarcoidosis raises the question of whether the relationship between these two conditions is causal or fortuitous. This report suggests that GN is secondary to sarcoidosis.

Adult↗
PubMed1982

Effects of percutaneous estradiol and conjugated estrogens on the level of plasma proteins and triglycerides in postmenopausal women.

Percutaneous administration of estradiol (E2) is a new substitutive treatment for postmenopausal women. In order to compare hepatic action of percutaneous E2 with that of conjugated estrogens, 18 postmenopausal women were allocated at random to receive one of these two types of natural estrogens for 21 days. Eight patients (group I) received conjugated estrogens orally, 1.25 mg daily. Ten patients (group II) were told to apply percutaneous E2 ointment, 5 gm (i.e., 3 mg of E2), each evening on the abdominal skin. E2, estrone (E1), follicle-stimulating hormone (FSH), and luteinizing hormone (LH), and several markers of estrogen action were evaluated before and after treatment. Both types of treatment were biologically effective, as indicated by the decrease in plasma gonadotropins and the increase in estrogen levels. However, conjugated estrogens produced a greater increase in E1 than in E2; hence, the E2/E1 ratio was 0.57 in group I, whereas it was approximately 1 in group II. Plasma renin substrate increased significantly (by 180%) in group I but not in group II. In the same way, conjugated estrogens produced a modest (12%) but significant decrease in antithrombin III, whereas there was no variation with percutaneous E2. Sex steroid-binding protein was the most sensitive parameter for the hepatic action of estrogen, and increased by 18.66% with percutaneous E2 and by 150% with conjugated estrogens. Plasma triglycerides tended to increase in group I and to decrease in group II, but not significantly. Therefore, percutaneous administration of of E2, in contrast to conjugated estrogens, can produce plasma levels of estrogens closer to those observed in the follicular phase and less alterations in protein synthesis. This lesser toxicity may be explained partially by the route of administration, since with percutaneous administration of E2, the steroid bypasses the liver.

Administration, Oral↗
PubMed1982

Bullous dermatosis associated with dysglobulinemia (two cases). Relationships with epidermolysis bullosa acquisita.

Two cases of bullous dermatosis with dysglobulinemia are described. The first one was associated with renal and neuromuscular amyloidosis and production of a monoclonal lambda IgG. Optical and electron microscopy showed amyloid deposits beneath basal lamina of the dermis. Results for direct and indirect immunofluorescence (IF) were negative. This bullous dermatosis is not an epidermolysis bullosa acquisita (EBA), in the strict sense, because the amorphous material deposited is amyloid. In the second case, associated with Waldenström's disease, there was no cutaneous or systemic amyloidosis. Direct IF was positive; linear IgM deposits were seen along the basal membrane of the bulla and the healthy skin. Indirect IF showed the presence of circulating antibodies against basal membrane zone. This bullous dermatosis is probably an EBA, despite the absence of IgG deposits. The absence of electron microscopy does not permit the confirmation of this diagnosis.

Aged↗
PubMed1979

[Critical study of the treatment of Grave's disease (author's transl)].

202 cases of Grave's disease were reviewed; among the 81 patients submitted to medical treatment, 53,1 p. 100 of patients failed to respond; 10 p. 100 relapsed and 35,9 p. 100 are euthyroid. The factors favouring a treatment failure were: age below thirty, severity of thyrotoxicosis, big enlargement of thyroid gland, duration of treatment shorter than 12 months. Relapses are more frequent after two years of medical treatment. Subtotal thyroidectomy was performed in 82 patients: 9,5 p. 100 relapsed, permanent hypothyroidism developed in 30,5 p. 100 and 50 p. 100 were euthyroid. The factors favouring post-operative hypothyroidism are estimated weight of the thyroid remnant, the moderate size of goiter and perhaps a six to twelve months preoperative medical treatment. 39 patients had I 131 therapy: among them, 24 p. 100 relapsed, 25,7 p. 100 had permanent hypothyroidism and 50,3 p. 100 are euthyroid.

Adolescent↗
PubMedDate not supplied

Hormonal regulation of apoptosis in breast cells and tissues.

Few studies have referred to the implication of apoptotic processes following hormonal treatment. No data are available on the effects of progesterone in breast cells. In order to gain insights on the effects of the gonadal steroids and antiestrogens in breast cells, we have carried out studies on apoptosis in different breast materials. We have developed a model of normal breast cells in cultures that remain hormone-dependent. On these cells and in some hormone-dependent breast cancer cell lines (T-47-D, ZR75-1, MCF-7) we have observed an antiapoptotic effect of estradiol (E(2)) and a potent proapoptotic effect of some antiestrogens. Progestins were also proapoptotic in normal as well as in hormone-dependent breast cancer cells. In order to understand the mechanisms of these hormones on apoptosis, we studied the bcl-2 family proteins. We demonstrated that E(2) increased the antiapoptotic proteins, bcl-2 and bclx(L), whereas, the progestins drastically decreased bcl-2 expression and weakly bclx(L) levels. We investigated the mechanisms by which E(2) increased bcl-2 expression. Our results using quantitative RT-PCR showed that E(2) increased bcl-2 mRNA levels at 48 h of treatment via a transcriptional mechanism. None of the hormone treatments altered the proapoptotic protein levels, bax and bak. We also studied the in vivo expression of bcl-2 and other members of its family in biopsies of normal breast tissues according to the menstrual cycle. Bcl-2 displayed a strong cyclical variation and seemed to be the most hormone-dependent member of the family.

Apoptosis↗
PubMedDate not supplied

Proapoptotic effects of antiestrogens, progestins and androgen in breast cancer cells.

The promoting action of E2 in breast cancer cells has been, until now, mainly linked to its action on prolifieration. Because of the importance of an increase in apoptosis in breast cancer prevention, we have studied the possible effects of various antiestrogens, progestins and an androgen on its occurrence in three hormone-dependent breast cancer cell lines. The antiestrogens were, a triphenylethylene derivative, 4 hydroxytamoxifen (4OHTAM) and two steroidal antiestrogens, IC1182780 and RU58668. The progestins were Org2058, a pregnane derivative, tibolone (OrgOD14), a normethyltestosterone derivative and OrgOM38 (the delta4 isomer of OrgOD14) and the androgen dihydrotestosterone (DHT). Apoptosis was studied in MCF-7, ZR75-1 and T47-D cells using morphological approaches and flow cytometry. The antiestrogens, the progestins and DHT were proapoptotic but to different potencies according to the cell line studied. Indeed, the 'pure' steroidal antiestrogens were more efficient than 4OHTam in increasing apoptosis. We have also studied the level of expression of some of the proteins involved in the regulation of apoptosis. Bcl-2 and bcxL, two antiapoptotic members of the bcl-2 family proteins, were inhibited by the progestins and the antiestrogens. In contrast, the proapoptotic proteins, bax and bak seemed to be constitutively expressed. Thus, since the ratio of proapoptotic and antiapoptotic proteins determines apoptosis or cell survival, the hormone effects are operating by modulating the antiapoptotic regulators of the balance. These data demonstrate that antiestrogens, progestins, and androgens can promote apoptosis in breast cancer cells, an effect which could be of importance in the therapeutic prevention of breast cancer.

Apoptosis↗