Pediatric endocrinologists were the only physicians interested in the arcana of GH metabolism and childrens growth, but their previously academic arguments took on new practical significance with major financial implications. The major scientific arguments dated back to the days of GH scarcity:
Everyone agrees on the nature and diagnosis of severe GH deficiency, but what are the edges and variations? How should marked constitutional delay be distinguished from partial GH deficiency? To what extent is "normal shortness" a matter of short children naturally making less growth hormone? Can a child make GH in response to a stimulation test but fail to make enough in "daily life" to grow normally? If a stimulation test is used to define deficiency, what GH cutoff should be used to define normal?It was the ethical questions that were new. Is GH not a wise use of finite healthcare resources, or is the physicians primary responsibility to the patient? If GH is given to most extremely short children to make them taller, will the definition of “extremely short” simply rise, negating the expected social benefit? If GH is given to short children whose parents can afford it, will shortness become a permanent mark of lower social origins? More of these issues are outlined in the ethics section. Whole meetings were devoted to these questions; pediatric endocrinology had become a specialty with its own bioethics issues. Despite the price, the 1990s became an era of experimentation to see what else growth hormone could help.
Hypocalciuria is a low level of calcium in the urine. It is a significant risk factor for predicting eclampsia in pregnancy. The most common causes for hypocalciuria is either thiazide diuretics or reduced dietary intake of calcium. The other cause is Familial hypocalciuric hypercalcemia (FHH). Low dietary sodium causes hypocalciuria. It is also common in patients with Gitelman syndrome. == References ==