Thyrotoxic crisis as an acute clinical presentation in a child.

A previously well, 4-year-old girl presented with a 4-6 weeks' history of increased appetite, weight loss, tiredness, sleep difficulty, excessive sweating, swelling in the neck and new-onset 'prominent, protruding eyes.' Family history revealed paternal grandmother receiving treatment for hyperthyroidism. Clinical assessment demonstrated features of thyrotoxicosis (tachycardia, warm peripheries, small smooth goitre with no nodules, exophthalmos). TFT (Free T4=101 pmol/L, thyroid-stimulating hormone <0.05 mIU/L) with raised thyroid peroxidase antibody levels (TPO=541 IU/mL) confirmed autoimmune hyperthyroidism. Observation on the ward showed features of thyrotoxic crisis with persistent severe tachycardia on ECG (sinus tachycardia with left ventricular hypertrophy (LVH)) and hypertension. Ultrasound thyroid showed diffuse thyroiditis with no focal lesion. Echocardiogram confirmed the above findings. A diagnosis of Graves' disease with thyrotoxic crisis was made. Antithyroid treatment (carbimazole) and beta-blocker (propranolol) was commenced. Thyrotoxic crisis resolved over 2 weeks and the child has continued to respond to carbimazole treatment at 1-year follow-up.

Kir2.6 regulates the surface expression of Kir2.x inward rectifier potassium channels.

Precise trafficking, localization, and activity of inward rectifier potassium Kir2 channels are important for shaping the electrical response of skeletal muscle. However, how coordinated trafficking occurs to target sites remains unclear. Kir2 channels are tetrameric assemblies of Kir2.x subunits. By immunocytochemistry we show that endogenous Kir2.1 and Kir2.2 are localized at the plasma membrane and T-tubules in rodent skeletal muscle. Recently, a new subunit, Kir2.6, present in human skeletal muscle, was identified as a gene in which mutations confer susceptibility to thyrotoxic hypokalemic periodic paralysis. Here we characterize the trafficking and interaction of wild type Kir2.6 with other Kir2.x in COS-1 cells and skeletal muscle in vivo. Immunocytochemical and electrophysiological data demonstrate that Kir2.6 is largely retained in the endoplasmic reticulum, despite high sequence identity with Kir2.2 and conserved endoplasmic reticulum and Golgi trafficking motifs shared with Kir2.1 and Kir2.2. We identify amino acids responsible for the trafficking differences of Kir2.6. Significantly, we show that Kir2.6 subunits can coassemble with Kir2.1 and Kir2.2 in vitro and in vivo. Notably, this interaction limits the surface expression of both Kir2.1 and Kir2.2. We provide evidence that Kir2.6 functions as a dominant negative, in which incorporation of Kir2.6 as a subunit in a Kir2 channel heterotetramer reduces the abundance of Kir2 channels on the plasma membrane.

Treatment of thyrotoxic crisis with plasmapheresis and single pass albumin dialysis: a case report.

Thyrotoxic crisis (thyroid storm) is a life-threatening condition. Standard therapy is based on thiamazole, prednisolone, and nonselective beta-blockers. Extracorporeal plasmapheresis is an additional tool for removing circulating thyroxine in patients who do not respond quickly to conventional standard therapy. As thyroxine can be bound by albumin, the aims of the present therapy report were to investigate the potential of extracorporeal single-pass albumin dialysis (SPAD) to remove thyroid hormones and to compare it with plasmapheresis. A 68-year-old female with thyrotoxic crisis refractory to conventional therapy underwent two sessions of plasmapheresis without clinical response. For the treatment dose to be increased, the patient was then treated with a modified continuous veno-venous hemodialysis with a dialysate containing 4% of human serum albumin (SPAD) intended to bind and remove thyroxines continuously. In total, the patient received three sessions of plasmapheresis and four SPAD treatments. Thyroxine levels were detected in the patient and in exchanged plasma or albumin dialysate, respectively, to calculate the amount removed. The main finding was that SPAD treatments were tolerated well by the patient. Due to continuous approach, SPAD sessions removed more thyroid hormone than plasmapheresis did, resulting in the improvement of the clinical status of the patient (reduction of heart rate and catecholamine dosage), which enabled bridging the patient to thyroidectomy as the ultimate surgical treatment. This is the first clinical report of the use of albumin dialysis in thyroid storm. SPAD represents a safe and efficient alternative to plasmapheresis as it can be performed continuously in this critical condition.

