Lithium carbonate is used to manage various mood disorders, but it can cause thyroid abnormalities, including goiter, hypothyroidism, and hyperthyroidism. In rare cases, it can lead to giant goiter and subclinical hyperthyroidism, which may require surgical intervention in severe cases.

This case represents a rare development of giant goiter and subclinical hyperthyroidism in a schizophrenia patient who was subjected to prolonged lithium carbonate treatment. The enlarged thyroid gland caused pressure on the airway and recurrent laryngeal nerve, which led to respiratory distress, hoarseness, and dysphagia. The immediate danger of suffocation required urgent surgical intervention. In this report, we describe the case of a 41-year-old Chinese woman. This sheds light on the etiology and challenges associated with managing a giant goiter. The patient underwent a subtotal thyroidectomy to relieve airway compression and facilitate airway expansion. Prior to the procedure, the patient was given iodine to prepare. Concurrently, changes were made to the psychiatric medication regimen. Following surgery, the patient's respiratory function and vocal cord functionality improved significantly, and her mental state remained stable.

It is essential to monitor thyroid function, test thyroid antibody levels, and perform thyroid ultrasounds consistently in all patients undergoing long-term lithium carbonate treatment. This vigilance helps prevent severe and potentially life-threatening thyroid enlargement.

Amiodarone-induced liver injury (AILI) is histopathologically similar to alcoholic steatohepatitis (ASH). We sought to elucidate their histologic differences and develop a scoring system to differentiate these two entities.

A cohort of 17 AILI and 17 ASH cases was included in the initial study. Cases from three different institutions were included for further validation.

Macrovesicular steatosis was usually below 10% of the liver parenchyma in AILI. Hepatocyte ballooning degeneration was more common in ASH than in AILI. "Balloon-like" hepatocyte was more common in AILI than in ASH. Lobular neutrophilic inflammation, satellitosis, and cholestasis were more common in ASH. Mallory-Denk bodies and pericellular fibrosis in AILI were mainly located in zone 1 compared with a panacinar or zone 3 distribution in ASH. A scoring system was developed in which points were assigned to different histologic features; a total sum of less than 5 suggests AILI, more than 5 is ASH, and 5 is equivocal. This scoring system was then evaluated on a test cohort comprising 14 AILI cases, in which 13 cases were correctly assigned with a score less than 5. The sensitivity, specificity, and accuracy for diagnosing AILI in the test cohort were 92.9%, 91.7%, and 92.3%, respectively.

This scoring system can aid pathologists to differentiate AILI from ASH.

Amiodarone-induced thyrotoxicosis (AIT) is caused by excessive hormone synthesis and release (AIT I), a destructive thyroiditis (AIT II), or a combination of both (AIT Ind). Although no gold-standard diagnostic test is available, technetium-99m sestamibi thyroid scintigraphy (99mTc-STS) has been previously reported to be an accurate tool for differentiating subtypes with important therapeutic implications. However, the information to guide reporting of 99mTc-STS is qualitative and highly subjective. This study aims to compare the interobserver reliability of 99mTc-STS before and after the use of quantitative thyroid-to-background ratios (TBRs) displayed on a time-activity curve for differentiation of AIT subtypes.

A retrospective audit of Nuclear Medicine Departments at Royal Melbourne Hospital (Parkville, Victoria, Australia) and Cabrini Hospital (Malvern, Victoria, Australia) identified 15 consecutive 99mTc-STS studies performed for AIT. Four nuclear medicine physicians reported the studies according to previously established criteria (series 1). Quantitative TBR and estimated 'normal' range TBR were subsequently provided before the studies were reordered and reported again (series 2). Interobserver reliability was calculated using Fleiss' κ statistic for each assessment.

The overall percentage of agreement (PoA) and κ statistics for use of conventional 99mTc-STS for diagnosis of AIT improved from 47 to 80% and from 0.30 to 0.67 following the use of quantitative TBR displayed on a time-activity curve with reference to a normal population. Interobserver reliability improved substantially under all diagnostic comparisons, particularly for differentiation of either AIT I (PoA 80% to 94%, κ: 0.48 to 0.84) or AIT Ind (PoA 47% to 82%, κ: -0.05 to 0.51) from other types of AIT.

