PTHmRNA and vitamin D_3 receptor RNA in primary hyperparathyroidism.

1.原发性甲状旁腺功能亢进症患者肾内碳酸氢盐代谢研究10例原发性甲状旁腺功能亢进症患者行甲状旁腺切除术前后肾内碳酸氢盐的处理及酸碱平衡的变化。手术前后酸碱平衡无明显改变.原发性甲状旁腺功能亢进症患者骨密度的研究本研究对15例原发性甲状旁腺功能亢进症患者行甲状旁腺切除术前后的骨密度进行了评价，结果显示，化学型和肾结石型原发性甲状旁腺功能亢进症患者骨密度降低。手术后，颅骨和腰椎的骨密度立即增加。手术前后下肢骨密度无明显变化.原发性甲状旁腺功能亢进症（甲状旁腺腺瘤）组织中PTHmRNA和维生素D_3受体RNA的表达然而，用北方螺栓法检测甲状旁腺腺瘤中PTHmRNA和维生素D_3受体RNA均失败。尽管过量的内源性PTH抑制了肾小管碳酸氢盐的阈值，并且增加了滤过负荷的尿碳酸氢盐排泄分数。原发性甲状旁腺功能亢进的碱平衡可能是由于肾外酸缓冲能力（可能是骨）增强所致。

1. Renal bicarbonate metabolism in patients with primary hyperparathyroidismThis study evaluated the acid-base balance and renal handling of bicarbonate in ten patients with primary hyperparathyroidism before and after parathyroidectomy.Renal tubular threshold of bicarbonate increased and fractional urinary bicarbonate excretion of the filtered load decreased after parathyroidectomy. However, no disturbances or changes in acid-base balance were observed before and after surgery.2. Bone mineral density in patients with primary hyperparathyroidismThis study evaluated the bone mineral density in 15 patients with primary hyperparathyroidism before and after parathyroidectomy.Bone mineral density decreased in the patient, with primary hyperparathyroidism of chemical and renal stone types. After surgery, bone mineral density of the skull and lumbar spine increased immediately. However, no changes in bone mineral density of the lower limbs were observed before and after surgery.3. PTHmRNA and vitamin D_3 receptor RNA in primary hyperparathyroidismTotal RNA of the parathyroid gland could be measured in five patients with primary hyperparathyroidism (parathyroid adenomas). However, the measurement of the PTHmRNA and vitamin D_3 receptor RNA in parathyroid adenomas using Northern bolt methods were failed.We conclude that primary hyperparathyroidism does not induce an acid-base disturbance, although the renal tubular threshold of bicarbonate is suppressed and fractional urinary bicarbonate excretion of filtered load is increased by excessiv endogenous PTH.Normal acid-base balance in primary hyperparathyroidism might be due to enhancement of extrarenal acid buffering capacyty (probably, bone).