Over-the-counter-drug-induced thyroid disorders.

OBJECTIVE: Excessive iodine ingestion may cause thyroid dysfunction. In this case series, we report four patients who developed significant thyroid dysfunction after ingesting over-the-counter (OTC) drugs containing large concentrations of iodine. METHODS: Four patients from a tertiary medical center are reported. RESULTS: Case 1 involved acute exacerbation of thyrotoxicosis induced by taking OTC Tri-iodine™ in a 35-year-old woman while still on methimazole therapy. Case 2 involved thyroid-extract-induced thyrotoxicosis following ingestion of Thyromine™, and was confirmed by laboratory studies and ¹³¹I thyroid uptake. Cases 3 and 4 involved severe, symptomatic hypothyroidism induced in 2 patients with underlying autoimmune thyroiditis (Hashimoto's disease) following ingestion of Iodoral™. In all cases, thyroid dysfunction resolved with appropriate management and discontinuation of the OTC drugs. CONCLUSION: These case reports demonstrate the significant risks associated with OTC preparations containing iodine in patients predisposed to thyroid dysfunction. There is no valid reason for taking high-dose OTC iodine supplements, which have been shown to cause harm and have no known benefit.

Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: a randomized, double-blind, crossover study.

CONTEXT: Patients previously treated with desiccated thyroid extract (DTE), when being switched to levothyroxine (L-T4), occasionally did not feel as well despite adequate dosing based on serum TSH levels. OBJECTIVE: Our objective was to investigate the effectiveness of DTE compared with L-T4 in hypothyroid patients. DESIGN AND SETTING: We conducted a randomized, double-blind, crossover study at a tertiary care center. PATIENTS: Patients (n = 70, age 18-65 years) diagnosed with primary hypothyroidism on a stable dose of L-T4 for 6 months were included in the study. INTERVENTION: Patients were randomized to either DTE or L-T4 for 16 weeks and then crossed over for the same duration. OUTCOME MEASURES: Biochemical and neurocognitive tests at baseline and at the end of each treatment period were evaluated. RESULTS: There were no differences in symptoms and neurocognitive measurements between the 2 therapies. Patients lost 3 lb on DTE treatment (172.9 ± 36.4 lb vs 175.7 ± 37.7 lb, P < .001). At the end of the study, 34 patients (48.6%) preferred DTE, 13 (18.6%) preferred L-T4, and 23 (32.9%) had no preference. In the subgroup analyses, those patients who preferred DTE lost 4 lb during the DTE treatment, and their subjective symptoms were significantly better while taking DTE as measured by the general health questionnaire-12 and thyroid symptom questionnaire (P < .001 for both). Five variables were predictors of preference for DTE. CONCLUSION: DTE therapy did not result in a significant improvement in quality of life; however, DTE caused modest weight loss and nearly half (48.6%) of the study patients expressed preference for DTE over L-T4. DTE therapy may be relevant for some hypothyroid patients.

Simultaneous occurrence of subacute thyroiditis and Graves' disease.