Use of quantitative TBR improves the interobserver reliability of reporting 99mTc-STS for investigation of different types of AIT. There is 'almost perfect' agreement upon differentiation of AIT I from AIT II and AIT Ind, with important implications for rationalizing the use of corticosteroid therapy. Prospective identification of AIT Ind is improved from 'poor' to a 'moderate' level of agreement to facilitate rational use of combination therapy at diagnosis.

Lithium is widely used to treat bipolar disorders. Lithium toxicity is generally caused by inappropriately high doses of lithium or impaired lithium excretion. Most lithium is eliminated via the kidneys and, since thyroid hormone increases tubular reabsorption of lithium, thyrotoxicosis could contribute to the development of lithium toxicity. We report a case of severe lithium toxicity that was apparently precipitated by the onset of thyrotoxicosis resulting from silent thyroiditis and dehydration.

The patient was a 64-year-old woman who was admitted for muscle weakness in the lower extremities, diarrhea, and palpitations. She had bipolar disorder and was being treated with lithium carbonate, which she discontinued one week before admission. Her circulating lithium levels had been monitored yearly. Early in her admission she was dehydrated and had febrile episodes, paroxysmal atrial fibrillation, and muscle weakness. Initially, fluid therapy was started, but she lost consciousness and had a cardiac arrest for 2 minutes due to prolonged sinus arrest. Chest compression and manual artificial ventilation were performed, and body surface pacing was started. Serum lithium was markedly elevated to 3.81 mEq/L (therapeutic range, 0.4-1.0 mEq/L), and thyroid hormone levels were increased (free triiodothyronine, 8.12 pg/mL; free thyroxine, 4.45 ng/dL), while thyrotropin (TSH) was suppressed (<0.01 μIU/mL). Hemodialysis was performed, and a temporary pacemaker was inserted for severe sinus bradycardia. The serum thyroglobulin was 4680 ng/mL (reference range, <32.7 ng/mL). A TSH receptor antibody test was negative. Glucocorticoid therapy and inorganic iodine (100 mg) were administered and continued until day 11. However, her neurological symptoms deteriorated with floppy quadriplegia and deep coma. She gradually recovered. On day 36, she was discharged without any neurological symptoms or thyrotoxicosis.

A 64-year-old woman taking lithium for bipolar disorder developed lithium toxicity in the setting of what seemed likely to be a recent onset of thyrotoxicosis due to silent thyroiditis.

Thyrotoxicosis may be a contributing cause of lithium toxicity, particularly if it is abrupt in onset and even with cessation of lithium therapy if renal function is compromised. Thyroid function should be assessed immediately in patients with suspected lithium toxicity.

Amiodarone is well recognized as an anti-arrhythmic drug containing a high dose of iodine with considerable potential to cause thyroid dysfunction. The present patient was a 66-year-old Japanese woman who developed a cardiac arrhythmia and was given amiodarone as an anti-arrhythmic agent for approximately 3 months, until the day before her death. However, 19 days after starting amiodarone, serum testing indicated a hypothyroid status that was not recognized clinically. At autopsy, microscopy showed that most of the thyroid follicles were enlarged with dense colloid substance and lined by flattened follicular cells (involuted follicles). There were a small number of damaged follicles infiltrated by macrophages, which were immunopositive for HAM56. Sudan IV staining indicated many lipid droplets in follicular cells. Ultrastructurally the follicular cells contained large residual bodies composed of abundant electron-lucent lipid droplets of variable size. Although it is difficult to be certain of the direct link of amiodarone on the basis of a single case, it is reasonable to presume that this histopathology is associated with amiodarone-induced hypothyroidism and that involution changes represent the hypofunctional status of this drug-induced disorder. This is the first report on the histopathological findings of thyroid tissue from a patient with amiodarone-induced hypothyroidism.

Therapy related alterations to the thyroid gland are associated with more or less specific morphological changes. The therapy (thyrostatic drugs, radio-iodine) may be administered for the treatment of thyroid dysfunction (hyperthyroidism), or the thyroid gland is involved during or after the treatment (irradiation, various drugs) of primarily non-thyroid related diseases. The present review summarizes the most important morphological changes related to therapy.

