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PubMed1987

Toxic multinodular goiter: a variant of autoimmune hyperthyroidism.

The aim of this study was to examine whether at least a subgroup of patients with toxic multinodular goiter may have autoimmune thyroid disease. Thyroid-stimulating immunoglobulin (TSI) activity, measured by a sensitive bioassay employing cultured human thyroid cells, was determined in patients with toxic multinodular goiter and other thyroid disorders. All patients with active Graves' disease (n = 47) had detectable serum TSI activity, whereas TSI was undetectable in patients with thyroid disease not believed to be of autoimmune origin: toxic adenoma (n = 13), cold nodule (n = 5), and nontoxic goiter (n = 19), with a single exception in the latter group. Toxic multinodular goiter (n = 26) was diagnosed based on clinical and laboratory evidence of hyperthyroidism associated with a multinodular goiter on palpation and scintiscan. The toxic multinodular goiter group was then subclassified according to scintiscan pattern (type A, diffuse but uneven distribution of technetium uptake; type B, multiple discrete nodules of varying size and function). All but 1 of the 11 TSI-positive toxic multinodular goiter patients had a type A scintiscan pattern. The patients with the type A scintiscan pattern were younger and more often had elevated antithyroid antibody titers, ophthalmopathy, and concurrent development of goiter and hyperthyroidism (rather than long-standing goiter preceding hyperthyroidism) compared to the type B patients. Thus, a subgroup of patients with clinically defined toxic multinodular goiter (type A) probably have autoimmune hyperthyroidism (a variant of Graves' disease), while in another subgroup (type B) hyperthyroidism is not related to an autoimmune etiology (a variant of toxic adenoma).

Adenoma↗
PubMed1993

Thyroid histology of hyperthyroid Graves' disease with undetectable thyrotropin receptor antibodies.

To determine the histological characteristics of hyperthyroid Graves' disease with undetectable TSH receptor antibodies (TRAb), we examined the thyroid histological findings of patients with hyperthyroidism who were referred for subtotal thyroidectomy and who lacked circulatory TRAb. Four patients had undetectable TRAb (6.4 +/- 4.2%) before treatment (group A). Their pathological and clinical findings were compared with those of four patients who had hyperthyroid Graves' disease with detectable TRAb (83.8 +/- 8.3%) before treatment (group B). The groups were matched for sex, age, duration of antithyroidal drug therapy, anti-Tg antibody, and antimicrosomal antibody levels. All patients were in a euthyroid state just before operation. Papillate hyperplastic epithelia in group A were significantly less severe than in group B. Enlarged colloids were not observed in two of the four patients in group A but were observed in all four patients in group B. Moderate or marked lymphocytic infiltrations were observed in all patients in group A but were virtually absent in group B. Based on these results, it is probable that hyperthyroid Graves' disease with undetectable TRAb titers represents an early stage or subtype of usual hyperthyroid Graves' disease in which there is marked or moderate lymphocytic infiltration.

Adolescent↗
PubMed2000

Age and gender predict the outcome of treatment for Graves' hyperthyroidism.

