Short stature and its treatment.

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The axiom that diagnosis must precede treatment holds true for the management of short stature. What matters is the current rate of growth and the potential for further growth; it is essential to measure accurately the rate of gain in height and the radio logical bone age. Early detection of subnormal rate of growth can lead to prevention of dwarfism, but a dwarf with epiphyses closed is beyond remedy. A child's rate of gain in height is determined by genetic factors that require a benign internal environment for their full expression. No form of therapy can alter a genetically determined height velocity; treatment is possible if an adverse internal environment can be corrected. Smith1 gave an excellent account of the various forms of dwarfism, including the many eponymous genetic syndromes. The genetic short stature of atypical Turner's syndrome may not be recognized unless the karyotype is known from chromosomal studies. A more common difficulty in diagnosis is the normal slow-growing short child of short parents; the normality is obvious only if the child's height is corrected for parental height, using the data of Tanner et al.2 Any prolonged illness creates an adverse environment that slows the rate of gain of height. In the same way cyanotic congenital heart disease, chronic hepatic or renal failure, and uncontrolled diabetes mellitus stunt growth. Deficient food intake or absorption are more easily rectified causes of subnormal rate of gain of height. The dietary intake, both in quantity and quality, must be discovered. Steatorrhoea may present as short stature with minimal symptoms referable to the gut. The curious phenomenon of low height velocity due to emotional deprivation3 is difficult to separate from the nutritional stunting that may affect such unfortunate children. Obviously successful treatment of short stature depends on identifying and removing these adverse environmental conditions. Endocrine causes of subnormal height velocity are not common. Primary thyroid failure severely limits statural growth and may not be immediately apparent. Adequate tests of thyroid function are always required in assessing growth failure. It is also difficult to distinguish primary from secondary failure of the thyroid due to pituitary lesions. Pituitary function is modi fied by primary thyroid failure and the secretion of growth hormone is diminished. Therefore, it is not possible to obtain an accurate measure of the pituitary's capacity to secrete growth hormone unless the level of circulating thyroid hormone is normal. That glucocorticoid excess can seriously diminish height velocity is well known from the study of Cushing's