Biomedical subjects
Publications and source records attributed to L Benassi.
Gynecologic and urinary congenital malformations are often associated and mostly diagnosed in teenagers. To update a 116-case international case registry, three cases of uterus didelphys with obstructed hemivagina and ipsilateral renal agenesis, detected in young girls, are reported. Diagnostic procedures and surgical treatment are discussed.
Skin biopsy specimens from five patients with pityriasis lichenoides et varioliformis acuta and from six patients with pityriasis lichenoides chronica were studied by direct immunofluorescence and by an immunoperoxidase technique using a panel of monoclonal antibodies. The dermal inflammatory infiltrate was composed of T cells, macrophages, and a small proportion of CD1a+ cells, mostly perivascular. CD8+ cells (cytotoxic/suppressor phenotype) predominated in the epidermis according to the degree of epidermal necroses, whereas CD4+ cells (helper/inducer phenotype) were superior in number among dermal T cells. A few B cells and Leu7+ cells were detected in only a small proportion of lesions. The results obtained confirm that the two conditions are variants of a single disease process and suggest that cell-mediated immune mechanisms may be important in the pathogenesis of the epidermal and vascular damage. Endothelial cells (HLA-DR+ and HLA-DQ+) and CD1a+ cells (epidermal and possibly dermal) could be primarily involved, acting as antigen-presenting cells.
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Cord blood and amniotic fluid thyrotropin (TSH), T4, T3, and rT3 concentrations were measured in 49 women who received 400 micrograms thyrotropin releasing hormone (TRH) iv during labor and in 16 control women who received saline. Cord blood serum TSH concentrations were elevated for as long as 4 hours after TRH administration and peak values (38.0 +/- 4.2 microU/ml) were observed from 61-120 minutes after TSH as compared to control values of 5.0 +/- 0.3 microU/ml. The elevations in fetal TSH concentration stimulated the fetal thyroid, resulting in a progressive increase in cord blood T4 and T3 but not rT3 concentrations. These TRH induced elevations in fetal cord blood TSH concentrations were not accompanied by increases in unconcentrated and 4 fold concentrated amniotic fluid TSH concentrations which were almost always below 0.6 microU/ml, the limit of assay sensitivity. Unconcentrated amniotic fluid T4 concentrations were barely detectable and no variation was observed between the TRH treated and saline treated mothers; amniotic fluid T3 was not detectable in any of the groups; and amniotic fluid rT3 concentrations ranged between 46.4 and 55.6 ng/dl and did not differ between groups. These findings suggest that term amniotic fluid TSH values do not reflect transient but marked elevations in fetal serum TSH concentrations and that amniotic fluid TSH determination is probably not useful in the detection of primary fetal hypothyroidism. It is possible, but unlikely, that long-term and even greater elevations in fetal serum TSH concentrations would result in increased amniotic fluid TSH concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Metoclopramide (MET), a potent dopamine receptor-blocking drug, or saline was administered to 125 term pregnant women at various time intervals (5-412 min) before delivery. Maternal serum was obtained before and after MET injection. Cord blood was obtained at delivery in MET-treated and saline-treated (control group) women. No significant changes in serum TSH, T4, T3, or rT3 concentrations were observed in maternal or cord blood after MET administration. These results suggest that, in contrast to euthyroid nonpregnant women and men, MET administration does not induce a rise in serum TSH concentration in term pregnant women or in the term fetus. Thus, the dopaminergic inhibitory effect on anterior pituitary TSH secretion may not be an important factor in TSH regulation during pregnancy or in the fetus, or the dose of MET employed may be unable to overcome the dopamine inhibitory effect.
The effect of TRH administration to the term pregnant women on the GH response in cord blood (CB) was evaluated in 138 subjects. Previous studies have demonstrated that TRH readily crosses the placenta. TRH (400 microgram) was administered iv to 59 pregnant women just before delivery. CB samples were obtained at delivery and assigned to 6 groups, depending upon the duration of time between TRH injection and CB sampling. The control group comprised 79 pregnant women who received saline. A progressive rise and then a fall in the CB GH concentration were observed after TRH administration. Values were significantly elevated 61-90 min after TRH administration compared to values in saline-treated subjects (19.3 +/- 3.1 vs. 13.1 +/- 0.9 ng/ml; P less than 0.05). The present study is the first report of the effect of TRH on the GH concentration in CB and suggests that TRH stimulates GH release in the fetus.
On the basis of recent demonstration in animals of the effect of some hormones on uteroplacental flow, the Authors examined the response of plasmatic Estetrol (15 alpha-hydroxy-estriol) after the administration of progesterone to pregnant women with low Estrogen values. The increase of this compound was related to an improvement of placental function, probably dependent on an increase of available O2, and therefore on uterine blood flow. This can justify a progesterone treatment in such pregnancies.
The Authors studied the levels of Estetrol (15 alpha-hydroxyestriol) in the amniotic fluid, in maternal and foetal plasma, by the RIA method, in near-term pregnancies. Higher concentrations of this steroid were found in the foetal plasma and in amniotic fluid than in the maternal plasma. These data, even though of little clinical importance, confirm the foetal origin of this compound and suggest further studies, especially in the amniotic compartment.
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TRH or saline was administered to 214 term pregnant women at various time intervals (8-820 min) before delivery. Cord blood (CB) was obtained, and plasma TSH, T4, T3, rT3, and thyroglobulin concentrations were measured by specific RIA. CB TSH was significantly elevated within 20 min after TRH administration and remained elevated for 180 min. CB T3 rose significantly by 60 min and remained elevated for 820 min. CB T4 was significantly increased from 120 to 820 min after TRH administration. There was no significant change in the CB thyroglobulin concentration. These findings demonstrate for the first time that TRH crosses the human placenta, that the fetal pituitary is responsive to TRH, and that endogenous TSH stimulates the fetal thyroid.
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The Authors have executed a retrospective study about the incidence of intrahepatic cholestasis in pregnancy in 85 patients hospitalized in the department of Obstetrics and Gynaecology, University of Parma. Particularly, they have investigated about the incidence of fetal distress, about the intrauterine death, and about poor intrauterine fetal growth.
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Neonatal urinary excretion of Estriol and their C(16) substituted precursors are considered in this study in fetus at birth. Besides the prognostic significance of different ormonal levels, we have examined the role played by these valuation in order to explain the data achieved during the pregnancy.