The response to treatment in Graves' hyperthyroidism is unpredictable, and factors postulated to predict outcome have not generally proved clinically useful or been widely adopted in clinical practice. We audited outcome in 536 patients with Graves' hyperthyroidism presenting consecutively to determine whether simple clinical features predict disease presentation and response to treatment. At presentation males had slightly more severe biochemical hyperthyroidism [free T4: males, 64.3 +/- 3.0 pmol/L (mean +/- SE); females, 61.3 +/- 1.7 (P = 0.45); free T3: males, 24.3 +/- 1.5 pmol/L; females, 21.0 +/- 0.6, (P = 0.04)]. Patients less than 40 yr at diagnosis had more severe hyperthyroidism than patients more than 40 yr old [free T4: <40 yr, 64.3 +/- 2.0; >40 yr, 56.7 +/- 2.3 (P = 0.02); free T3: <40 yr, 22.8 +/- 0.8; >40 yr, 19.0 +/- 0.9 (P = 0.003)]. Males had a lower remission rate than females after a course of antithyroid medication [19.6% vs. 40%; odds ratio, 0.37; 95% confidence interval (CI), 0.17-0.79; P < 0.01]. Similarly, patients aged less than 40 yr had a lower remission rate than older patients (32.6% vs. 47.8%; odds ratio, 0.53; 95% CI, 0.32-0.87; P = 0.01). One dose of radioiodine cured hyperthyroidism in fewer males than females (47% vs. 74%; P < 0.0001). Logistic regression analysis demonstrated male sex (odds ratio, 2.80; 95% CI, 1.31-5.98; P = 0.008), serum free T4 concentration at diagnosis (odds ratio, 1.02; 95% CI, 1.0-1.04; P = 0.01), and dose of radioiodine administered (odds ratio, 0.99; 95% CI, 0.99-1.00; P = 0.001) were contributing factors associated with failure to respond to a single dose of radioiodine. As males and younger patients are more likely to fail to respond to medical treatment, and male patients are likewise less likely to respond to a single dose of radioiodine, we suggest that those groups with low remission rates should be offered definitive treatment with radioiodine or surgery soon after presentation and that the value of higher initial doses of radioiodine in males be evaluated.

Adolescent↗
PubMed2000

Cloning and characterization of the novel thyroid and eye muscle shared protein G2s: autoantibodies against G2s are closely associated with ophthalmopathy in patients with Graves' hyperthyroidism.

Serum autoantibodies against eye muscle antigens are closely linked with thyroid-associated ophthalmopathy (TAO), although their significance is unclear. The two antigens that are most often recognized are eye muscle membrane proteins with molecular masses of 55 and 64 kDa, as determined from immunoblotting with crude human or porcine eye muscle membranes. We cloned a fragment of the 55-kDa protein by screening an eye muscle expression library with affinity-purified anti-55 kDa protein antibody prepared from a TAO patient's serum. A complementary DNA (cDNA) encoding a novel protein, which we have called G2s, was sequenced on both strands, and its size was 411 bp. The open reading frame of G2s corresponded to a 121-amino acid peptide with a size of 1.4 kb. Using the rapid amplification of 5'-cDNA ends technique we were able to clone an additional 0.3 kb of the protein. G2s did not share significant homologies with any other entered protein in computer databases and had one putative transmembrane domain. Using the 1.4 kb cDNA as probe in Northern blotting of a panel of messenger ribonucleic acids prepared from human tissues, the parent protein was shown to correspond to a large molecule of about 5.8 kb with a calculated molecular mass of approximately 220 kDa, consistent with earlier immunoblot studies performed in the absence of reducing agents. G2s was strongly expressed in eye muscle, thyroid, and other skeletal muscle and to a lesser extent in pancreas, liver, lung, and heart muscle, but not in kidney or orbital fibroblasts. We tested sera from patients with Graves' hyperthyroidism with and without ophthalmopathy and from control patients and subjects for antibodies against a G2s fusion protein by immunoblotting and enzyme-linked immunosorbent assay. In immunoblotting, antibodies reactive with G2s were identified in 70% of patients with TAO of less than 3 yr duration, 53% with TAO of more than 3 yr duration, 36% with Graves' hyperthyroidism without evident ophthalmopathy, 17% with Hashimoto's thyroiditis, 3% with type 1 diabetes, 23% with nonimmunological thyroid disorders, and 16% of normal subjects. The prevalences, compared to normal values, were significant for the two groups of patients with TAO, but not for the other groups. Tests were positive in 54% of patients with active TAO, 33% with chronic ophthalmopathy, 36% with Graves' hyperthyroidism, 54% with Hashimoto's thyroiditis, 23% with type 1 diabetes, and in 11% of normal subjects using enzyme-linked immunosorbent assay. The antibodies predicted the development of the ocular myopathy subtype of TAO in six of seven patients and the congestive ophthalmopathy subtype in seven of eight patients, respectively, with Graves' hyperthyroidism studied prospectively during and after antithyroid drug therapy. Antibodies reactive with G2s may be early markers of ophthalmopathy in patients with Graves' hyperthyroidism. Because G2s is expressed in both thyroid and eye muscle, immunoreactivity against a shared epitope in the two tissues may explain the well known link between thyroid autoimmunity and ophthalmopathy.