BACKGROUND: Rare cases of Graves' disease occurring years after subacute thyroiditis (SAT) have been reported. Here, we present the first known case of simultaneous occurrence of Graves' disease and SAT. PATIENT FINDINGS: A 41-year-old woman presented with 10 days of neck pain, dysphagia, and hyperthyroid symptoms. Neck pain had initially started at the base of the right anterior neck and gradually spread to her upper chest, the left side of her neck, and bilateral ears. Physical examination revealed a heart rate of 110 beats/minute and a diffusely enlarged tender thyroid gland without evidence of orbitopathy. There was a resting tremor of the fingers and brisk deep tendon reflexes. Laboratory values: thyrotropin<0.01 mcIU/mL (nL 0.39-5.33), free thyroxine 2.0 ng/dL (nL 0.59-1.60), free T3 6.6 pg/mL (nL 2.3-4.2), thyroglobulin 20.1 ng/mL (nL 2.0-35.0), thyroglobulin antibody 843 IU/mL (nL 0-80), thyroperoxidase antibody 130 IU/mL (nL 0-29), thyroid stimulating hormone receptor antibody 22.90 IU/L (nL<1.22), thyroid stimulating immunoglobulins 299 units (nL<140), erythrocyte sedimentation rate 120 mm/h (nL 0-20), and C-reactive protein 1.117 mg/dL (nL 0-0.5). Human leukocyte antigen (HLA) typing revealed DRB1, DR8, B35, B39, DQB1, DQ4, and DQ5. A thyroid ultrasound showed an enlarged heterogeneous gland with mild hypervascularity. Fine-needle aspiration (FNA) biopsies of both thyroid lobes revealed granulomatous thyroiditis. The thyroid scan showed a diffusely enlarged gland and heterogeneous trapping. There was a focal area of relatively increased radiotracer accumulation in the right upper pole. The 5-hour uptake ((123)I) was 6.6% (nL 4-15). The patient was symptomatically treated. Over the next several weeks, she developed hypothyroidism requiring levothyroxine treatment. SUMMARY: This case illustrates a rare simultaneous occurrence of Graves' disease and SAT. Previous case studies have shown that Graves' disease may develop months to years after an episode of SAT. A strong family history of autoimmune thyroid disorders was noted in this patient. Genetic predilection was also shown by HLA typing. CONCLUSION: Although the occurrence of SAT with Graves' disease may be coincidental, SAT-induced autoimmune alteration may promote the development of Graves' disease in susceptible patients. Genetically mediated mechanisms, as seen in this patient by HLA typing and a strong family history, may also be involved.

Multinodular goiter as the initial presentation of systemic sarcoidosis: limitation of fine-needle biopsy.

Sarcoidosis is a chronic systemic disease characterized by noncaseating granulomas. Thyroid involvement is rare, with a prevalence of 1-4% in large series of autopsied patients with systemic sarcoid. We report a case of a 65-year-old woman with a nontoxic multinodular goiter, dyspnea in the supine position, and rightward tracheal deviation as the initial presentation of systemic sarcoidosis. Fine-needle biopsy of the thyroid mass was consistent with benign adenomatoid goiter. A total thyroidectomy was performed because of compression symptoms. Histopathology revealed numerous diffuse noncaseating granulomata typical of thyroid sarcoidosis. Subsequent chest computed tomography showed extensive bulky mediastinal and hilar adenopathy and multiple small pulmonary nodules consistent with sarcoidosis. Transbronchial fine-needle biopsy also revealed noncaseating granulomas. The patient's supine dyspnea resolved quickly after total thyroidectomy. This case report illustrates that in patients with known sarcoidosis, careful thyroid examination is essential and supine dyspnea may be directly related to tracheal compression by a multinodular goiter rather than pulmonary sarcoidosis.

Management of coexisting thyrotropin/growth-hormone-secreting pituitary adenoma and papillary thyroid carcinoma: a therapeutic challenge.

BACKGROUND: A thyrotropin (TSH)-secreting pituitary adenoma coexisting with differentiated thyroid carcinoma is rare. There have been only four previously reported cases; three were treated with thyroidectomy followed by pituitary resection and one was treated with thyroidectomy alone. METHODS: We hereby report the fifth case, in which a patient presented with a TSH/growth-hormone-secreting pituitary macroadenoma coexisting with papillary thyroid carcinoma (PTC). RESULTS: She underwent biochemical testing, ophthalmologic examination, thyroid ultrasonography, Tc-99m-pertechnetate thyroid scan, whole-body positron emission tomography, (111)In-octreotide scan, thyroid fine-needle aspiration biopsy, octreotide treatment, total thyroidectomy, recombinant human TSH radioactive iodine remnant ablation, and continued treatment with octreotide and levothyroxine after thyroidectomy. She has remained asymptomatic for 24 months without biochemical or radiological evidence of pituitary hormone oversecretion, pituitary adenoma enlargement, and PTC recurrence. CONCLUSION: To our knowledge, this is the first case of a TSH/growth-hormone-secreting pituitary macroadenoma coexisting with PTC being successfully treated with octreotide and levothyroxine after thyroidectomy and recombinant human TSH-stimulated radioactive iodine remnant ablation.

Symptomatic hyponatremia in association with a low-iodine diet and levothyroxine withdrawal prior to I131 in patients with metastatic thyroid carcinoma.

