Secondary Hypothyroidism

Secondary hypothyroidism occurs after pituitary gland malfunction results in reduced release of thyroid stimulating hormone (TSH). TSH, in turn, activates the thyroid gland, leading to a release of thyroxine or T4 and triiodothyronine or T3 hormones. Thus clinical presentation will be dependent on dysfunctional pituitary and on the hypothyroid state of the patient. Secondary hypothyroidism can be acquired or congenital. The latter is linked to more severe dynamics, retardation of skeletal growth, and disturbed mental development [1].

Pituitary dysfunction can occur due to a tumor that compresses the gland and interferes with its functioning. Craniopharyngiomas, brain tumors, and hematologic malignancies can present the etiologic factor in children [2]. Chemotherapy administration in leukemic children can also cause damage to the gland [3]. Adults generally present with macroadenoma of the pituitary or have had previous exposure to iatrogenic factors such as radiation therapy or surgeries with a high risk of pituitary trauma [4]. Reduced secretion of hormones from the pituitary gland apart from TSH also contributes to clinical presentation. Failed release may lead to amenorrhea, infertility, weight loss, hypoglycemia, and diabetes insipidus [5].

Clinical presentation of a hypothyroid state differs by some factors. Such factors are the age of onset, duration of hypothyroidism, the cause of the disease, and extent of additional contribution to the presentation by the pituitary gland. Generally, hypothyroidism is associated with slower basal metabolic rate, patients may gain weight by retention of salt, water, and an increase in body fat. About 10% increase in body weight is usually observable. Fat tissue is affected by disrupted lipolysis and biosynthesis of fatty acids. Other manifestations include fatigue, headaches, periorbital edema, adynamia, constipation, dryness of skin, intolerance to cold, and cardiovascular signs such as bradycardia [5].

Secondary hypothyroidism diagnosis is based on clinical presentation and evaluation of thyroid stimulating hormone (TSH), T3, and T4 hormone levels in the serum. TSH measurement exhibiting high levels of TSH implies primary hypothyroidism disregarding the etiological factor or severity of the disease and excludes secondary hypothyroidism as a possible cause [6]. The acceptable range of TSH in a healthy human is 0.4 mIU/L to 4.0 mIU/L and may vary between age groups, nationalities, and races. For example, blacks tend to have lower levels of TSH than other races. This finding established a ground for the introduction of TSH reference range regulations based on variables of age and ethnicity [7].

Laboratory findings indicative of secondary hypothyroidism is subnormal or decreased TSH due to this hormone's delayed or disturbed secretion into the bloodstream. Because TSH is secreted improperly, FT4 levels (standing for free thyroxine or free T4) will be low as well due to hypostimulation of the thyroid gland [8].

By definition, secondary hypothyroidism occurs in cases of pituitary impairment. That is why imaging studies such as MRI scan of the head are essential diagnostic tools for discovering the cause of the disease [8].

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