Normalization of serum thyrotrophin by means of radioiodine treatment in subclinical hyperthyroidism: effect on bone loss in postmenopausal women.

BACKGROUND: Patients with subclinical hyperthyroidism (reduced serum TSH and normal free T4 and T3 concentrations) have slightly increased bone turnover and might have reduced bone mass, especially among postmenopausal women (due to concomitantly reduced oestrogen production), as also seen during suppressive L-T4 treatment. OBJECTIVE: We have evaluated whether normalization of serum TSH using radioiodine treatment (RAI) in postmenopausal women with a nodular goitre and subclinical hyperthyroidism, protects against bone loss? DESIGN: Prospective, non-randomized study, outpatients 2 years follow-up. PATIENTS: Postmenopausal women with a nodular goitre, biochemically subclinical hyperthyroidism (TSH < 0.2 mU/I, and signs of a growing goitre or compression symptoms. Sixteen were treated with RAI (median dose 555 MBq) (+RAI), whereas 12 were followed without treatment (-RAI). MEASUREMENTS: Serum TSH (third generation technology), free T4 and T3 indices, and bone mass (BMD) as measured by Dual Photon Absorptiometry (4 in each group) (only spine) or Dual X-ray Absorptiometry (DEXA) (both spine and hip), were measured yearly for up to 2 years. RESULTS: The two groups did not differ regarding age, thyroid hormone parameters, and absolute levels of BMD at spine and hip. RAI resulted in normalization of TSH in all 16 women, and FT4I as well as FT3I decreased to 78% after one year (P < 0.01). These parameters did not change in the untreated group, thus serum TSH remained reduced. BMD at the spine tended to increase (n.s.) after RAI to (median) 101.9% after one year, and 101.5% after 2 years. In contrast the -RAI group experienced a continued fall in BMD to 97.3% after one year, and 95.5% after 2 years, both reduced as compared to the +RAI group (P < 0.02). BMD of the hip also increased after RAI, to 102.3% after one year, and 101.7% after 2 years. In contrast BMD in the -RAI group decreased to 94.8% after one year, and 98.0% after 2 years, both lower than in the +RAI group (P < 0.01). CONCLUSIONS: Subclinical hyperthyroidism due to a nodular goitre in postmenopausal women resulted in a continued loss of bone mass of about 2% per year. Radioiodine treatment resulting in normalization of serum TSH prevented this continued bone loss for at least 2 years. Our study supports earlier intervention in such patients.

Plasma 6-keto-PGF1 alpha, thromboxane B2 and PGE2 during diabetic ketoacidosis.

In 10 patients admitted to hospital with diabetic ketoacidosis plasma prostanoids 6-keto-PGF alpha, thromboxane B2 and PGE2 were studied before treatment and following recovery. During ketoacidosis the median plasma 6-keto-PGF1 alpha and PGE2 were significantly increased compared to those of a normal reference group: 5.2 pg/ml and 3.9 pg/ml versus 1.7 pg/ml and 0.4 pg/ml (p less than 0.01 and p less than 0.05). In response to therapy both prostanoids decreased significantly towards a normal level, 6-keto-PGF1 alpha: 0.5 pg/ml p less than 0.01 and PGE2: 0.08 p less than 0.05 respectively. The changes in plasma 6-keto-PGF1 alpha were negatively correlated to changes in pH, rho: -0.7788 p = 0.0135, whereas the changes in PGE2 were positively correlated to serum creatinine at admittance, rho: 0.6976, p = 0.0368 and to the amount of intravenous fluid and insulin used during treatment, rho: 0.7500 p = 0.0126 and rho: 0.8424, p = 0.0023 respectively. Plasma thromboxane B2 concentrations were not elevated and did not change after treatment of the ketoacidosis.

Depression and magnesium deficiency.

The psychiatric symptoms of magnesium deficiency are unspecific, ranging from apathy to psychosis, and may be attributed to other disease processes associated with poor intake, defect absorption, or excretion of magnesium. Serum magnesium should be determined when there are symptoms consistent with magnesium deficiency and/or in conditions which can lead to a deficiency, e.g., malabsorption, malnutrition, alcoholism and diuretic treatment. A low serum value suggests magnesium deficiency, but the diagnosis is reinforced with analyses of magnesium in the urine and a loading test with magnesium. Magnesium can be given orally or intramuscular/intravenously.

