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Results for “thyroid dysfunction”

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At least 595 records · Page 33Linked to original sources
PubMed1999

High prevalence of thyroid dysfunction in adult patients with beta-thalassemia major submitted to amiodarone treatment.

Amiodarone may induce hyper- or hypothyroidism. Patients with beta-Thalassemia Major (beta-Thal) have an increased prevalence of primary hypothyroidism and often require amiodarone for hemosyderotic cardiomyopathy. Aim of this study was to retrospectively evaluate thyroid function in beta-Thal adult patients on long-term amiodarone. The study group consisted of twenty-two (21 males, 1 female; age: 23-36 yr) beta-Thal patients submitted to long-term (3-48 months) amiodarone therapy from January 1991 to July 1996. Controls included 73 beta-Thal patients (23 males and 50 females aged 25-35 yr) not treated with amiodarone. In all cases serum free thyroid hormones, thyrotropin and thyroid autoantibodies were evaluated. A higher prevalence of overt hypothyroidism (5/22 [22.7%]) as compared to controls (3/73 [4.1%], p=0.02) was found in beta-Thal patients < or = 3 months after starting amiodarone, while the prevalence of subclinical hypothyroidism was similar in amiodarone-treated (18.2%) and untreated (15%) beta-Thal patients. Overt hypothyroidism resolved spontaneously after amiodarone withdrawal in 1 case, while the remaining patients were maintained euthyroid on amiodarone by L-thyroxine administration. After 21-47 months of amiodarone therapy, 3 patients (13.6%) developed thyrotoxicosis (2 overt and 1 subclinical), which remitted shortly after amiodarone withdrawal. No case of hyperthyroidism was observed in beta-Thal controls (p=0.012 vs amiodarone-treated patients). In conclusion, amiodarone administration is often associated in adult beta-Thal patients to a rapid progression of the pre-existing subclinical hypothyroidism, but transient thyrotoxicosis may also be observed after a longer period of therapy. These findings should be carefully considered in the management of these patients.

Adult↗
PubMed1993

Thyroid dysfunction in African trypanosomiasis: a possible role for inflammatory cytokines.

OBJECTIVE: Sleeping sickness (African trypanosomiasis) is an anthropozoonosis transmitted by the tsetse fly. The treatments of choice are the antiparasitic agents suramin and/or melarsoprol. Experimental infection of animals with Trypanosoma brucei results in inflammatory lesions in the pituitary and/or the thyroid gland. In biochemical terms, these animals have hypothyroidism. We evaluated the functional integrity of the hypothalamic-pituitary-thyroid axis in patients with African trypanosomiasis before, during and after specific therapy. DESIGN: Prospective, controlled, cross-sectional study. PATIENTS AND MEASUREMENTS: Sixty-five patients with sleeping sickness (31 female, 34 male; aged 18-66; 32 with haemolymphatic sleeping sickness receiving suramin i.v., 33 with cerebral sleeping sickness receiving melarsoprol) and 13 control subjects (6 female, 7 male; aged 21-60) were enrolled in a cross-sectional study after giving informed consent. Fourteen patients were studied shortly after admission for sleeping sickness, 19 in the middle of the course of treatment, 18 at the end of the 5-week treatment period, and 14 patients after cure. All subjects underwent a TRH stimulation test at 1200 with bolus injection of 400 micrograms TRH i.v. Blood was drawn for determination of fT3, fT4, TSH, rT3, TNF-alpha, IL-1 and IL-6 at 0 minutes and TSH at 60 minutes. All hormones and cytokines were determined by RIA or ELISA. RESULTS: Baseline TSH concentrations (mean +/- SEM) were elevated in unmedicated patients with sleeping sickness compared to normal subjects (2.6 +/- 0.4 vs 1.4 +/- 0.2 mU/l; P = 0.01), whereas fT3 (2.7 +/- 0.5 vs 5.8 +/- 0.3 pmol/l; P = 0.0002) and fT4 concentrations (10.3 +/- 1.2 vs 15.4 + 0.8 pmol/l; P = 0.007) were low. Stimulated TSH concentrations did not significantly differ from normal controls. Reverse T3 concentration in patients with sleeping sickness were normal (2.2 +/- 0.3 vs 2.4 +/- 0.2 nmol/l; P = NS). During the course of treatment, baseline TSH, fT3 and fT4 concentrations slowly returned to normal and were indistinguishable from controls after cure. Plasma concentrations of TNF-alpha (16.0 +/- 4.1 vs 2.9 +/- 1.4 ng/l in controls; P = 0.003) and interleukin-6 (19.2 +/- 7.3 vs 1.3 +/- 0.2 ng/l; P = 0.0001), but not interleukin-1 beta (2.0 +/- 0.2 vs 0.9 +/- 0.2, ng/l P = NS), were elevated, when thyroid function impairment and disease activity were at their maximum, but gradually decreased into the normal range with therapy. We found a negative correlation between baseline cytokine concentrations and fT3 concentrations (TNF-alpha: r = -0.34, P = 0.003; IL-6: r = -0.43, P = 0.0001). CONCLUSIONS: We conclude that unmedicated sleeping sickness is associated with significant impairment of thyroid function, which is reversed with specific therapy. Elevated TSH concentrations and low fT3 and fT4 concentrations suggest primary hypothyroidism in patients with sleeping sickness. However, an additional pituitary and/or hypothalamic component cannot be excluded. This impairment may be due to the elevated plasma cytokine concentrations found in these patients or may be the result of parasitic thyroiditis.

