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Biomedical subjects

V Scafidi

Publications and source records attributed to V Scafidi.

At least 37 records · Page 2Linked to original sources
PubMed1988

[Improvement of glucose tolerance in diabetics under nicardipine therapy].

Present study was carried out in order to control if glucose tolerance and insulin secretion changed during nicardipine treatment in healthy or in non-insulin dependent diabetics. In the 8th day of therapy with nicardipine (40 mg/day), glucose tolerance and insulin secretion were unmodified in a group of 20 non-diabetic patients. At the same time glucose tolerance was found improved in the group of 14 non-insulin dependent diabetic without a contemporary variation of insulin secretion. Such a result, note-worthy for a drug frequently administered to diabetics, could be due to inhibited glucagon secretion, or to increased glucose uptake by hepatocytes.

Adult↗
PubMed1986

[Evaluation of the parameters used in monitoring hypothyroid patients treated with L-thyroxine].

Hormonal and clinical data on 38 tests performed in 7 hypothyroid patients given substitutive treatment with L-thyroxin were analysed. The aim of the survey was to assess the dependability of the various parameters used to estimate dose adequacy in substitutive treatment. Examination of individual cases revealed that overdoses of thyroxin increased T4 to above normal limits without increases in T3, FT3, FT4 or hypophyseal suppression. Chronological discrepancies between clinical data and normal parameters were also noted. However on the data as a whole significant correlations were noted between T4 and TSH (p less than 0.001), between T4 and delta-TSH (p less than 0.001), between T3 and TSH p less than 0.01), between FT3 and delta-TSH (p less than 0.01), between FT4 and delta-TSH (p less than 0.01). FT4 and delta-TSH were also significantly correlated (p less than 0.02) with the Billewicz clinical index of hypothyroidism. It is concluded that the clinical and hormonal data in treated hypothyroid cases have the same significance as in normal or untreated hypothyroid cases. However, it must be borne in mind that unusual relations between the various thyroid hormone fractions including TSH and the standardised clinical examination may arise while doses are being established. In this case the data cannot be automatically interpreted but merely carefully assessed in the light of experience.

Adult↗
PubMed1986

Mild hyperthyroidism with inappropriate secretion of TSH in postmenopausal women.

In a previous study on the function of the hypothalamus - pituitary - thyroid axis, about 10% of postmenopausal women with the climacteric syndrome were found to have borderline high values of T3 and T4 and signs of pituitary decreased sensitivity to the suppressive effect of increased thyroid hormones. The present report concerns 5 women in the first phase of their menopause who showed a mild hyperthyroidism under basal conditions and after suppression test with liothyronine. Each patient had borderline increased levels of serum total and free T4 and T3 and a marked TSH responsiveness to exogenous TRH. After liothyronine, the serum levels of T4, FT4, TSH and the responsiveness to TRH-test clearly decreased. These data suggest an inappropriate TSH secretion with a decreased pituitary sensitivity to thyroid hormones. These cases could represent a modification of the hypothalamus-pituitary-thyroid axis associated with that of the gonadal axis, secondary to the absence of rapid adaptation of neurotransmitters.

Female↗
PubMed1984

[Hepatic clearance of 99mTc-p-butyl HIDA in liver diseases. Correlations with routine hematochemical parameters of liver function].

The aim of the present investigation was to study the clearance of 99mTc-p-butyl IDA in some acute and chronic liver diseases, it being considered that the typical parameters obtained with this method are as indicative as any of the others put forward for the study of liver function using radioisotopes. 46 subjects were examined: 6 with acute hepatitis, 10 with chronic hepatitis, 18 with liver cirrhosis and 12 with dyspepsia but otherwise normal haematochemical tests. Two basic 99mTc-p-butyl IDA clearance parameters, Tu (semi-take up time) and Te (semi-excretion time), were determined plotting the data obtained using a Gamma-Camera on semi-logarithmic paper. Mean Tu values were as follows: 5'06'' +/- 1'24'' in dyspeptics, 12'30'' +/- 6'31'' in subjects with acute hepatitis, 6'30'' +/- 1'45'' in subjects with chronic hepatitis and 13'30'' +/- 4'30'' in subjects with cirrhosis. The values were: 34'30'' +/- 4'30'' in dyspeptics, 49'54'' +/- 2'36'' in subjects with acute hepatitis, 42'24'' +/- 12'24'' in subjects with chronic hepatitis and 65'30'' +/- 39'36'' in subjects with cirrhosis. The Tu parameter was found to be delayed more significantly in cirrhotic patients and less in subjects with acute or chronic hepatitis, compared to dyspeptics with normal haematochemical parameters. Te was significantly delayed in subjects with cirrhosis and acute hepatitis, while there was no difference for subjects with chronic hepatitis. Of the routine haematochemical tests, the albumin/gamma-globulin ratio and unconjugated bilirubin were found to correlate significantly with the Tu parameter, whereas conjugated bilirubin was found to bear a significant correlation to the Te parameter.

