Thyrotoxic periodic paralysis in a Caucasian man in treatment for Graves' disease

Thyrotoxic periodic paralysis (TPP) is the main secondary form of hypokalemic periodic paralysis and is mostly associated with Graves' disease. Initially diagnosed in Asian countries, TPP has been sporadically reported in different populations of the Western World. Increased Na+/K(+)-ATPase activity seems to be responsible for the marked hypokalemia observed during the transient paralysis attacks. We report on a 35-year-old Italian man without history of hypokalemic periodic paralysis and hyperthyroidism, in treatment for Graves' disease, who suffered episodes of flaccid paralysis even with normal thyroid hormone levels. An insulin-glucose provocation test confirmed our diagnosis. Oral and parenteral potassium reverse the symptoms. Monitoring of thyroid function is also important to prevent further attacks.     

Surgical management in Graves' disease

Graves' disease is most often managed with radioiodine in the United States today. Surgical therapy, however, is a safe and effective form of treatment when performed by an experienced thyroid surgeon. Surgery can be particularly helpful when rapid control of hyperthyroidism is essential, in large gland disease, in children and in women of child-bearing age.     

Hypokalemic paralysis following administration of intravenous methylprednisolone in a patient with Graves' thyrotoxicosis and ophthalmopathy

Glucocorticoids are commonly used in the treatment of patients with thyroid disorders, in particular Graves' ophthalmopathy. Thyrotoxic hypokalemic periodic paralysis (TPP) is an infrequent but potentially serious condition characterised by recurrent episodes of weakness associated with hypokalemia. We describe the development of acute hypokalemic paralysis in a middle-aged Caucasian man with recently diagnosed thyrotoxicosis and severe, active Graves' opthalmopathy who developed progressive flaccid paralysis 12 hours following intravenous administration of methylprednisolone. Rechallenge with the same dose after the patient had been rendered euthyroid did not provoke TPP. Clinicians should exercise caution when administering high-dose glucocorticoids during thyrotoxicosis as there is a risk of provoking hypokalemic paralysis in susceptible patients.     

Unaltered glucose-induced thermogenesis in Graves' disease

The thermogenic response to a 100-g oral glucose challenge was studied in 12 patients with Graves' disease using continuous indirect calorimetry. Seven hyperthyroid patients were reinvestigated under the same experimental conditions after medical therapy. The mean net increase in energy expenditure (delta EE) following the glucose challenge was the same in hyperthyroid patients as compared to a control group (delta EE = +0.15 +/- 0.02 and 0.15 +/- 0.01 kcal/min, respectively) and the treated patients (delta EE = +0.11 +/- 0.03 kcal/min ns). When expressed as a percentage of the energy content of the glucose challenge, the mean glucose induced thermogenesis was similar in all three groups: 7.0 +/- 1.0%, 7.4 +/- 0.5%, and 5.5 +/- 1.3% in hyperthyroid, control subjects, and treated patients, respectively. It is concluded that the high energy requirement of hyperthyroid patients is due primarily to an elevated resting energy expenditure. The postprandial thermogenesis in itself does not contribute to the elevated fuel utilization in Graves' disease.     

Risk factors for Graves' disease

A case-control study of 100 newly diagnosed patients with Graves' disease and the same numbers of controls matched with respect to sex, age (± 2 years) and type of residence (rural-urban) was carried out. According to the matched analysis (McNemar's test and t-test) seventeen variables recognized as risk factors were included into the model of multivariate conditional logistic regression. The following factors were significantly associated with the occurrence of Graves' disease: change in time spent on work -- much overtime work, second job, much less work than usual (RR = 6.62; CI = 2.08--21.01), lack of readiness of relatives and friends to help the subject (RR = 1.48; 95% CI = 1.14--1.93), increased arguments with spouse (RR = 14.12; 95% CI = 1.63--121.87), unemployment for at least one month (RR = 9.80; 95% CI = 1.13--85.02), and family history of Graves disease in the first degree of relation (RR = 7.20; 95% CI = 0.85--60.70).     

Kennedy disease in a patient with progressive speech disorder

Kennedy disease is an adult onset neuromuscular disease characterized by slowly progressive proximal and bulbar muscle weakness. The disease associates with gynecomastia, adult onset infertility and sensory neuropathy, and caused by pathologic expansion of CAG repeats at the N-terminal region of the androgen-receptor gene at Xq11-q12. We report on a patient presenting with slowly progressive muscle weakness of the lower extremities, progressive dysartry and swallowing difficulties. The clinical symptoms were not fully specific for the disease. Moreover the family history was suggestive for an autosomal dominant trait meaning a diagnostic pitfall at the original examination. Finally the firm diagnosis of the Kennedy disease was established by a polimerase chain reaction based method.