RETARDED linear growth in hypothyroidism has been attributed to three causes: (1) secondary hypopituitarism with decreased growth hormone (GH) secretion; (2) reduced sensitivity of peripheral tissues to GH; and (3) fall in the caloric intake.1 Shiekholislam et al2 have reported abnormally low levels of plasma GH in seven of ten hypothyroid children after stimulation with insulin hypoglycemia. The children with impaired GH responses were subsequently restudied when they were euthyroid and experiencing normal growth. Their GH responses to hypoglycemia were then found to be normal.
This article is concerned with the results of serial evaluations of plasma GH responses in eight children with hypothyroidism. The study was designed to determine whether GH responsiveness estimated by established stimuli becomes normal prior to, concurrent with, or after the clinical and growth improvements which accompany thyroid replacement. Therefore, GH responses, growth rates, thyroid hormone levels, and bone maturation were assessed