Adult↗
PubMedDate not supplied

Prospective study on thyroid autoimmunity and dysfunction related to chronic hepatitis C and interferon therapy.

This study was designed to assess patients with chronic hepatitis C (CHC) for the presence of thyroid autoimmunity and dysfunction, to evaluate the risk of thyroid disorders associated with interferon (IFN) therapy, and to survey the outcome of possible treatment-related thyroid injury. Out of 104 consecutive untreated patients (30 women and 74 men; mean age, 52.7 years), 8 (7.7%) were found seropositive for thyroid autoantibodies (ThyAb), whereas seropositivity in healthy controls was 1/98 (1.3%). The relative increase in risk of developing thyroid autoimmunity associated with CHC was 760% (95% CI, 220-1300%). No patients had abnormalities of thyroid function tests, but on IFN treatment, 3/3 patients showed a rapid over-range rise in circulating thyrotropin, which returned to normal after therapy discontinuation. In the other 5 seropositive patients who refused treatment, thyroid function remained normal. Out of the 58 initially seronegative patients who consented to IFN treatment, 9 (15.5%) developed thyroid autoimmunity. Seven of them (77.7%) had thyroid dysfunction: hypothyroidism in 4 cases, transient thyrotoxicosis in 2 cases. The last patient developed TSH-receptor antibodies and Graves' disease, requiring methimazole therapy. Thyroid function recovered in the former 6 cases following IFN discontinuation. In the 28 initially seronegative patients who refused IFN and participated in a preliminary tauroursodeoxycholic acid trial, antithyroglobulin antibodies alone appeared in one case, but no thyroid dysfunction was observed. The relative risk of thyroid autoimmune disorder associated with IFN therapy was 342% (28-636%). The patients with CHC were unlikely to develop thyroid dysfunction in the absence of IFN therapy, in spite of being ThyAb seropositive. Moreover, a considerable proportion of seronegative patients, when IFN-treated, developed thyroid autoimmunity and then thyroid dysfunction. Both in seropositive and seronegative patients immediate IFN discontinuation normalized thyroid function and hormone replacement therapy was not necessary.

Adult↗
PubMedDate not supplied

Prospective study on thyroid function anomalies in severely ill patients.

Patients with severe non-thyroidal illness (NTI) often evidence concomitant anomalies in thyroid function (TF). In order to shed light on the implications of these anomalies and/or changes and disease course, we monitored TF changes in a selected cohort of 45 patients with serious NTI (21 with liver cirrhosis, 15 with renal failure and 9 with malignancy) from April 1985 to October 1989. TF test results on admission were as follows: all patients had normal thyroid stimulating hormone (TSH) levels; 16 patients had no TF abnormalities; 28 had decreased serum triiodothyronine (T3) and increased serum reverse triiodothyronine (rT3) levels, (8 of them had low serum free T3 values as well); 1 patient had subnormal level of both T3 and thyroxine (T4). Fifteen (53.5%) of the 28 subjects with initial low T3 sustained a subsequent decline in total and free serum T4 to subnormal levels; in 13 of these patients the drop occurred shortly before death. Patients in critical condition with below normal serum T4 also had decreased serum TSH concentrations: the so-called "low T3 and low T4 syndrome" might thus result from decreased TSH concentrations: due to failure of the usual feedback mechanism. Eighteen patients (40%) had died by the end of the study period. The mortality rate was 89% in patients with initial T3 level less than 0.40 nmol/L. This finding leads us to the hypothesis that initial low T3 levels in NTI patients are indicative of a poor prognosis.

Aged↗
PubMedDate not supplied

[Changes in blood levels of the pituitary-thyroid axis observed during therapy with protirelin ++ in hospitalized euthyroid patients with cerebrovascular disease].

