Hypothyroidism: Prognosis and Future Perspectives

Hypothyroidism - Prognosis and Future Perspectives

Differential Diagnosis.
The differential diagnosis of hypothyroidism includes nonthyroidal illness (i.e., decreased T3 or T4 , or both, without clinical hypothyroidism), euthyroid hypothyroxinemia (decreased T4 caused by decreased thyroid-binding globulin), and drugs that inhibit T4 binding (salicylates, phenytoin, and phenobarbital). Once hypothyroidism has been diagnosed, the most important clinical distinction is between primary and secondary hypothyroidism. The clinical and laboratory similarities between myxedema coma and other life-threatening causes of the comatose state may make its diagnosis extremely difficult. Regarding hypothyroid myopathy, the muscular appearance, stiffness, and exacerbation by cold may suggest a mild form of myotonia congenita, which can present in adulthood. Although the stiffness noted in patients with pyramidal and extrapyramidal diseases may appear similar to that of hypothyroid myopathy, the characteristic history, appearance, and laboratory studies usually permit the diagnosis of hypothyroidism.

Evaluation.
The combination of a low T4 level and an elevated thyroid-stimulating hormone (TSH) level is virtually diagnostic of primary hypothyroidism, because TSH elevation does not occur in central hypothyroidism. Further delineation between primary and secondary hypothyroidism is dependent on history, examination, and other laboratory studies. In addition to TFTs, other laboratory abnormalities have been described, including anemia (normocytic-normochromic, microcytic-hypochromic, or macrocytic) and hyponatremia (factitious due to hyperlipidemia or secondary to impaired free water excretion), as well as elevated serum creatine kinase, myoglobin, and prolactin. Because of the possibility of concomitant adrenal insufficiency, a serum cortisol level should also be obtained. The EEG may show slowing of the posterior dominant rhythm and a generalized voltage decrease, as well as triphasic waves that disappear with replacement therapy. CSF analysis may reveal an elevated protein content which may exceed 100 mg/dl.

Management.
The treatment of hypothyroidism, regardless of cause, consists of thyroid hormone replacement. Even in the setting of hypothyroid-induced seizures, achievement of the euthyroid state facilitates control. Precipitants of myxedema coma (e.g., infection, cold exposure, certain drugs phenothiazines, narcotics, and sedative-hypnotics, phenytoin, rifampin , and other stressors surgery, trauma ) require correction.

Prognosis and Future Perspectives.
With early recognition and treatment, as well as improved intensive supportive care, the mortality rate of myxedema coma has decreased from roughly 50 to 70 percent to around 15 to 20 percent.
Without early recognition and prompt institution of replacement therapy, the prognosis is grave.

Data from Mitehell JM: Thyroid disease in the emergeney department: Thyroid fune~tion tests and hypothyroidism and myxedema eoma Emerg Med Clin North Am 1989;7:885-902; Mazzafern EL: Adult hypothyroidism: 1. Manifestations and elinical presentation. Postgrad Med 1986;79:64 72; Myers L, Hays J: Myxedema eoma. Cnt Care Clinie 1991;7:43 56.