BACKGROUND: Strategies to improve I131 uptake in thyroid carcinoma include levothyroxine (LT4) withdrawal or thyrotropin (TSH) administration along with a low-iodine diet. We report five patients with papillary or follicular thyroid carcinoma who developed symptomatic hyponatremia during LT4 withdrawal and low-iodine diet. RESULTS: Four patients had pulmonary and/or brain metastases. All had restricted iodine intakes during LT4 withdrawal. Presenting complaints included weakness, dizziness, fainting spells, lethargy, and/or nausea. Baseline serum sodium levels while on LT4 suppression were normal. During presentation all were hypothyroid and serum sodium ranged from 110 to 121 mmol/L (normal 135-148). Despite hyponatremia, the plasma renin activity and serum aldosterone levels were suppressed, indicating volume expansion. The hyponatremia responded to fluid restriction and normalized after LT4 replacement. Low sodium intake, inappropriate antidiuretic hormone secretion syndrome (SIADH)-like disorder secondary to hypothyroidism and/or lung or cerebral metastases may have contributed to hyponatremia. CONCLUSIONS: The development of hyponatremia during LT4 withdrawal and low-iodine diet in otherwise healthy patients with thyroid carcinoma is extremely rare. However, elderly patients with metastatic thyroid carcinoma need observation during LT4 withdrawal combined with a low-iodine diet and should receive instruction to take iodine-free sodium chloride. Free water restriction may be necessary in some patients.

Palpation thyroiditis causing new-onset atrial fibrillation.

OBJECTIVE: Surgery-induced thyroiditis can pose a significant clinical problem that is underappreciated. We present a case of new-onset atrial fibrillation as a consequence of palpation thyroiditis in a 70-year-old man who underwent radical right neck dissection for malignant melanoma and review the limited literature on this topic. DESIGN: Biochemical parameters including thyrotropin, free thyroxine, triiodothyronine, erythrocyte sedimentation rate, C-reactive protein, thyroglobulin, thyroid stimulating immunoglobulins, thyroid binding inhibitory immunoglobulins, thyroid peroxidase, thyroglobulin antibodies, and 24-hour urine iodine were measured. Thyroid ultrasound and technetium-99m pertechnetate scintigraphy with radioactive iodine 131 uptake were employed for diagnostic purposes. MAIN OUTCOME: Following right neck exploratory dissection, the patient developed hyperthyroidism and atrial fibrillation. Imaging studies were compatible with right lobar thyroiditis. Other etiologies of thyroiditis were excluded. Despite normalization of thyroid function after 2 weeks, atrial fibrillation persisted and required cardioversion. CONCLUSIONS: Manipulation of the thyroid gland during neck exploratory surgery can result in hyperthyroidism with atrial fibrillation as a consequence. To avoid this complication, careful attention should be paid during surgical procedures or other clinical situations in which the thyroid gland is manipulated.

Catecholamine-induced cardiomyopathy.

OBJECTIVE: To review the pathogenesis as well as the clinical and laboratory features of catecholamine-induced cardiomyopathy associated with pheochromocytoma and other disorders and discuss the various treatment options available. METHODS: Materials used for this article were identified through MEDLINE, PubMed, and Google Scholar searches of the relevant literature from 1955 to the present. RESULTS: Catecholamines and their oxidation products cause a direct toxic effect on the myocardium. Catecholamines also exert a receptor-mediated effect on the myocardium. Catecholamine-mediated myocardial stunning has been implicated in the pathogenesis of stress-induced cardiomyopathy. Biopsy of the myocardium in patients with pheochromocytoma or those with stress-induced cardiomyopathy shows similar pathologic findings. The clinical features in pheochromocytoma-related cardiomyopathy include hypertension, dilated or hypertrophic cardiomyopathy, pulmonary edema due to cardiogenic and noncardiogenic factors, cardiac arrhythmias, and even cardiac arrest. Stress-related cardiomyopathy such as takotsubo cardiomyopathy occurs primarily in postmenopausal women. These patients may present with clinical features suggestive of an acute myocardial infarction or a hemodynamically compromised state. The definitive management of cardiomyopathy associated with pheochromocytoma includes medical treatment with alpha-adrenergic blockade, possibly along with angiotensin converting enzyme blockers and beta1-adrenergic receptor blockers, followed by excision of the tumor. Stress-induced cardiomyopathy is usually self-limiting; patients may require support with nonadrenergic inotropes. CONCLUSION: Recognition of catecholamine-induced cardiomyopathy, especially in patients with pheochromocytoma, before surgical treatment is important to minimize morbidity and mortality.

