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Biomedical subjects

P Bianchi

Publications and source records attributed to P Bianchi.

At least 19 recordsLinked to original sources
PubMed1992

Steroidal and non-steroidal factors in plasma sex hormone binding globulin regulation.

Sex hormone binding globulin (SHBG) is a specific steroid-binding plasma glycoprotein regulated by several factors. Sex steroids are currently considered to be the main physiological regulators of this protein. SHBG levels, in fact, increase during estrogen treatment and decrease after androgen administration. It is well known, however, that in many physiological and pathological conditions SHBG concentrations cannot be explained only on the basis of steroidal control mechanisms. The regulation of SHBG levels is in fact more complex and other factors can also affect its plasma values. Between the steroidal factors our attention was focused on the role of androgens, of glandular and peripheral origin, in their capacity to lower SHBG plasma levels. We studied hyperandrogenic conditions in prepubertal (65 subjects with precocious adrenarche and 16 girls with prepubertal hypertrichosis, aged between 4 and 8 years) and in adult age (51 hirsute patients aged between 14-35 years and 51 acneic patients aged between 15-40 years). The effects of dexamethasone and ACTH administration on SHBG plasma levels were also evaluated. The results obtained showed that in adult hyperandrogenic patients SHBG levels, significantly lower than in controls, were not always inversely correlated with androgen levels, which, on the contrary, were higher than in controls. In patients with precocious adrenarche we found an inverse correlation only between SHBG, which was significantly lower than normal, and body mass index or bone age but not with androgens, suggesting that in this condition other factors may be more relevant than steroids in SHBG regulation. Between the non-steroidal factors our attention focused on insulin. We studied 40 non-obese hyperandrogenic patients with or without ultrasonographic evidence of polycystic ovaries, aged 18-39 years, and 35 obese patients, aged 19-37 years, with or without hyperandrogenism or evidence of PCO. Low levels of SHBG were found not only in hyperandrogenic obese patients but also in obese patients with normal androgens. It is possible to conclude that (1) several factors (calorie intake, energy balance and growth factors), other than steroids, may be involved in the regulation of SHBG levels in plasma; and (2) each regulating factor may act to a different extent depending on the various periods of the life cycle.

Adolescent↗
PubMed1992

Lack of linear relationship between hyperinsulinaemia and hyperandrogenism.

OBJECTIVE: Because of continued debate about the role of insulin in the development of hirsutism and in the induction of the polycystic ovary syndrome, we have evaluated the hormonal pattern in a group of hirsute patients. PATIENTS: Fifty-four hirsute patients (age range 18-39 years) of whom 26 patients were obese (O) (BMI 28-53 kg/m2 and W/H greater than 0.85), 12 with ultrasonographic evidence of polycystic ovaries (O PCO) and 14 with normal ovaries. Twenty-eight patients were within normal weight range, and, of these, 14 presented ultrasonographic evidence of polycystic ovaries and 14 had normal ovaries. Two groups of age-matched subjects (obese and normal weight), normally menstruating, without hirsutism or history of endocrinopathies or ultrasonographic evidence of polycystic ovaries, served as controls. MEASUREMENTS: Androstenedione and testosterone were evaluated in all patients by RIA, following ether extraction, DHEAS, LH, FSH and insulin were evaluated directly by RIA. SHBG was evaluated by the concanavalin method. Free testosterone (FT%) was calculated according to the formula FT = 4.038-1.607 log SHBG. Integrated areas under the response curve were calculated for LH and insulin respectively following i.v. administration of GnRH (100 micrograms) or oral administration of glucose (75 g). RESULTS: Results (mean +/- standard deviation) showed comparable values of androstenedione in all groups of obese patients and in obese controls (7.3 +/- 2.6 in patients with polycystic ovaries, 7.1 +/- 2.9 in non-polycystic ovary patients and 7.4 +/- 2.6 nmol/l in obese controls, respectively), regardless of baseline and area insulin, the presence or absence of polycystic ovaries, or hirsutism. SHBG levels showed a similar pattern (24 +/- 10, 23.8 +/- 7.9 and 36 +/- 19 nmol/l) as did the percentage of free testosterone, regardless of the presence or absence of hirsutism. Regression analysis of the insulin and LH values (baseline and area) against the androgens and SHBG plasma levels showed that only LH area correlated positively with testosterone (r = 0.36, P less than 0.03), androstenedione (r = 0.44, P less than 0.02), % free testosterone (r = 0.53, P less than 0.001), testosterone/SHBG ratio (r = 0.39, P less than 0.03) and inversely with SHBG (r = -0.57, P less than 0.001). CONCLUSIONS: These results showed (1) no linear relationship between high levels of insulin, ovarian androgen production or free hormone availability, and (2) make it very doubtful that insulin plays a primary role in polycystic ovarian syndrome or hirsutism.