Adult↗
PubMed2000

An elevation of serum immunoglobulin E provides a new aspect of hyperthyroid Graves' disease.

In hyperthyroid Graves' disease, short-term methimazole is sufficient to induce lasting remission in some patients, but even long-term treatment fails to do so in others. We have evaluated the role of autoimmune abnormalities in the helper T cell type 2 (TH2)-interleukin-13 (IL-13)-TSH receptor system in maintaining hyperthyroidism by comparing IgE levels in patients with various thyroid diseases. One hundred and ninety-three patients with hyperthyroid Graves' disease were treated with methimazole, and blood samples were obtained to measure serum levels of T4, T3, TSH, thyroglobulin, antimicrosomal antibody, TSH binding inhibitory Ig (TBII), thyroid-stimulating antibody, thyroid stimulation-blocking antibody, IgE, interferon-gamma, IL-4, and IL-13. Elevation of serum IgE (> or = 170 U/mL) was found in 35.5% of patients with hyperthyroid Graves' disease, and serum levels of T4, T:1, antimicrosomal antibody, and TBII were significantly greater in patients with IgE elevation than in those with normal serum IgE. During methimazole treatment, there was a parallel decrease in the serum T4 concentration in the presence or absence of an IgE elevation. However, there was a significantly smaller decrease in TBII in patients with elevated IgE than in those with normal IgE. As a result, the remission rate was significantly greater in patients with normal IgE than in those with IgE elevation. Serum levels of IL-13 were elevated in 64.7% of patients with IgE elevation in the absence of detectable TH1 marker, interferon-gamma. These findings suggest that in one third of patients with hyperthyroid Graves' disease, TH2 cells are stimulated and secrete excess amounts of IL-13, which subsequently stimulates B cells to synthesize more TSH receptor antibody and IgE, so that during methimazole treatment TBII decreases less in patients with IgE elevation, producing a lower remission rate.

Adolescent↗
PubMed2003

Bone and calcium metabolism in subclinical autoimmune hyperthyroidism and hypothyroidism.

Bone turnover is reported to increase in favour of resorption in overt hyperthyroidism and the rate of resorption is associated with the levels of thyroid hormones. Hypothyroidism, on the other hand, was shown to cause no disturbance of calcium kinetics and found to associate lower trabecular resorption surfaces and increased bone cortical thickness. Similar studies are very rare in subclinical thyroid disorders and consequently we aimed to examine calcium and bone metabolism in subclinical thyroid disorders. Thirteen patients with subclinical hyperthyroidism secondary to untreated Graves' disease, 20 patients with subclinical hypothyroidism and 10 healthy subjects participated in this survey. Briefly calcium, phosphorus, and creatinine (Cre), urinary deoxypyridinoline (U-DPD) and serum osteocalcin (OC) were measured as biochemical markers for calcium metabolism. Concerning serum Ca and phosphorus levels, there were no differences between three of the groups, but urinary Ca excretion was higher in subclinical hyperthyroid patients compared to control and hypothyroid subjects. Hypothyroid patients had similar U-DPD levels with control subjects (p = 0.218). Serum OC and U-DPD were higher in subclinical hyperthyroid compared to control subjects (p<0.001 and p<0.001 respectively). We demonstrated a higher bone turnover and greater calcium excretion in subclinical hyperthyroid patients. Additionally, we found that subclinical hypothyroidism is not associated with disturbed calcium metabolism. As persistent increase in bone turnover is responsible for accelerated bone loss, patients with Graves' disease may have increased risk for osteoporosis.

Adult↗
PubMed2005

Graves' hyperthyroidism showing transient hypothyroidism during interferon therapy for chronic hepatitis type C.