Plasma glucagon levels suppressed by a glucose load in a man with incidental pancreatic glucagonoma.

OBJECTIVE: To describe a patient with a histologically proven pancreatic glucagonoma, noted incidentally during a follow-up visit for high aminotransferase levels, and to evaluate its autonomy with a standard 75-g oral glucose tolerance test. METHODS: We present the results of a 2-hour oral glucose tolerance test, with plasma glucagon and blood glucose levels measured every 30 minutes after an oral glucose load. In addition, we provide a brief review of the literature on the diagnosis and management of glucagonomas and the importance of long-term surveillance. RESULTS: In our patient, who had a 1-year history of impaired fasting glucose, plasma glucagon levels were persistently suppressed to within the normal range after oral glucose challenge. Octreotide scintigraphy revealed abnormal uptake in the pancreatic tail, and a 2.8-cm mass was removed at laparoscopic distal pancreatectomy. Immunohistochemical staining of the tumor tissue showed intense reactivity for glucagon. Plasma glucagon levels were reduced to <50 pg/mL postoperatively, and scintigraphic study at 4-month follow-up showed no residual uptake at the previous tumor site or elsewhere. CONCLUSION: Glucagon-secreting pancreatic tumors are extremely rare. A substantially elevated plasma level of glucagon is usually seen in patients with metastatic tumors. In the early stage of a glucagonoma, however, the plasma glucagon level may be only modestly elevated and may still be susceptible to normal negative feedback inhibition. We demonstrated plasma glucagon complete suppressibility after oral glucose challenge in a patient with a glucagonoma, the first such report in the literature.

Combined levothyroxine plus liothyronine compared with levothyroxine alone in primary hypothyroidism: a randomized controlled trial.

CONTEXT: Standard therapy for patients with primary hypothyroidism is replacement with synthetic thyroxine, which undergoes peripheral conversion to triiodothyronine, the active form of thyroid hormone. Within the lay population and in some medical communities, there is a perception that adding synthetic triiodothyronine, or liothyronine, to levothyroxine improves the symptoms of hypothyroidism despite insufficient evidence to support this practice. OBJECTIVE: To evaluate the benefits of treating primary hypothyroidism with levothyroxine plus liothyronine combination therapy vs levothyroxine monotherapy. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind, placebo-controlled trial conducted from May 2000 to February 2002 at a military treatment facility that serves active duty and retired military personnel and their family members. The trial included a total of 46 patients aged 24 to 65 years with at least a 6-month history of treatment with levothyroxine for primary hypothyroidism. INTERVENTION: Patients received either their usual dose of levothyroxine (n = 23) or combination therapy (n = 23), in which their usual levothyroxine dose was reduced by 50 micro g/d and substituted with liothyronine, 7.5 micro g, taken twice daily for 4 months. MAIN OUTCOME MEASURES: Scores on a hypothyroid-specific health-related quality-of-life (HRQL) questionnaire, body weight, serum lipid levels, and 13 neuropsychological tests measured before and after treatment. RESULTS: Serum thyrotropin levels remained similar and within the normal range in both treatment groups from baseline to 4 months. Body weight and serum lipid levels did not change. The HRQL questionnaire scores improved significantly in both the control group (23%; P<.001) and the combination therapy group (12%; P =.02), but these changes were statistically similar (P =.54). In 12 of 13 neuropsychological tests, outcomes between groups were not significantly different; the 1 remaining test (Grooved Peg Board) showed better performance in the control group. CONCLUSION: Compared with levothyroxine alone, treatment of primary hypothyroidism with combination levothyroxine plus liothyronine demonstrated no beneficial changes in body weight, serum lipid levels, hypothyroid symptoms as measured by a HRQL questionnaire, and standard measures of cognitive performance.