Adolescent↗
PubMedDate not supplied

Serum concentrations of somatomedins and growth hormone in relation to bone metabolism in acromegaly and thyroid dysfunction.

Many hormones are involved in the complex process of formation and resorption of bone. However, only somatomedin is found to directly stimulate cell replication and collagen synthesis in bone. This study was undertaken to examine a possible regulatory role of somatomedin in mediating the effects of growth hormone and thyroid hormones on bone metabolism. Bone metabolism and concentrations of somatomedins and growth hormones were studied in 17 acromegalic, 15 thyrotoxic and 14 hypothyroid patients, before and during treatment. During treatment of acromegalic and thyrotoxic patients parameters of bone turnover, both formation and resorption, decreased parallel to the decrease in concentration of somatomedin. During treatment of hypothyroid patients parameters of bone turnover increased. A positive correlation was found in acromegalic patients between changes in somatomedins and parameters of bone resorption (R = 0.82, P less than 0.01) as well as bone formation (R = 0.63, P less than 0.05) and in thyrotoxic patients between changes in somatomedin and bone resorption (R = 0.87, P less than 0.05). These data suggest that somatomedin may indeed play a role in the regulation of bone turnover. In addition, secondary effects on growth hormone concentrations were observed.

Acromegaly↗
PubMed1988

Occult thyroid dysfunction in patients with refractory depression.

Assessment of metabolic rate was useful in evaluating refractory depression in six of 15 women. Five of the six had normal levels of T3 and T4; however, each had an elevated thyrotropin-stimulating hormone level or a low metabolic rate. The depressions responded to medication with thyroid hormone.

Adult↗
PubMedDate not supplied

[Thyroid dysfunction and disorders in deamination of nitrogenous compounds in experimental atherosclerosis].

A decrease in monoamine deamination with simultaneous appearance of cadaverine deaminating activity in the mitochondrial fractions of the rabbit liver, brain and heart was more noticeable under conditions of hypothyroidism combined with hypercholesterolemia developing in the presence of normal function of the thyroid. A decrease in monoamine deamination, the appearance of cadaverine deaminating activity and a significant increase in AMP deamination were observed in the mitochondrial fraction of the rabbit heart muscle under conditions of hyperthyroidism.

Adenosine Monophosphate↗
PubMedDate not supplied

CD5 B cells in autoimmune and non immune-mediated thyroid dysfunctions.

In a previous study we demonstrated a significant increase of CD5+ B subset in patients with Graves' disease (GD) compared with normal controls. The aim of this study was to compare the percentage of CD5+ B and CD5- B cells in GD with that in different forms of autoimmune and non immune-mediated thyroid diseases. Seventy-two patients were studied: 28 patients with GD, 20 with silent thyroiditis (ST), 12 with Hashimoto's disease (HD), and 12 subjects affected by hyperthyroidism due to toxic adenoma (TA). Eleven out of 28 patients with GD were also evaluated after six months of methimazole treatment. The study was performed by cytometric analysis. In GD the percentage and the absolute number of CD5+ B cells were significantly increased compared with normal controls (42.5 +/- 18.2% versus 19 +/- 6.3%, p < 0.0001; 142 +/- 153.3/cmm versus 46.9 +/- 22/cmm, p < 0.003, respectively. CD5+ B cells tended to normalise after six months of treatment. In ST the percentage of CD5+ B cells was increased (28.6 +/- 10.2%); conversely the absolute number was in the normal range. Patients affected by HD did not show any significant modification in B cells and their subsets in comparison with controls. In TA, CD5+ B were 7.6 /- 4.4% and 14.3 /- 10.9/cmm. Our results demonstrated a marked increase in both percentage and absolute number of CD5+ cells, only in active GD. The expansion of CD5+ B cells could play a role in the immune imbalance present in this disease.

Adenoma↗