We report a patient with Graves' disease in whom thyroid function was changed from initial hyperthyroidism to transient hypothyroidism and back to hyperthyroidism during interferon (IFN) therapy. A 43-year-old man was admitted to our hospital to receive IFN treatment for chronic active hepatitis (type C) in June 1998. His thyroid function was normal and testing for thyroid gland antibodies (TSH binding inhibitor immunoglobulins; TBII, anti-thyroglobulin antibodies; TgAb and anti-thyroid peroxidase antibodies; TPOAb) was negative before IFN therapy. The patient had neither history of thyroid disease nor any particular family history. He developed hyperthyroidism four months after its initiation of IFN therapy. When he was hyperthyroid, TBII, the activity of thyroid-stimulating antibodies (TSAb) and thyroid stimulation-blocking antibodies (TSBAb) were 40.2% (normal range, -15 approximately +15.0%), 1201% (normal range, <or=180%) and 52.0% (normal range, <or=45.6%), respectively. Thyroid 99mTc(technetium)-uptake ratio (Tc-UTR) was 1.07% (normal range, 0.5-3.0%). He transiently developed hypothyroidism in December 1998 and recurrent hyperthyroidism in February 1999. When he was hypothyroid, TBII, TSAb and TSBAb were 74.3%, 769% and 95.9%, respectively. To investigate the mechanism of his fluctuating thyroid status, we serially assessed the serum levels of cytokines (TNF-alpha, IFN-gamma, IL-1beta, IL-2, IL-4) and the soluble form of ICAM-1 (sICAM-1) as well as the activities of two types of TSH receptor antibodies (TRAb), TSAb and TSBAb, before and after IFN therapy. There were no characteristic changes of cytokines or sICAM-1 during the follow-up period. The transient hypothyroid state may be explained by two possible mechanisms: one may be due to the shift in the balance between the stimulating and blocking types of TRAb, and the other may be due to the complication of destructive thyroiditis that developed during IFN therapy.

Adult↗
PubMed1989

Neutrophil chemotaxis, random migration, and adherence in patients with hyperthyroidism.

We have examined neutrophil adherence, chemotactic activity, and random migration in 35 hyperthyroid patients with Graves' disease and 106 normal volunteers. No statistically significant differences were found between granulocyte adherence of 17 hyperthyroid subjects (67 +/- 15.6%) and 81 healthy volunteers (63.1 +/- 17%). In 3 thyrotoxic patients, impaired neutrophil adherence was found, which resolved when thyroid function returned to normal. The neutrophil chemotactic activity of 32 normal controls was 107.5 +/- 21.4 cells, and the random migration 36 +/- 15.5 cells. No statistically significant difference was demonstrated in 13 hyperthyroid patients who had a neutrophil chemotactic activity of 102 +/- 14.6 cells and a random migration of 31.2 +/- 13.2 cells. Defective chemotactic activity and random migration was found in 2 patients. Neutrophil functions returned to normal in one of the two subjects who were re-evaluated when thyroid function recovered. In summary, 14% of hyperthyroid patients had impaired leukocyte functions. However, severe pyogenic infections are quite rare in hyperthyroid patients, indicating that the observed alterations in function of phagocytic cells are not clinically important.

Cell Migration Inhibition↗
PubMed1992

Thyroid hypoechogenic pattern at ultrasonography as a tool for predicting recurrence of hyperthyroidism after medical treatment in patients with Graves' disease.

An abnormal thyroid echographic pattern characterized by a diffuse low echogenicity has been described in Hashimoto's thyroiditis and Graves' disease. The aim of the present work was to study the relationship between thyroid hypoechogenicity and the outcome of treatment for hyperthyroidism with antithyroid drugs in patients with Graves' disease. The study group included 105 patients who underwent a course of methimazole treatment. Thyroid ultrasonography was carried out at diagnosis, and autoantibodies to thyrotropin receptor (TR-ab) were measured at the end of treatment. During the follow-up after methimazole treatment, 87/105 (83%) patients had relapse of hyperthyroidism and 18/105 (17%) were in remission. Recurrence of hyperthyroidism occurred in 71/76 (93%) patients with thyroid hypoechogenicity and in 16/29 (55%) of those with normal thyroid echogenicity (chi 2 = 19.0; p less than 0.0001). Positive TR-ab values at the end of methimazole treatment were found in 59/76 (78%) patients with thyroid hypoechogenicity and in 12/29 (41%) patients with normal thyroid echogenicity (chi 2 = 10.9; p less than 0.0001). Sixty-five/87 (74%) patients with relapse of hyperthyroidism and 6/18 (33%) of those who remained euthyroid were TR-ab-positive at the end of methimazole treatment (chi 2 = 9.8; p less than 0.002). The finding of thyroid hypoechogenicity at diagnosis had higher specificity (0.81) and sensitivity (0.72) with respect to TR-ab positivity at the end of methimazole treatment (0.74 and 0.66 respectively) for the prediction of relapse of hyperthyroidism. Therefore, the evaluation of thyroid echographic pattern can be considered a useful prognostic tool in patients with Graves' disease.

