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Hypothyroidism is one condition that many of us want to choose if we had the opportunity to choose our disease. It is easily correctable, with a minimum of fuss and cost.
Disorders of thyroid are second only to diabetes mellitus in endocrine practice. Of the thyroid disorders hypothyroidism is most frequent in these parts of the country.
Deficient thyroid function results commonly from inadequate hormone secretion from the thyroid gland (primary hypothyroidism). Secondary hypothyroidism is rare in which pituitary TSH is deficient, although the thyroid is intrinsically normal.
In India iodine deficiency disorder is a significant problem of goitrous hypothyroidism. Hyperthyroidism treated by radio iodine ablation can result in thyroid deficiency. Spontaneous atrophic hypothyroidism, or Hashimotos thyroiditis are other causes, along with dyshormonogenesis.
The symptoms depend on how complete and how rapid the thyroid failure occurred. The clinical features of our patients included:
In areas where endemic goitre is severe, endemic cretins are present; they are defined epidemiologically by their associated with endemic goitre and iodine deficiency, by mental deficiency and by other features such as defects of hearing and speech, squint, stance and gait disorders, retarded growth and hypothyroidism. Endemic cretins can be subdivided into myxedematous and neurological cretinism.
Once the clinical suspicion of hypothyroidism occurs, biochemical confirmation is possible by showing low levels of serum thyroxine (T4) and triiodiothyronine (T3). In the usual variety of primary hypothyroidism serum TSH level may be elevated even before serum thyroid hormone levels fall. Therefore primary hypothyroidism can be confirmed by elevated TSH levels alone. However a correlation between the clinical picture and the lab investigations is necessary.
Should the clinical suspicion of thyroid deficiency be strong and the serum TSH is in the normal range, secondary hypothyroidism should be considered, when low levels of serum T4 are due to deficiency of pituitary TSH. Such conditions are rare and may be seen in relevant conditions eg Sheehans syndrome, pituitary tumour operated on, congenital hypopituitarism in newborns and infants.
Available of reliable assays of thyroid hormones has rendered redundant the older indirect methods such as basal metabolic rate, serum cholesterol level.
Once hypothyroidism is confirmed treatment consists of thyroxine replacement. Sodium thyroxine, a synthetic compound is the drug of choice.
Replacement can be started with the full dose (0.1-0.15 mg a day) in the young, otherwise healthy adult without evidence of other endocrinopathies (eg Addisons disease).
If in doubt a smaller starting dose is gradually increased. One should consider possible coexistence of other auto immune disorders such as Addisons disease, when Addisonian crisis may be precipitated by thyroxine, without corticosteroids. Sometimes polyglandular auto immune failure or hypopituitarism are diagnosed this way.
Thyroxine replacement is best done first thing in the morning on an empty stomach; in the usual forms of hypothyroidism therapy is for life. One should consider rare exceptions such as transient reversion to euthyroid state, or even followed by spontaneous hyperthyroidism. The latter are extremely rare.
The usual replacement dose of thyroxine is 0.1-0.15 mg a day; larger doses may suppress pituitary TSH and lead to osteoporosis long term.
The dose of thyroxine replacement in neonatal hypothyroidism and in childhood is as follows
|Age||Dosage (ug/kg/d)||Range of dose|
|Birth to 6 mo
|Above 12 years
Neonatal screening for hypothyroidism is done in developed countries. With a prevalence of nearly 1:4000 such screening should be initiated in other countries also.
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