Background: Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), often termed Hashimoto encephalopathy, is a poorly understood and often misdiagnosed entity. Objective: To characterize the clinical, laboratory, and radiologic findings in patients with SREAT to potentially improve recognition of this treatable entity. Design: Retrospective analysis of clinical features and diagnostic test data. Setting: Two affiliated tertiary care referral institutions. Patients: Twenty consecutive (6 male) patients diagnosed as having SREAT from 1995 to 2003. Main Outcome Measures: Clinical features and ancillary test findings associated with SREAT. Results: The median age at disease onset was 56 years (range, 27-84 years). The most frequent clinical features were tremor in 16 (80%), transient aphasia in 16 (80%), myoclonus in 13 (65%), gait ataxia in 13 (65%), seizures in 12 (60%), and sleep abnormalities in 11 (55%). All patients were assigned an alternative misdiagnosis at

Subacute thyroiditis (SAT), or granulomatous thyroiditis, is an inflammatory thyroid condition associated with pain and systemic symptoms. Few community studies are available. We studied the 160 patients with SAT in Olmsted County, Minnesota, seen between January 1, 1960, and December 30, 1997. Subjects were identified through the medical diagnostic index of the Rochester Epidemiology Project. The overall age- and sex-adjusted incidence from 1960 through 1997 was 4.9 cases per 100,000/yr. In the most recent 28-yr period (1970-1997), 94 patients were identified. In this group, pain was the presenting symptom in 96%. SAT recurred in 4% of the patients 6-21 yr after the initial episode. Corticosteroid therapy was given to 36%. Early-onset hypothyroidism occurred both in patients receiving corticosteroid therapy (29%) and in those not receiving corticosteroid therapy (37%). At latest follow-up, significantly more patients who had received corticosteroid therapy had a diagnosis of hypothyroidism than the group without corticosteroid therapy (25% vs. 10%, P < 0.05; overall rate of hypothyroidism, 15%). Early transient hypothyroidism is common in SAT. Permanent hypothyroidism is less common, and only 15% of the patients are receiving T(4) therapy after 28 yr of follow-up. Symptomatic relief is achieved with corticosteroid therapy, but such therapy does not prevent early- and late-onset thyroid dysfunction.

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The glucagonoma syndrome is a rare disorder characterized by weight loss, necrolytic migratory erythema (NME), diabetes, stomatitis, and diarrhea. We identified 21 patients with the glucagonoma syndrome evaluated at the Mayo Clinic from 1975 to 1991. Although NME and diabetes help identify patients with glucagonomas, other manifestations of malignant disease often lead to the diagnosis. If the diagnosis is made after the tumor is metastatic, the potential for cure is limited. The most common presenting symptoms of the glucagonoma syndrome were weight loss (71%), NME (67%), diabetes mellitus (38%), cheilosis or stomatitis (29%), and diarrhea (29%). Although only 8 of the 21 patients had diabetes at presentation, diabetes eventually developed in 16 patients, 75% of whom required insulin therapy. Symptoms other than NME or diabetes mellitus led to the diagnosis of an islet cell tumor in 7 patients. The combination of NME and diabetes mellitus led to a more rapid diagnosis (7 months) than either symptom alone (4 years). Ten patients had diabetes mellitus before the onset of NME. No patients had NME clearly preceding diabetes mellitus. Increased levels of secondary hormones, such as gastrin (4 patients), vasoactive intestinal peptide (1 patient), serotonin (5 patients), insulin (6 patients, clinically significant in 1 only), human pancreatic polypeptide (2 patients), calcitonin (2 patients) and adrenocorticotropic hormone (2 patients), contributed to clinical symptoms leading to the diagnosis of an islet cell tumor before the onset of the full glucagonoma syndrome in 2 patients. All patients had metastatic disease at presentation. Surgical debulking, chemotherapy, somatostatin, and hepatic artery embolization offered palliation of NME, diabetes, weight loss, and diarrhea. Despite the malignant potential of the glucagonomas, only 9 of 21 patients had tumor-related deaths, occurring an average of 4.91 years after diagnosis. Twelve patients were still alive, with an average age follow-up of 3.67 years.

Subclinical hypothyroidism (SCH), also called mild thyroid failure, is diagnosed when peripheral thyroid hormone levels are within normal reference laboratory range but serum thyroid-stimulating hormone (TSH) levels are mildly elevated. This condition occurs in 3% to 8% of the general population. It is more common in women than men, and its prevalence increases with age. Of patients with SCH, 80% have a serum TSH of less than 10 mIU/L. The most important implication of SCH is high likelihood of progression to clinical hypothyroidism. The possibility that it is a cardiovascular risk factor has been a subject of debate. Large-scale randomized studies are needed for evidence-based recommendations regarding screening for mild thyroid failure and levothyroxine therapy for this condition. Currently, the practical approach is routine levothyroxine therapy for persons with a persistent serum TSH of more than 10.0 mIU/L and individualized therapy for those with a TSH of less than 10.0 mIU/L. © 2009 Mayo Foundation for Medical Education and ResearchOn completion of this article you should be able to: (1) S ubclinical hypothyroidism (SCH) is defined as a serum thyroid-stimulating hormone (TSH) level above the upper limit of normal despite normal levels of serum free thyroxine. 1 Serum TSH has a log-linear relationship with circulating thyroid hormone levels (a 2-fold change in free thyroxine will produce a 100-fold change in TSH). Thus, serum TSH measurement is the necessary test for diagnosis of mild thyroid failure when the peripheral thyroid hormone levels are within normal laboratory range. 1 The individual range for peripheral thyroid hormones is narrower than the population reference laboratory range; therefore, a slight reduction within the normal range will result in elevation of serum TSH above the normal range.Subclinical hypothyroidism or mild thyroid failure is a common problem, with a prevalence of 3% to 8% in the population without known thyroid disease. 2,3 The prevalence increases with age and is higher in women. 2 After the sixth decade of life, the prevalence in men approaches that of women, with a combined prevalence of 10%. 2 Antithyroid antibodies can be detected in 80% of patients with SCH, and 80% of patients with SCH have a serum TSH of less than 10 mIU/L.Before diagnosis of SCH, other causes of an elevated TSH level, such as recovery from nonthyroidal illness, assay variability, presence of heterophile antibodies interfering with the TSH assay, and certain cases of central hypothyroidism with biologically inactive TSH and thyroid hormone resistance, should be excluded. However, the most common cause of elevated TSH is autoimmune thyroid disease. 1 Previous radioiodine therapy, thyroid surgery, and external radiation therapy can also result in mild thyroid failure. Transient SCH may occur after episodes of postpartum, silent, and granulomatous thyroiditis. 1,4 The clinical importance of and therapy for mild elevation of serum TSH (<10 mIU/L) 5 and the exact upper limit of normal for the serum TSH ...