Adult↗
PubMedDate not supplied

Hyperthyroidism during lithium therapy for depression.

OBJECTIVE: To report three cases of hyperthyroidism encountered within a period of 32 months in patients receiving lithium therapy for depression. METHODS: Three detailed case reports are presented, and the related literature is discussed. RESULTS: Although hypothyroidism during lithium therapy is well recognized and documented, appearance of cases of hyperthyroidism during lithium therapy is considered uncommon. The antithyroid effect of lithium through inhibition of generation of cyclic adenosine monophosphate tends to mask the underlying hyperthyroidism. Nevertheless, during a 32-month period, three cases of hyperthyroidism were encountered in patients who had received lithium treatment (900 to 1,200 mg/day) for 7 months to 17 years. These patients had symptoms of heat intolerance, palpitations, and tremor, and they were subsequently treated successfully with radioactive iodine. CONCLUSION: Most likely, cases of hyperthyroidism that occur during lithium therapy may be under-diagnosed, underreported, or both.

Journal Article↗
PubMed2002

Nerve growth factor and norepinephrine concentrations in weight-bearing and non-weight-bearing bones of euthyroid and hyperthyroid rats.

UNLABELLED: Thyroid hormone, nerve growth factor (NGF) and norepinephrine (NE) and weight-bearing affect bone metabolism, yet interactions between these factors and osseous tissue have not been investigated. Therefore, the aims of the study were to measure NGF and NE concentrations in weight-bearing and non-weight-bearing bones from euthyroid (control) and hyperthyroid (HT) rats. Hyperthyroidism was induced by oral intake of triiodothyronine (90 mg/kg/day) for 21 days. Histomorphometry on distal femurs verified significant trabecular bone loss in HT rats compared to euthyroid animals. NGF concentrations were assayed via ELISA, whilst NE concentrations were measured via HPLC and ECD. In euthyroid rats: (i) the concentration of NGF in ribs (914 ng/g) was almost 3-fold greater than in femurs (326 ng/g wet weight of tissue) (ii) the concentrations of NE in ribs (74.7 ng/g) and calvaria (87.4 ng/g) were 2.5-3.5-fold greater than either femurs (24.0 ng/g) or tibiae (30.5 ng/g) and (iii) NE concentrations were comparable between ribs (74.7 ng/g) and calvaria (87.4 ng/g) and similar between tibiae (30.5 ng/g) and femurs (24.0 ng/g). In HT rats: (i) the concentration of NGF in ribs (1802 ng/g) was 4-fold greater than in femurs (402 ng/g) (ii) NE concentrations in ribs (23.3 ng/g) and calvaria (13.6 ng/g) were 4.5-fold and 2.6-fold greater respectively than in tibiae (5.2 ng/g), while ribs had almost a 2-fold higher concentration of NE than calvaria. In HT rats compared to euthyroid animals: (i) NGF concentrations almost doubled in ribs but there was little change in the NGF concentration in femurs (ii) there was a reduction in NE concentrations in calvaria by 84%, in ribs by 69% in tibiae by 83% and 55% in femur (NS). CONCLUSIONS: (i) Non-weight-bearing is associated with higher concentrations of NGF and NE than weight-bearing in bones in euthyroid and HT rats; (ii) Hyperthyroidism exerts opposite effects on NGF and NE in bone and (iii) Hyperthyroidism interacts with weight-bearing to determine NGF and NE concentrations in bone. Therefore, the influence of thyroid hormone on NGF and NE in bone may need to be taken into account when considering the action of thyroid hormone on bone in either euthyroid or hyperthyroid states.