The effects of a TRH-T (protireline tartrate) treatment at a dose of 2 mg/day for 3 weeks on the serum levels of the pituitary-thyroid axis hormones, have been studied in a randomized group of 10 elderly euthyroid hospitalized patients with cerebrovascular disease. At the end of the treatment an 8.3% mean increase of serum T3 level and a 12.5% mean increase of serum FT3 level (p less than 0.02 in both cases) have been observed. At the same time a 34% mean decrease of the basal TSH (p less than 0.05) and a 26% mean decrease of the delta-TSH after TRH-test (p less than 0.025) have been noted. However, the hormone concentrations changes never exceeded the normal values. In a randomized group of 9 hospitalized untreated patients with cerebrovascular disease used as controls (matched for age and sex), no significant changes of studied hormones have been recorded. In the treated patients, one week after the withdrawal of therapy serum levels of thyroid hormones and TSH went back to the levels observed before treatment. TRH-T seems to cause these modest hormone changes by decreasing the number of TRH receptors and the activity of TSH secreting cells. Nevertheless, the presence of the normal feedback in the pituitary-thyroid axis, allows a good tolerance to such a treatment.

Aged↗
PubMedDate not supplied

[Changes in the thyroid hormone picture that may be found in severely decompensated type II diabetics].

Thyroid hormone picture of 28 patients (15 males and 13 females), mean age 56.6 yr (range 45-65 yr), with seriously decompensated type II diabetes mellitus has been studied. In each patient the study was repeated after 3 months of treatment of diabetes. The patients showed significantly lower serum T3 levels and significantly higher serum rT3 levels (P less than 0.001), in comparison with a group of 16 normoglicemic subjects. After 3 months of strict control of diabetes T3 and FT3 significantly increased (P less than 0.01), whereas significant variations of rT3 were not found. Among the whole group of diabetics 5 patients had low levels of serum T4 (P less than 0.01 vs. controls), high levels of serum TSH (P less than 0.001 vs. controls) and an exaggerated responsiveness to exogenous TRH (P less than 0.001 vs. controls). After the 3 months of treatment these patients showed a significant decrease of rT3 (P less than 0.02) and of delta-TSH (P less than 0.01). In the whole group of diabetics significant statistical correlations between glycometabolic and thyroid parameters were not found. The study, on the whole, showed in patients with seriously decompensated type II diabetes, a hormone picture like the low-T3 syndrome, in some cases, however, pituitary TSH secretion suggested the existence of incipient failure of thyroid hormones. A connection between alterations in thyroid hormone picture and glycometabolic imbalance, even statistically labile, is however indicated by improvement of thyroid function when diabetes is carefully controlled.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

[Stimulated secretion of TSH in patients with depression of mild nature].

Several studies have demonstrated that a consistent part of patients with severe depression shows anomalous responses of neuroendocrine axes. In the last years, altered TSH responsiveness to exogenous TRH have been reported also in patients with panic disorders. Because of these suggestions we studied stimulated TSH secretion in 24 untreated hospitalized patients (8 males and 16 females), aged from 21 to 76, in whom the psychiatric examination disclosed mild but inequivocal signs of persistent depression (score range on Rufin and Ferreri Iventory from 20 to 35). The TRH-test (200 mcg i.v.) was started between 9.00 and 9.30 a.m.. The same test was performed also in 14 sex- and age-matched volunteers defined without psychiatric disorders. As comparison parameter, delta-TSH (maximum increase during TRH stimulation) was accounted. All the patients had normal serum thyroid hormone levels. TSH responsiveness of patients with minor depressive disorders was not found statistically different when compared with normal control volunteers, but a reverse significant correlation was found between delta-TSH and percentage score of anxiety in group of patients (with blunted TSH response in 6 (25%) patients), that was not found in normal subjects. A significant correlation between delta-TSH and depression degree was not found. The present data, although preliminary, could indicate the existence of depressed subjects in whom blunted TSH response to TRH seems related to anxiety degree. Additional studies, particularly on the medullo-adrenal function, might clarify the nature of these alterations, that at state is unclear, although the mechanisms suggested also for alterations of pituitary hormone responses in major depression could be taken in account.

Adult↗
PubMedDate not supplied

[Insulin resistance in patients with Graves' disease and reduced glucose tolerance. The normalization of fasting insulin secretion in parallel with the restoration of thyroid function].