The clinical features and the laboratory aspects of the amiodarone-induced hypothyroidism (AIH) in the elderly as well as the effects of amiodarone treatment in aged AIH people have not yet been well clarified. In the present paper, we evaluated 18 subjects of both sexes (7 females, 11 males), aged 65-83 years, affected by AIH, recruited in Central Tuscany, Italy. The patients were divided in two subsets on the basis of thyroid stimulating hormone (TSH) values: mild (TSH < 20 mU/l; Group A, n=11) and severe (TSH > 20 mU/l; Group B, n=7) hypothyroid patients. On the basis of clinical features, hypothyroidism was diagnosed only in two patients (out of Group B). Concerning the hormonal pattern, we found that free tetraiodothyronine (fT4) levels were significantly lower than the normal range only in Group B subjects; TSH and thyroglobulin were higher than normal in both groups; free triiodothyronine (fT3) were always in the normal range. Thyroid autoantibodies were found positive only in one patient out of Group A and in two patients out of Group B. In 5/18 patients T4 substitutive therapy was rapidly assigned, because of severe degree of hypothyroidism. In the remaining 13/18 patients, we evaluated the clinical behavior of AIH. After additional cardiac evaluation, amiodarone was withdrawn in 5/13 patients: during follow-up period (4-10 months) four patients became quickly euthyroid while one worsened. In 8/13 patients, amiodarone treatment had to be carried on; during follow-up (2-48 months), four patients remained mildly hypothyroid, while other four patients became severely hypothyroid. In conclusion, in amiodarone treated elderly people, diagnosis of hypothyroidism is reliable only on the basis of high values of TSH; clinical features and fT3 serum levels never enable diagnosis.

To investigate whether amiodarone increases interleukin-6 (IL-6) production in thyrocytes, human follicles obtained from subtotally thyroidectomized patients with Graves' disease were cultured in serum-free medium supplemented with various concentrations of bovine thyrotropin (bTSH) and amiodarone. The follicles gradually formed monolayer cells and secreted triiodothyronine (T3), thyroglobulin (Tg), and IL-6 for at least 14 days. TSH dose-dependently increased T3 and Tg but not IL-6 levels in the conditioned medium. Amiodarone exerted no significant effect on T3, Tg, or IL-6 concentrations at 0.1-1 microM. In contrast, at 10-20 microM, it decreased T3 and Tg, but increased IL-6 levels, and these changes were accompanied by increased expression of IL-6 mRNA. Amiodarone-induced IL-6 production was inhibited by prednisolone at 10(-7) M. Electron microscopic examination revealed that the thyroid follicles in the suspension culture remained intact at 1 microM, but that cytotoxic effects (decreased microvilli and increased onion-like inclusion bodies) occurred at higher concentrations (10-25 microM). These in vitro findings indicate that amiodarone does not impair thyroid function at clinically attainable serum levels (1 microM), but exerts cytotoxic effect by inducing the production of a proinflammatory cytokine (IL-6) at higher concentrations. Because amiodarone-induced IL-6 production was inhibited by prednisolone, it is reasonable to administer glucocorticoids to patients with amiodarone-induced destructive thyrotoxicosis (type II).

Although amiodarone is regarded as a highly effective anti-arrhythmic agent, its use may lead to alterations in thyroid gland function and/or thyroid hormone metabolism, partly because of its rich iodine content. Patients treated with amiodarone may manifest altered thyroid hormone profile without thyroid dysfunction, or they may present with clinically significant amiodarone-induced hypothyroidism or amiodarone-induced thyrotoxicosis. The former results from the inability of the thyroid to escape from the Wolff-Chaikoff effect. It prevails in areas with high dietary iodine intake, and it is readily managed by discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis occurs more frequently in areas with low iodine intake; it may arise from iodine-induced excessive thyroid hormone synthesis (type I) or destructive thyroiditis with release of preformed hormones (type II). Type I should be treated with thionamides alone or in combination with potassium perchlorate, whereas type II benefits from treatment with glucocorticoids. Surgery may be a feasible option for patients who require long-term amiodarone treatment.

We have critically reviewed the available information on iodine-induced hyperthyroidism (IIH) from published sources and other reports as well as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induce an episode of thyrotoxicosis (IIH). This has been observed in epidemic incidence in several countries when iodine has been given as prophylaxis in a variety of vehicles, but the attack rate as recorded has been low. IIH is most commonly encountered in older persons with long standing nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs after an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing drugs such as radiocontrast media or amiodarone are administered. The biological basis for IIH appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient and iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyroidism (Graves' disease) is not expressed because of iodine deficiency. The risks of IIH are principally to the elderly who may have heart disease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health impact of IIH or "subclinical" IIH, especially in the course of prophylaxis programs with iodized salt or iodinated oil in regions where access to health care is limited.