Journal Article↗
PubMed2005

Clinical presentation and treatment of hyperthyroidism associated with thyroid cancer.

OBJECTIVE: Hyperthyroidism apparently does not protect the patients from thyroid cancer as believed before. In contrast, hyperthyroidism with concurrent thyroid cancer can be diagnosed after pathological examination of unsuspect nodules. The aim of this study was to evaluate the coexistence of hyperthyroidism and thyroid carcinoma and to discuss the advantages of total thyroidectomy in such cases. METHODS: Between January 2002 and October 2004, 120 hyperthyroid patients underwent surgical treatment in our clinic. All patients with hyperthyroidism in this study underwent fine-needle aspiration biopsy and cytologic examination. Frozen section evaluation was performed in all of these patients during the operation. RESULTS: Among these patients 10 had concurrent thyroid cancer. Only one of these patients was examined by fine needle aspiration biopsy prior to operation, while the rest of malignancies was diagnosed from unsuspect nodules. CONCLUSIONS: The selection of appropriate operation procedure appears very important to find out and treat concurrent thyroid cancers. We diagnosed 90 % of thyroid cancers incidentally. If there are no technical difficulties, we prefer total thyroidectomy for the patients with toxic multinodular goiter and Graves' disease with nodules.

Adult↗
PubMed1979

Iodine-131: optimal therapy for hyperthyroidism in children and adolescents?

To assess the medium- to long-term effects of I-131 therapy of hyperthyroidism in children and adolescents, we studied 51 patients (age range 6--18; boys, 43 girls) treated with I-131 for Graves' disease with hyperthyroidism at the University of Michigan Medical Center (1951--1972). Patients received total doses ranging from 3 to 81.6 mCi. The mean followup period was 14.6 +/- 7.9 yr. Hyperthyroidism was effectively treated in 49 within 1 to 12 mo. One patient failed to respond to three treatment doses, and hyperthyroidism recurred in two patients: 2 and 11 yr after initial therapy. Of these three patients, two were treated by thyroidectomy and one was retreated successfully with I-131. There were no cases of thyroid cancer, other malignancies or leukemia. The patients' reproductive histories and the health of their offspring were as in the general population. At the time of study, the prevalence of hypothyroidism was 92%, with no recurrent goiters or thyroid nodules. Iodine-131 is found to be safe and effective treatment of hyperthyroidism in children and adolescents and should be the preferred mode of therapy.

Adolescent↗
PubMed1998

Radioiodine treatment outcomes in thyroid glands previously irradiated for Graves' hyperthyroidism.

UNLABELLED: Persistent or recurrent Graves' hyperthyroidism after an initial treatment dose of radioactive iodine (RAI) is not uncommon and usually necessitates additional administrations. The radiation sensitivity of the previously irradiated thyroid gland is unknown but is of importance in selecting the retreatment dose. METHODS: A retrospective analysis of patients receiving RAI for Graves' hyperthyroidism was undertaken. A first treatment dose was given to 1076 patients, and 168 of these patients subsequently required a second dose for persistent or recurrent hyperthyroidism (interval between RAI treatments, 8.5 +/- 17.1 mo). RESULTS: Paired comparisons for retreated patients showed similar RAI doses (291 +/- 95 MBq and 283 +/- 129 MBq; p = ns) and treatment intensities (3.26 +/- 1.87 MBq g(-1) and 3.48 +/- 1.88 MBq g(-1); p = ns) for first and second treatments. Hypothyroidism occurred significantly earlier and more frequently after the first RAI dose (p = 0.002), but there was no difference for persistent or recurrent hyperthyroid events (p = 0.14). Multivariate regression established that the RAI treatment number (first or second) was a significant independent determinant of hypothyroid (p = 0.008) and combined (p = 0.001) events, whereas RAI dose and dose intensity were not. CONCLUSION: We conclude that previous RAI treatment failure does not lessen the chance of successfully eradicating Graves' hyperthyroidism with additional RAI treatment. Furthermore, the previously irradiated thyroid gland may be less susceptible to early hypothyroidism than the RAI-naive thyroid gland.