In order to investigate the nature of impaired glucose tolerance (IGT) in 3 young patients with Graves' disease we have studied their insulin secretion fasting and in response to oral glucose by means of measurement of serum C-peptide. Fasting levels of serum C-peptide of these patients were beyond the range of 15 age-matched normal subjects; the C-peptide/glucose ratio was also significantly higher (p less than 0.001) in the patients than in the controls. Following glucose ingestion serum levels of C-peptide resulted high in the range of normals, with a mean C-peptide/glucose ratio greater than in the controls, but without reaching of statistical significance. To investigate whether the anomaly in fasting insulin secretion of these patients had any correlation with their hyperthyroidism, afterwards we surveyed fasting concentrations of serum C-peptide in parallel with progressive variations of serum free thyroxine and triiodothyronine (FT4 and FT3) and thyrotrophin (TSH) during antithyrotoxic treatment with methimazole. The data of 23 tests on serum FT3 and FT4 levels, carried out during 16-18 months, resulted in significant correlation with contemporaneous measurements of fasting serum C-peptide (p less than 0.001). No significant correlation was found between serum TSH and fasting C-peptide levels. The results suggest that IGT of the patients in this study is not dependent on lacking insulin secretion, but on mild insulin resistance. Such glucose metabolic anomaly appears to be in clear correlation with the degree of hyperthyroidism, even if its pathogenesis remains to be further investigated.

Adult↗
PubMedDate not supplied

[The thyroid hormone picture of alcoholics in connection with their liver status].

This work was performed in order to analyze thyroid hormone picture of alcoholic patients with reference to hepatic damage. Forty consecutive patients of male sex, aged 28-64 years, were investigated. They consumed more of 50 g ethanol/day for at least 2 years. According to investigations on hepatic condition, 2 cases had normal liver, 22 cases had steatosis and 16 had cirrhosis. None of patients disclosed a clinical and/or hormonal behaviour pointing to alterations of thyroid function. In alcoholics serum T3 levels resulted significantly lower compared to a control group of 40 healthy males (P less than 0.001), independently of degree of hepatic damage. Instead, serum T4 levels did not result significantly different in the comparison between alcoholics and controls. Serum FT3 and FT4 levels resulted significantly higher (P less than 0.001) only in alcoholics with liver cirrhosis. In comparison with normals, serum rT3 was significantly lower in alcoholics without liver cirrhosis (P less than 0.001), but significantly higher in alcoholics with liver cirrhosis (P less than 0.005). Serum TBG behaved in the same manner. According to euthyroidism in our alcoholic patients basal and TRH-stimulated TSH were normal, however significantly lower when compared to controls (P less than 0.005). On the whole these results suggest the existence of an autonomous ethanol-dependent mechanism that determine decreased serum T3 levels in the alcoholics, in absence of serum T4 variations. In the alcoholic with liver cirrhosis, an increased conversion of T4 in rT3, correlated to hepatic damage, joins to previous mechanism. The tendency to low secretion of pituitary TSH might be dependent of action of alcohol on neuromodulation of TRH secretion.

Adult↗
PubMedDate not supplied

[Role of high blood glucagon in the reduction of serum levels of triiodothyronine in severe non-thyroid diseases].

In healthy subjects intravenous glucagon administration induces a prompt (at 1 h) fall in serum T3 concentration and a later (at 4 h) rise in biologically inactive rT3. Since high levels of plasma glucagon have frequently been found in some patients with severe chronic illnesses, together with an anomalous thyroid condition (low serum T3, high serum rT3), it has been supposed that hyperglucagonemia could play a pathogenetic role in causing selective T3 deficiency. In the present study fasting plasma glucagon concentration was measured in 48 patients with low T3 and severe nonthyroidal illnesses: hepatic cirrhosis in 16 cases, chronic non-A non-B hepatitis in 4 cases, uncontrolled type II diabetes mellitus in 5 cases, renal failure in 12 cases, congestive heart failure in 5 cases, tumor in 16 cases. In comparison with a group of 21 healthy controls fasting plasma glucagon concentration was significantly higher in the patients (198.75 +/- 13.20 pg/ml vs. 127 +/- 6.80 pg/ml; p less than 0.001). However, only 29 patients (60.4%) had elevated plasma glucagon levels, whereas 19 (39.5%) had abnormal plasma glucagon levels. Furthermore, no significant difference was found between the thyroid hormone pattern of the patients with hyperglucagonemia and of the patients with normal glucagonemia. On the other hand, a significant correlation between plasma glucagon concentrations and serum T3 and rT3 concentrations was not found. All these findings indicate that in patients with severe chronic illnesses the fall in circulating T3 cannot be due to hyperglucagonemia only which, therefore, might simply be a contributory factor together with other as yet unidentified disorders.

Adult↗