There was no rebound effect following withdrawal of treatment, but a gradual return to pre-treatment bowel movement frequency should be expected. Minimal distribution of the drug occurs beyond the immediate gastrointestinal tissues. Lubiprostone is rapidly metabolized by reduction/oxidation, mediated by carbonyl reductase. There is no metabolic involvement of the hepatic cytochrome P450 system. The measurable metabolite, M3, exists in very low levels in plasma and makes up less than 10% of the total administered dose. Data indicate that metabolism occurs locally in the stomach and jejunum. References
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Functions of the calcium-sensing receptor
Parathyroid gland: mediates negative feedback mechanisms relating to PTH secretion. In normal individuals, PTH secretion decreases with increasing blood calcium levels. Loss of function abnormalities in the CaSR here cause hypercalcemia. Kidneys: mediates negative feedback mechanisms relating to calcium reabsorption from the tubular system. In normal individuals, reabsorption of calcium and other electrolytes decreases with increasing blood calcium level. Loss of function abnormalities in the CaSR here contribute to both hypercalcemia and hypocalciuria. Diagnosis
As most cases of FHH are asymptomatic and benign, the diagnosis of FHH is less likely to be made. Typically, diagnosis is made in the pursuit of uncovering the etiology of hypercalcemia. Calcium levels are often in the high normal range or slightly elevated. Commonly, the parathyroid hormone level is checked and may be slightly elevated or also on the high normal end. Normally, high calcium should cause low PTH and so this level of PTH is inappropriately high due to the decreased sensitivity of the parathyroid to calcium. This may be mistaken for primary hyperparathyroidism. However, evaluation of urine calcium level will reveal a low level of urine calcium. This too is inappropriate as high serum calcium should result in high urine calcium. If urine calcium is not checked, this may lead to parathyroidectomy for presumed primary hyperparathyroidism 
Additionally as the name implies, there may be a family history of benign hypercalcemia.Ultimately, diagnosis of familial hypocalciuric hypercalcemia is made—as the name implies—by the combination of low urine calcium and high serum calcium.