Graves Disease↗
PubMed2003

Pregnancy with hyperthyroidism.

OBJECTIVE: The purpose of the study was (i) to diagnose the pregnant women suffering from hyperthyroidism by differentiating their symptoms from normal pregnancy and confirming this disease biochemically and (ii) to treat such patients medically to achieve euthyroid state of the mother while monitoring the developing fetus for better obstetrical outcome. DESIGN: A descriptive comparative study. PLACE AND DURATION OF STUDY: This was a hospital-based study carried out on the patients presented at Federal Government Services Hospital, Islamabad from 1997 to 1998. SUBJECTS AND METHODS: A total of 30 patients in reproductive age group, suffering from hyperthyroidism with pregnancy, were studied. Patients were recruited in the study in their first trimester having no associated medical problems. The patients were divided into two groups. Group I patients were diagnosed for hyperthyroidism for the first time during pregnancy by biochemical methods. These patients were treated medically. After treatment effects on their previous obstetrical complications, general health and fetal well-being were monitored. The group II patients were already under medical treatment and served as control. Their thyroid status in all trimesters, types of medicine, dose adjustment and maternal and fetal well-being were compared with the patients of group I. The patients of both the groups were treated medically with beta blockers and anti-thyroid drugs mainly carbimazole. For fetal monitoring, ultrasonography (USG) and cardiotocography (CTG) were carried out. RESULTS: The most common type of hyperthyroidism, in patients of both the groups, was toxic nodular goiter that affected 70% of the patients. The most common previous obstetrical complication in patients of both the groups was abortion (85.7%), followed by premature labour (7%). Carbimazole was the drug of choice given to 70% and 60% patients of group I and group II respectively. Having achieved euthyroid state, dose reduction was possible in 65% patients of group I and 83% patients of group II. CONCLUSION: Euthyroid state in mothers, by the time of delivery, can be easily achieved with antithyroid drugs and b blockers and the aim to improve obstetrical outcome can be successfully achieved. Hence obstetrical complications, which otherwise affect 93.33% of such patients, can easily be avoided through medical treatment.

Adult↗
PubMed1982

Hyperthyroidism caused by inappropriate thyrotropin hypersecretion: studies in patients with selective pituitary resistance to thyroid hormone.

We have identified the condition of thyrotropin (thyroid-stimulating hormone [TSH])-induced hyperthyroidism secondary to selective pituitary insensitivity to thyroid hormone in three patients. Each patient was clinically hyperthyroid, with elevated serum levels of thyroxine (T4) and triiodothyronine (T3) and detectable levels of serum TSH before therapy. After therapy each patient had notably elevated TSH levels at a time that peripheral levels of thyroid hormones were in the hyperthyroid range. Before and after therapy, serum levels of TSH were suppressed by therapy with liothyronine sodium and were stimulated by protirelin (thyrotropin-releasing hormone) both before and after liothyronine and dexamethasone treatment. Dexamethasone therapy decreased the levels of TSH, protirelin-stimulated TSH, and circulating T4 and T3. Serum levels of glycoprotein alpha-subunit were 0.6 to 2.4 ng/ml, values considerably lower than found in patients with TSH-secreting pituitary tumors. We suggest that the frequency of TSH-induced hyperthyroidism secondary to pituitary insensitivity to thyroid hormone may be higher than presently indicated in the medical literature.

Adolescent↗
PubMed1983

Serum angiotensin-converting enzyme. Alterations in hyperthyroidism, hypothyroidism, and subacute thyroiditis.

