Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) influence hair follicles through paracrine and intracrine routes. There is significant evidence that PTH and PTHrP influence the proliferation and differentiation of hair follicle cells. The PTH/PTHrP receptor signalling plays an important role in the hair follicle cycle and may induce premature catagen-telogen transition. Transgenic mice with an overexpression or blockade (PTH/PTHrP receptor knockout mice) of PTHrP activity revealed impaired or increased hair growth, respectively. Some findings also suggest that PTHrP may additionally influence the hair cycle by inhibiting angiogenesis. Antagonists of the PTH/PTHrP receptor have been shown to stimulate proliferation of hair follicle cells and hair growth. A hair-stimulating effect of a PTH/PTHrP receptor antagonist applied topically to the skin has been observed in hairless mice, as well as in mice treated with cyclophosphamide. These data indicate that the PTH/PTHrP receptor may serve as a potential target for new (topical) hair growth-stimulating drugs, especially for chemotherapy-induced alopecia.
A 43-year-old man was admitted to the Endocrinology Department because of hypocalcaemia and hypomagnesaemia developed after surgical treatment of hyperparathyroidism. There was no history of coronary heart disease and hypercholesterolemia before admission, only moderate hypertension. At about 2 pm the patient experienced sudden chest pain radiating to the jaw and upper limbs. Electrocardiogram revealed temporary horizontal ST-segment elevation in II, III and aVF leads (Fig. 1). The patient was referred to the Cardiology Department and coroangiography was performed. There were neither atherosclerotic changes nor contraction of coronary arteries during angiography (Fig. 2A-C). Laboratory test made shortly after the onset of pain revealed severe ionised hypocalcaemia -0.69 mmol/L (1.13-1.29 mmol/L) and hypomagnesaemia -0.52 mmol/L (0.7-1.0 mmol/L). Troponin I level was within the normal range -0.039 ng/mL (0.0-0.056 ng/mL) but a slight elevation of creatine kinase-MB mass was present -4.6 ng/mL (0.0-3.6 ng/mL). The chest pain ceased following intravenous administration of calcium and magnesium. Two-dimensional transthoracic echocardiography showed normal left ventricular size and function with ejection fraction of 57%, mild left ventricular hypertrophy and mild mitral and tricuspid regurgitation (Fig. 3). Although coronary spasm secondary to hypocalcaemia is a very rare facet of angina, failing to consider it in differential diagnoses in all cases of variant angina might pose a grave threat to the patient's life.
Milk-alkali syndrome (MAS), characterized by renal failure, metabolic alkalosis and hypercalcemia, is a severe and life-threatening complication of the treatment of hypoparathyroidism. The clinical course is often sudden and is not preceded by any prodromal symptoms. Occurrence does not depend on the duration of hypoparathyroidism treatment, although it is closely related to the applied therapy, especially the dose of calcium carbonate and active vitamin D preparations. Drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate routine control, changing the calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i.e. vegetarian diet), pregnancy and other associated conditions are listed among the factors triggering MAS. A higher calcium carbonate dose is directly associated with an increased risk of milk-alkali syndrome. In case of a high calcium demand it is necessary to control renal function and monitor the level of calcium in the serum more frequently, aiming for the lower end of the reference range. If MAS has been confirmed or if there are alarming neurological symptoms suggestive of hypercalcemia, the patient must be sent to the hospital immediately. Treatment of MAS involves: discontinuation of calcium and vitamin D supplementation, and intravenous infusion of normal saline solution to eliminate volume deficiencies and to achieve forced diuresis while maintaining proper fluid balance. As soon as there is improvement in the patient's clinical condition, it is necessary to begin the treatment of comorbidities increasing the risk of renal failure or alkalosis (i.e. vomiting, diarrhea).
(1) Background: Parathyroid cystic adenomas (PCA) are rare entities representing only 0.5–1% of parathyroid adenomas, accounting for 1–2% of cases of primary hyperparathyroidism (PHPT). The purpose of this study was to compare classical and functional/secreting cystic parathyroid lesions and identify risk factors for severe hypercalcemia; (2) Methods: A total of 17 patients with PHPT and parathyroid cysts (study group) were compared with the group of 100 patients with hyperparathyroidism caused by adenoma or hyperplasia (control group). In both groups the majority were women (88% vs. 12%, with gender ratio 7, 3:1). The patients were examined preoperatively and postoperatively: PTH, creatine, calcium and phosphate serum and urine concentrations and calcidiol serum levels were assessed; (3) Results: Patients with parathyroid cyst had statistically higher PTH and calcium serum concentration, higher calciuria and lower serum phosphate concentration. There were no statistically significant differences in the concentration of creatine in serum and urine and tubular reabsorption of phosphorus (TRP); (4) Conclusions: Due to higher PTH and calcium levels, cystic parathyroid adenomas could be one of the rare risk factors for severe hypercalcemia and hypercalcemic crisis which can be life threatening.
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