Pituitary-thyroid axis in critical illness.

Severe nonthyroidal illness has been claimed to cause secondary hypothyroidism. We reevaluated this concept measuring serum free T4 and free T3 by an ultrafiltration method and serum TSH by an ultrasensitive technique (detection limit, and serum TSH by an ultrasensitive technique (detection limit, 0.05 mU/L). Forty-five critically ill patients suffering from hepatic coma (n = 10), terminal cancer (n = 9), stroke (n = 8), and respiratory insufficiency not treated (n = 7) and treated (n = 11) with dopamine were studied. The mortality rate was 80%. No patients received glucocorticoids, and only patients in the last group received dopamine. Serum total as well as free thyroid hormone index values were grossly reduced in the majority of the patients. The 34 patients not receiving dopamine in general had normal values of serum free T4 (32 of 34) and free T3 (31 of 34), measurable TSH (33 of 34), and detectable TSH responses to iv TRH (33 of 34). In contrast, the dopamine-treated patients had reduced serum free T4 and TSH levels compared to normal subjects (P less than 0.05), as well as reduced TSH responses to TRH (P less than 0.01). Serum free T4 and free T3 were below the normal range in 3 patients and 1 patient, respectively, and serum TSH was below the detection limit in 2 patients. We conclude that critically ill patients with nonthyroidal illness not receiving dopamine have normal pituitary-thyroid function, whereas dopamine induces some degree of secondary hypothyroidism.

Plasma 6-keto-PGF1 alpha, thromboxane B2 and PGE2 in type 1 (insulin-dependent) diabetic patients during exercise.

The capacity of prostacyclin production determined as plasma 6-keto-PGF1 alpha was investigated in 12 type 1 (insulin-dependent) diabetic patients with a median duration of diabetes of 14 years during ordinary metabolic control. Using high pressure liquid chromatography preceding radioimmunoassay, the plasma concentration of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, was determined at rest and after a standardised bicycle exercise test. The plasma 6-keto-PGF1 alpha in diabetic patients at rest did not differ from that of 25 healthy volunteers; 2.9 pg/ml (range less than 0.2-15.3) versus 1.7 pg/ml (range less than 0.2-16.6). During the exercise test plasma 6-keto-PGF1 alpha increased significantly in the diabetic patients as well as in the control group (p less than 0.05). The increment of 6-keto-PGF1 alpha in the diabetic patients was neither related to the metabolic regulation, duration of diabetes nor to changes in platelet volume, platelet number or the production of thromboxane B2 and prostaglandin E2. Our results do not support the hypothesis that Type 1 diabetic patients have a decreased capacity of prostanoid production, as suggested from in vitro studies.

Familial dysalbuminemic hyperthyroxinemia.

A family with familial dysalbuminemic hyperthyroxinemia is described. The syndrome is inherited as an autosomal dominant trait and is characterized by marked elevation of serum thyroxine, due to increased binding of thyroxine to albumin, whereas serum triiodothyronine is normal. Serum free thyroxine is normal when measured with ultrafiltration or equilibrium dialysis, but artefactually high when measured with an analogue assay. The importance of the condition, which is harmless, lies in the misinterpretation of values with subsequent erroneous treatment of thyrotoxicosis. By using an ultrasensitive TSH method it is possible to discriminate between euthyroid and hyperthyroid patients and thereby to avoid incorrect diagnosis in subjects with euthyroid hyperthyroxinemia.

Bilateral papilledema with normal CT-scan in neurosarcoidosis.

A 74-year-old woman was admitted with fever, muscle and joint pain and a mild hypercalcemia. Rather suddenly she turned unconscious and bilateral papilledema was found. A subsequent CT of the brain, however, did not disclose signs of space-occupying masses or increased intracranial pressure. She died two days later and at autopsy there were no signs of incarceration. Microscopic examination revealed non-caseating epithelioid granulomas throughout the meninges and brain consistent with sarcoidosis.