Adolescent↗
PubMed1992

Precision of gestational age assessment in the neonate.

The precision of the Ballard scale for assessing gestational age (GA) was evaluated in a consecutive sample of 227 preterm and/or low-birth-weight neonates. Each newborn was rated independently by two neonatologists and the difference in GA estimation between them was computed. The estimated precision was not high, the 95% tolerance interval estimate being as large as 7.4 weeks. The precision of the neurologic and physical parts of the scale was poorer than that of the complete scale (95% of differences less than 10.5 and 9.2 weeks respectively), and more influenced by the type of delivery. These findings are not unexpected from statistical theory, and cast doubts on the use of only the physical part of the Ballard scale in assessing GA, since greater accuracy could be accompanied by reduced precision.

Anthropometry↗
PubMed1992

[Mondor syndrome. Etiopathogenesis and case report].

The Authors observed and report a case of Mondor's syndrome in a male. In the attempt to identify the real origin in this peculiar thrombophlebitis they reviewed the recent literature. It is apparently impossible to drawn definitive conclusions from the different studies on this subject. Anyway Mondor's syndrome looks suitable for inclusion in the group of jumping thrombophlebitis. Therefore the real cause of the venous accident should be a pathologic situation next to the venous branch where the thrombophlebitis has broken out.

Adult↗
PubMed1991

Mapping the gene encoding the human erythroid transcriptional factor NFE1-GF1 to Xp11.23.

The X-linked NFE1 gene encodes an erythroid factor involved in globin gene transcription. Using a human cDNA clone encoding this factor, we show, by in situ hybridization and by analysis of human-rodent hybrid cell lines, that this gene is located in Xp11.23. In the absence of polymorphisms in the NFE1 gene, these results allow the study of the possible relationships between NFE1 mutations and X-linked hereditary persistence of fetal hemoglobin by linkage analysis with RFLP markers of the region. A female patient, hemizygous for the NFE1 locus, shows essentially normal hematological parameters.

Cell Line↗
PubMed1991

Patterns of gastrin secretion in patients with nonfunctioning pituitary adenomas.

The presence of gastrin in pituitary tissue as well as gastrin hypersecretion by some pituitary adenomas have been documented using different methodological approaches. In the present study, serum gastrin levels were measured in 93 patients with nonfunctioning pituitary adenoma, i.e. a condition lacking a reliable marker of the disease. Elevated gastrin levels (85-2, 180 ng/l; normal range: 15-80 ng/l) were found in 14/93 patients (15%), the highest values being observed in one patient with MEN I syndrome. In all but MEN I hypergastrinemic patient, a severe gastric hypochlorhydria (Basal Acid Output: 0.04 +/- 0.1 mmol H+/h) unresponsive to pentagastrin (Maximum Acid Output: 0.1 +/- 0.2 mmol H+/h) was seen. Secretin injection caused gastrin to increase in the patient with MEN I and in another hypergastrinemic patient. Antiparietal cells autoantibodies were positive in 3/11 patients. No changes in gastrin concentrations were found after administration of several agents usually employed in the evaluation of pituitary function, except a significant gastrin reduction after octreotide injection. In two hypergastrinemic patients who underwent pituitary adenomectomy, the high gastrin levels did not change after surgery. Finally, gastrin was undetectable in the culture media of 15 pituitary adenomas surgically removed from both normo- and hypergastrinemic patients and immunocytological studies of tumor cells did not show any gastrin staining. In conclusion, although in patients with pituitary adenomas serum gastrin evaluation is indicated in order to document the presence of a MEN I syndrome, the present data show that high gastrin levels cannot be taken as a specific marker of nonfunctioning pituitary adenomas unless the peripheral origin of hypergastrinemia is excluded.

Adenoma↗
PubMed1991

Cerebrospinal fluid estrone in pseudotumor cerebri: a change in cerebral steroid hormone metabolism?