Angiotensin-converting enzyme (ACE) activity was measured in the serum samples of 247 patients with varying thyroid states. In 60 hyperthyroid patients, the mean (+/- SD) ACE level of 29.5 +/- 9.7 units/mL was higher than in all other groups. The serum ACE level was 17.0 +/- 5.1 units/mL in 129 euthyroid subjects and differed from the level of 13.9 +/- 5.1 units/mL observed in 34 hypothyroid patients. Twenty-four patients receiving exogenous thyroid hormone had elevated serum thyroxine values. Their mean serum triiodothyronine level was in the normal range, and the mean ACE level did not differ from the euthyroid mean. The mean serum ACE level fell from 30.8 to 17.4 units/mL in 35 hyperthyroid patients studied before and after therapy. In 12 hypothyroid subjects, the mean serum ACE level rose from 11.6 to 15.8 units/mL after thyroid hormone replacement. In eight of ten patients with transient hyperthyroidism (subacute thyroiditis or painless thyrotoxic thyroiditis), their highest ACE levels were observed in the hyperthyroid or transition phase and fell progressively with the lowest values being recorded during the hypothyroid or early recovery phases. Thus, ACE activity may respond to thyroid hormone, and interpretation of serum ACE levels may require knowledge of the patient's thyroid status. Serum ACE may be useful as a probe for exploring peripheral thyroid hormone action.

Adolescent↗
PubMed2005

Thyroid function and mortality in patients treated for hyperthyroidism.

CONTEXT: Hyperthyroidism has been reported to cause excess all-cause and circulatory mortality. Whether this can be reversed is unknown, as is the influence of mild persisting thyroid dysfunction and treatment-induced hypothyroidism. OBJECTIVES: To determine whether radioiodine treatment is associated with increased mortality and to determine the influences of mild thyroid dysfunction and the development of overt hypothyroidism treated with thyroxine (T(4)). DESIGN, SETTING, AND PARTICIPANTS: A population-based study of 2668 individuals aged 40 years or older treated for overt hyperthyroidism with radioiodine in the West Midlands region of England from 1984-2002. MAIN OUTCOME MEASURES: Cause of death compared with age- and period-specific mortality in England and Wales and assessment of the influence of T(4) therapy for radioiodine-induced hypothyroidism and subclinical thyroid dysfunction on mortality. RESULTS: In 15,968 person-years of follow-up, 554 died vs 487 expected deaths (standardized mortality ratio [SMR], 1.14; 95% confidence interval [CI], 1.04-1.24, P=.002). Increased risks of all-cause and circulatory deaths vs age- and period-specific mortality were observed in follow-up in those not requiring, or prior to, T(4) therapy. These increased risks were not observed during follow-up on T(4) therapy (circulatory disease SMR prior to T(4), 1.33; 95% CI, 1.14-1.53 vs SMR, 0.91; 95% CI, 0.70-1.17 during T(4)). Patients receiving T(4) had decreased risk of mortality vs risk in the period not requiring, or prior to, T(4) therapy (all-cause mortality hazard ratio [HR], 0.65; 95% CI, 0.54-0.79; circulatory mortality HR, 0.65; 95% CI, 0.48-0.87). Increased all-cause mortality vs the background population was observed in the period prior to T(4) therapy in follow-up associated with low, normal, and high serum thyrotropin. The SMR for ischemic heart disease increased slightly when analyzed by serum thyrotropin, high serum thyrotropin being the highest SMR (low thyrotropin SMR, 1.06; 95% CI, 0.75-1.45; normal thyrotropin SMR, 1.17; 95% CI, 0.76-1.71; high thyrotropin SMR, 1.48; 95% CI, 0.86-2.37). Comparison within the cohort showed that mild hypothyroidism prior to T(4) therapy was associated with increased risk of mortality from ischemic heart disease vs biochemical euthyroidism (HR, 2.08; 95% CI, 1.04-4.19). CONCLUSIONS: Patients treated with radioiodine for hyperthyroidism had increased mortality vs age- and period-specific mortality in England and Wales, a finding no longer evident during T(4) therapy. This supports treating hyperthyroidism with doses of radioiodine sufficient to induce overt hypothyroidism. The association within the cohort of mortality from ischemic heart disease with subclinical hypothyroidism suggests T(4) replacement should be considered should this biochemical abnormality develop after radioiodine therapy.

Adult↗