Autoimmune Thyroid Disorders in Autoimmune Addison Disease.

CONTEXT: Autoimmune thyroid disease is the most common endocrine comorbidity in autoimmune Addison disease (AAD), but detailed investigations of prevalence and clinical course are lacking. OBJECTIVE: This work aimed to provide comprehensive epidemiological and clinical data on autoimmune thyroid disorders in AAD. METHODS: A nationwide registry-based study including 442 patients with AAD and autoimmune thyroid disease were identified through the Norwegian National Registry of Autoimmune Diseases. RESULTS: Of 912 registered AAD patients, 442 (48%) were diagnosed with autoimmune thyroid disease. A total of 380 (42%) had autoimmune hypothyroidism. Of the 203 with available thyroid function tests at time of diagnosis, 20% had overt hypothyroidism, 73% had subclinical hypothyroidism, and 7% had thyroid levels in the normal range. Negative thyroid peroxidase antibodies was found in 32%. Ninety-eight percent were treated with levothyroxine, 5% with combination therapy with liothyronine or thyroid extracts, and 1% were observed without treatment. Seventy-eight patients (9%) were diagnosed with Graves disease (GD), of whom 16 (21%) were diagnosed with autoimmune hypothyroidism either before onset or after remission of GD. At the end of follow-up, 33% had normal thyroid hormone levels without antithyroid-drugs or levothyroxine treatment. The remaining had either active disease (5%), had undergone ablative treatment (41%), or had developed autoimmune hypothyroidism (21%). CONCLUSION: The true prevalence of hypothyroidism in AAD is lower than reported in the current literature. Careful consideration of the indication to start thyroxin therapy is warranted. Long-term remission rates in GD patients with AAD are comparable to recent reports on long-term follow-up of patients without AAD.

Does thyroid function influence fracture risk? Prospective data from the HUNT2 study, Norway.

OBJECTIVE: To prospectively study the relation between TSH and risk of hip and forearm fractures. DESIGN: A population-based cohort study. METHODS: In a substudy of the second survey of the Nord Trøndelag Health Study, Norway (HUNT2, 1995-97), linked with a hospital-based fracture registry, we investigated the relation between baseline TSH and risk of hip and/or forearm fractures. POPULATION: A total of 16 610 women and 8595 men aged 40 years or more, without previous self-reported thyroid disease and hip or forearm fractures. RESULTS: During 12.5 years follow-up, a total of 1870 women and 342 men experienced hip or forearm fractures. Overall, there was no relation between baseline TSH and fracture risk. However, there was weak evidence that women with TSH <0.5 and >3.5 mU/l had a slightly increased risk of hip fractures (hazard ratio (HR) 1.30, 95% CI 0.97-1.94 and HR 1.19, 95% CI 0.93-1.52) compared with the reference group with TSH of 1.5-2.4 mU/l. Supplementary analyses showed higher hip fracture risk in women with TSH >4.0 mU/l and negative thyroid peroxidase antibodies (TPOAb) compared with the reference group (HR 1.75, 95% CI 1.24-2.46). CONCLUSION: We found no statistically significant relation between baseline TSH and subsequent fracture risk, but the data suggest a weak positive association with hip fracture risk among women with both low and high TSH. The latter association was confined to women with negative TPOAb status.

Serum TSH related to measures of body mass: longitudinal data from the HUNT Study, Norway.