Estrogen and androgen hormones were studied in the plasma and cerebrospinal fluid (CSF) of five patients affected by pseudotumor cerebri (PTC). Six men and six women without cerebral or endocrine diseases were selected as controls. Androstenedione (A), testosterone (T), 17-hydroxyprogesterone (17OH-P), E1 and E2 were measured in plasma and CSF in baseline conditions and following 1 month prednisone therapy (2 mg/die, per os) using RIA following chromatographic separation on celite microcolumns. Men and women affected by PTC show increased CSF E1 levels and marked decreased CSF A levels, with respect to controls. In plasma, on the contrary, normal values of these parameters were observed in PTC. In normal subjects A/E1 ratio shows the same values in plasma and CSF, suggesting for the two hormones analogous feasibility to cross the blood brain barrier. In PTC patients A/E1 ratio is comparable to controls in plasma, but lower in CSF as a result of decreased A and increased E1 contents. The CSF imbalance between A and E1 attenuates but does not disappear after treatment. No correlation is found between pressure levels and steroid pattern both in baseline condition or after one month of treatment. In conclusion, our results demonstrate that PTC is not only associated with increased CSF E1 levels, as previously suggested, but, above all, with decreased CSF A levels and this hormonal impairement seems to be confined to the CSF compartment and not observed in plasma. These data do not lead to any definitive conclusion about the role of altered CSF estrogen and androgen levels in PTC pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Measurement of alkaline phosphatase activity in serum with N-methyl-D-glucamine as a buffer: evaluation of the method for routine use.

Some aspects of the measurement of alkaline phosphatase activity concentration in human serum, using N-methyl-D-glucamine as a buffer, were evaluated with a view to the possible routine use of the method. The evaluated characteristics included: the temperature-dependence of the pH of the buffer; the effect of adding the magnesium/zinc ions buffer; the effect of the serum volume fraction; the substrate-starter versus the serum-starter mode; the effect of modifying the formulation of reagents; the within-run and the between laboratory imprecision; the correlation with an alternative routine method. Also, sex- and age-related reference values were produced, based on 2968 values from selected reference sample groups in 7 laboratories. In general, the results demonstrate the robustness of the method, its adaptability to a variety of mechanized analysers, and hence its feasibility as a routine measurement method.

Adolescent↗
PubMed1991

Signs and symptoms in samples with and without temporomandibular disorders.

Factors commonly associated with signs and symptoms of temporomandibular disorder were investigated in two groups. The patient group consisted of 41 subjects seeking treatment at the UCSF Temporomandibular Disorders Clinic, and the control group consisted of 40 incoming and first-year students. Questionnaires and clinical examinations were used to identify and measure factors in the areas of history, functional signs, and occlusion. Only four factors emerged as statistically significant between groups: frequent headaches, masticatory muscle tenderness, cervical muscle tenderness, and maximum opening.

Adult↗
PubMed1991

Use of immunoglobulin heavy-chain and light-chain measurements in a multicenter trial to investigate monoclonal components: I. Detection.

We assessed the combined use of serum protein electrophoresis (SPE) and nephelometric measurement of immunoglobulin heavy- and light-chain components for detecting serum monoclonal immunoglobulins (monoclonal components, MC) in 4788 unselected samples from 4173 patients. MC were detected in 514 samples from 390 patients. In 356 these were detected by SPE; the other 34 had a normal SPE pattern but an abnormal kappa:lambda light-chain ratio (KLR). Only 208 of the 356 (58%) samples with bands by SPE had abnormal KLRs. Samples with MC concentrations greater than 5 g/L had a higher proportion of abnormal KLRs (75%) than those with concentrations less than 5 g/L (42%). The KLR was abnormal in 13% of samples in which no MC were visible by SPE or immunofixation electrophoresis (IFE). Compared with quantitative measurements of immunoglobulin heavy and light chains, high-quality SPE remains the method of choice for the detection of MC. Quantitative methods, however, are able to detect additional MC, especially those containing free light chains, and in the absence of SPE and IFE will detect about 75% of MC present at greater than 5 g/L.

Antibodies, Monoclonal↗
PubMed1991

Use of immunoglobulin heavy-chain and light-chain measurements in a multicenter trial to investigate monoclonal components: II. Classification by use of computer-based algorithms.

We describe a computer algorithm for classifying serum monoclonal proteins (MC) based on serum protein electrophoresis (SPE) and the automated measurement of kappa and lambda light chains and IgG, IgA, and IgM. We developed the algorithm by using a large database of unselected samples containing MC collected in a multicenter study. The performance of the algorithm was optimized by using iterative computational procedures and was tested on both the development database and on an independent set of MC-containing samples. With the development database, the algorithm correctly classified 50% and misassigned 2.5% of the MC. Where the MC were present in concentrations greater than 10 g/L, the rate of successful classification increased to 72% with 3% misclassification. When the algorithm was tested on a group of 101 MC-containing samples from an independent source, 67% were correctly classified and 8% misclassified, half of the latter being unusual IgD myelomas. We discuss the scope for the application of the algorithm in routine laboratory practice involving personal computer software.

