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Biomedical subjects

N Custro

Publications and source records attributed to N Custro.

51 records · Page 3Linked to original sources
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

Evidence of transient IgA anti-endomysial antibody positivity in a patient with Graves' disease.

BACKGROUND: Anti-endomysial antibodies (EmA) have been shown to have a high specificity and sensitivity in celiac disease (CD) diagnosis, and their use is considered effective in improving the diagnostic accuracy of CD screening. AIMS: To report the clinical details of transient IgA EmA positivity in a patient with Graves' disease. METHODS: We screened 48 patients (7 males, age range 19-79, median 58.3 years) for CD. They were hospitalized for thyroid disorders (30 patients had autoimmune hypothyroidism and 18 had Graves' disease with clinical hyperthyroidism associated with diffuse goitre). CD screening was carried out on all patients by assaying serum anti-gliadin antibodies (AGA) and EmA. RESULTS: None of the 48 patients in our study were positive for IgA and/or IgG-class AGA and none showed IgA deficiency. Only 1 patient was positive for EmA; however, intestinal biopsy in this subject was normal both when thyroiditis was first diagnosed and subsequently after 2 and 3 years. Furthermore, EmA became negative after 2 years. New gastroenterological investigations performed 3 years after the diagnosis confirmed the normal intestinal histology and absorption capacity. Moreover, AGA, EmA and tissue transglutaminase antibodies were negative. CONCLUSIONS: This study underlines the possibility of transient EmA positivity without any signs of CD in patients with autoimmune thyroid disorders.

Aged↗
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↗
PubMedDate not supplied

Effects of verapamil on platelet aggregation and serum thromboxane synthesis in vitro and in vivo.

The aim of this study was to evaluate the in vitro effects of verapamil on platelet aggregation and serum thromboxane formation. We also studied the in vivo effects of verapamil retard on platelet aggregation and serum thromboxane formation. The incubation of verapamil with PRP produced a dose-dependent decrease of in vitro platelet aggregation for all the agents used. Potentiation by verapamil of antiaggregating activity of prostacyclin was also demonstrated; in fact when verapamil and prostacyclin were added simultaneously a synergistic inhibition of platelet aggregation by ADP was observed. In whole blood verapamil partially inhibited thromboxane production only at a higher concentration. In vivo verapamil significantly decreased platelet aggregation induced by ADP and epinephrine while no changes were observed after arachidonic acid. No significant changes occurred in serum TXB2 levels. The observations suggest a potential role for verapamil in antithrombotic therapy as an antiplatelet agent.

Dose-Response Relationship, Drug↗