OBJECTIVE: Thyroid function and body mass are related, but the causal relationship remains unclear. Our objective was to investigate the longitudinal relationship between thyroid stimulating hormone (TSH) and body mass measures [body weight, body mass index (BMI), waist circumference (WC) and waist-hip-ratio (WHR)]. DESIGN: We used data from two waves of a population-based study: HUNT 2 (1995-1997) and 3 (2006-2008). Average follow-up time was 10·5 years. Multivariable general linear and logistic regression models were used to assess the relation between TSH and the body mass measures. PARTICIPANTS: In total 9954 women and 5066 men without self-reported thyroid disease and TSH within the reference range (0·5-3·5 mU/l) at baseline and <10 mU/l at follow-up. RESULTS: For each mU/l increase in TSH among women, weight increased 0·9 kg (95% CI 0·8, 1·1), BMI 0·3 kg/m(2) (95% CI 0·3, 0·4) and WC 0·6 cm (95% CI 0·3, 0·8). In men, the corresponding figures were 0·8 kg (95% CI 0·5, 1·0), 0·2 kg/m(2) (95% CI 0·2, 0·3) and 0·5 cm (95% CI 0·2, 0·8). In line with this, a weight gain of more than 5 kg was associated with a TSH increase of 0·08 mU/l (95% CI 0·06, 0·11) in women and 0·15 mU/l (95% CI 0·12, 0·18) in men. Women who lost more than 5 kg decreased their TSH by 0·12 mU/l (95% CI 0·09, 0·16) and men by 0·03 mU/l (95% CI -0.02, 0·09). CONCLUSION: Weight gain is accompanied by increasing TSH, and weight loss in women is related to decreasing TSH.

[Do we really need more non-forensic autopsies?]. / Trenger vi virkelig flere obduksjoner?

There has been a decline in the rate of non-forensic autopsies during the last decades. Pathologists consider this trend to be an unfortunate, and believe the rate of such autopsies should rather increase to help reduce clinical mistakes. This chronicle summarises the most important arguments for increasing the rate of autopsies and concludes that an increase is not warranted.

A patient presenting with symptomatic hypomagnesemia caused by metformin-induced diarrhoea: a case report.

INTRODUCTION: Metformin is licensed for treatment of diabetes mellitus type 2. This report describes a patient on metformin who developed diarrhoea and symptomatic hypomagnesemia. To the author's knowledge, this is the first report on metformin-induced symptomatic hypomagnesemia. CASE PRESENTATION: The patient was a 57-year old Caucasian male with diabetes mellitus type 2. He had been on metformin for nine years and presented with chronic diarrhoea, spasms, paresthesias, pain, and malaise. Blood tests revealed hypomagnesemia, hypocalcemia, and hypokalemia. CONCLUSION: Drugs associated with diarrhoea may induce malabsorption. If malabsorption is substantial it may result in further symptoms of clinical importance. In some cases potentially life-threatening conditions may occur.

Hyperthyroid levels of TSH correlate with low bone mineral density: the HUNT 2 study.

OBJECTIVE: To study the relationship between TSH and forearm bone mineral density (BMD) in a general female population. Design Cross-sectional, population-based study. METHODS: In a substudy of the Nord-Trøndelag Health Study 1995-1997 (HUNT 2), 5778 women without and 944 with self-reported thyroid disease aged > or =40 years had their serum TSH and distal and ultra-distal forearm BMD measured. In range-based categories of TSH, excluding women with previous thyroid disease, a general linear model was used to calculate adjusted mean BMD, and a logistic regression model to compute adjusted odds ratio (OR) for osteopenia and osteoporosis. Corresponding models were used to compare BMD in women with self-reported hypothyroidism or hyperthyroidism to euthyroid women. RESULTS: In women without self-reported thyroid disease, those with TSH <0.5 mU/l had 10.7 mg/cm(2) (95% confidence interval (CI) 0.2-21.1) lower distal and 9.1 mg/cm(2) (95% CI -0.7-18.9) lower ultra-distal BMD than women in the reference category (TSH 0.50-1.49 mU/l). No differences were found between the categories with TSH > or =0.50 mU/l. Compared to self-reported euthyroid women, self-reported hyperthyroid women had increased odds for osteoporosis both distally (OR 1.35, 95% CI 1.00-1.82) and ultra-distally (OR 1.48, 95% CI 1.10-1.99). CONCLUSION: Women with the lowest TSH (<0.5 mU/l) had lower forearm BMD than the reference category. No differences were observed between the TSH categories > or =0.50 mU/l. The prevalence of osteoporosis was higher in women who reported hyperthyroidism than in women without self-reported thyroid disease.