Algorithms↗
PubMed1991

Intraglomerular metastases. A possibly maldiagnosed entity.

Intraglomerular metastases are rare. We observed a case of lung cancer which gave rise to liver metastases and to exclusively intraglomerular kidney metastases, mimicking angio-endotheliomatosis. Differential diagnosis and histological features of the lesion are discussed.

Adenocarcinoma↗
PubMed1990

Ovarian 17-ketosteroid reductase deficiency as a possible cause of polycystic ovarian disease.

The deficiency of ovarian 17-ketosteroid reductase (17-KSR) was recently discovered to be a possible cause of polycystic ovarian disease (PCOD) in hirsute women. Forty three patients with PCOD (age range, 18-38 yr) were reevaluated to search for a hormonal pattern that might suggest an ovarian 17-KSR deficiency. Androstenedione, testosterone, FSH, LH, 17-hydroxyprogesterone, and dehydroepiandrosterone sulfate were evaluated basally on the day 17 of the menstrual cycle, when present, and after dynamic tests (ACTH stimulation, 1 mg im for 2 consecutive days; dexamethasone inhibition, 0.5 mg four times a day for 14 days; and cyproterone acetate treatment, 50 mg each day for 14 days) in three successive menstrual cycles or at 30-day intervals. All patients studied presented with hyperestronemia, abnormal gonadotropin pattern, and hyperandrogenism, but showed different responses of androstenedione and testosterone to dynamic tests. In two patients the hormonal pattern suggested an ovarian 17-KSR deficiency: in fact they showed plasma values of androstenedione (22 and 31.3 nmol/L, respectively) and estrone (628 and 849 pmol/L, respectively) that were greatly increased compared with other patients and with controls. Androstenedione did not increase after ACTH stimulation (21.5 and 32.1 nmol/L, respectively) and did not decrease after dexamethasone inhibition (21 and 29 nmol/L, respectively), but only decreased after cyproterone acetate treatment (8 and 10.8 nmol/L, respectively). An hCG test, performed during dexamethasone suppression, confirmed the diagnosis of ovarian 17-KSR defect in one of these two patients (patient 1). Two of three brothers of patient 1 (aged 25 and 34 yr) presented with persistent important pubertal gynecomastia; one brother also had severe oligospermia. These clinical findings and the high values of androstenedione/testosterone (0.85) and estrone/estradiol (4.1) ratios of baseline plasma levels compared with controls (0.18 and 2.1, respectively) suggested a partial testicular 17-KSR deficiency. Five other patients showed PCOD secondary to nonclassic 21-hydroxylase defect diagnosed on the basis of high 17-hydroxyprogesterone plasma values and highly responsive to ACTH. The remaining 36 patients showed increased values of androstenedione and testosterone after ACTH stimulation and a decrease of these two parameters after both dexamethasone inhibition and cyproterone acetate treatment. The discovery of the 17-KSR deficiency in men and women in the same family demonstrates genetic control of this enzyme similar in both sexes, confirming the hypothesis that this disorder is inherited as an autosomal recessive character. Finally, it is strongly supported that ovarian 17-KSR defect may cause a syndrome closely resembling PCOD.

17-Hydroxysteroid Dehydrogenases↗
PubMed1990

Bone mineral density in adult celiac patients and the effect of gluten-free diet from childhood.

Peripheral single photon absorptiometry was used to measure forearm bone mineral density in 22 celiacs on gluten-free diet from childhood (male 14, female 8, age 13-20) and 29 untreated adult celiacs at diagnosis (male 5, female 24, age 18-56, 14 with subclinical disease), compared with healthy sex- and age-matched controls. Bone mineral density was similar in patients treated from childhood and their controls [(668.4 +/- 65.3 vs. 654.9 +/- 69.6 mg/cm2, (mean +/- SD)], but significantly lower in untreated patients than in their controls (598.3 +/- 83.1 vs 673.2 +/- 42.7 mg/cm2, p less than 0.001). It was also significantly lower in the 12 younger untreated celiacs (18-28 yr) versus controls (619.4 +/- 68.5 vs 669.1 +/- 39.3 mg/cm2, p less than 0.01). In the untreated women, but not their controls, a negative correlation (p less than 0.05) was observed between bone mineral density and age. Bone mineral density did not correlate with severity of clinical or biochemical abnormalities. These results suggest that bone derangements are common in celiacs diagnosed in adulthood, even if they never presented evident malabsorption symptoms, and emphasize the importance of early diagnosis and treatment.

Absorptiometry, Photon↗