Thyroid storm after intensity-modulated radiation therapy: a case report and discussion.

A 43-year-old man with locally advanced squamous cell carcinoma of the base of tongue was treated with induction chemotherapy followed by intensity-modulated radiation therapy (IMRT). Within 20 days post-treatment, the patient developed clinical symptoms highly suggestive of hyperthyroidism. Two and one half months after completion of therapy, the patient developed severe thyrotoxicosis, which, in retrospect, appears to have met the criteria for thyroid storm. This case history illustrates a previously unreported, life-threatening complication of external-beam radiation that should be considered in patients receiving IMRT therapy involving the thyroid. Diagnosis of the patient's hyperthyroidism and probable thyroid storm was difficult to recognize because of the significant overlap between the signs and symptoms of severe thyrotoxicosis and the expected toxicities of his cancer therapy.

Palm vitamin E improves bone metabolism and survival rate in thyrotoxic rats.

The effects of vitamin E derived from palm oil on bone turnover in thyrotoxic rats were studied. Palm vitamin E reduced bone resorption to a greater extent than bone formation in thyrotoxic rats, suggesting a net reduction in bone loss. The action of palm vitamin E is probably due to its antioxidant properties. Survival rates were also significantly increased in thyrotoxic rats given palm vitamin E, suggesting the role of free radicals in the overall morbidity and mortality in thyrotoxicosis.

Differential diagnosis of thyroid crisis and malignant hyperthermia in an anesthetized porcine model.

The intra-operative differential diagnosis between thyroid crisis and malignant hyperthermia can be difficult. Also stress alone can trigger MH. The purposes of this study were: 1) to investigate the metabolic and hemodynamic differences between thyroid crisis and MH, 2) determine how thyroid crisis affects the development of MH, and 3) determine if the stress of thyroid crisis can trigger MH in susceptible individuals. We studied MH susceptible and normal swine. Two groups of animals (MH susceptible and normal) were induced into thyroid crisis (critical core hyperthermia, sustained tachycardia and increase in oxygen consumption) by pretreatment with intraperitoneal triiodothyronine (T3) followed by large hourly intravenous injections of T3. Two similar groups were given intravenous T3 but no pretreatment. These animals did not develop thyroid crisis and served as controls. Thyroid crisis did not result in metabolic changes or rigidity characteristic of an acute episode of MH. When the animals were subsequently challenged with MH triggering agents (halothane plus succinylcholine) dramatic manifestations of fulminant MH episodes (acute serious elevation in exhaled carbon dioxide, arterial CO2, rigidity and acidemia) were noted only in the MH susceptible animals. Although thyroid crisis did not trigger MH in the susceptible animals it did decrease the time to trigger MH (14.1 +/- 7.2 minutes versus 47.2 +/- 17.7 minutes, p < 0.01) in susceptible animals. Hormone induced elevations in temperature and possibly other unidentified factors during thyroid crisis may facilitate the triggering of MH following halothane and succinylcholine challenge.

Thyroid storm and myxedema coma.

This article describes the clinical recognition of, and pathophysiological mechanisms underlying the development of, thyroid storm and myxedema coma. Effective therapeutic management of these conditions depends on a clear understanding of the physiological adaptations occurring in hyperthyroidism and hypothyroidism, and of how precipitating events may produce these decompensated states.