自身免疫性多内分泌腺病综合征Ⅰ型1例

本文报道1例特发性甲状旁腺功能减退症(idiopathic hypoparathyroidism,IHP)并发桥本甲状腺炎的自身免疫性多内分泌腺病综合征(autoimmune polyendocrinopathy syndrome,APS)Ⅰ型。患者为22岁女性,情绪悲观2年,反复四肢强直性痉挛1年半,长期服用抗抑郁药物和抗癫痫药物治疗效果差,实验室检查发现低钙血症、高磷血症,甲状腺自身抗体阳性、甲状腺素、甲状旁腺素水平降低,血清肌酶水平明显升高,给予钙剂、维生素D制剂、左甲状腺素钠治疗后,随血钙上升,血磷、肌酶恢复正常,情绪好转,停用抗癫痫药物后无肢体抽搐,同时对相关文献进行复习和总结。     

妊娠糖尿病孕妇骨代谢状况的研究

目的探讨妊娠糖尿病（GDM）孕妇与正常孕妇骨代谢特点的异同。方法比较67例妊娠糖尿病患者（GDM组）与13例正常糖耐量孕妇（NGT组）血钙、磷、ALP、250HD、CTx、24h尿钙、跟骨超声（SOS）等骨代谢指标的异同。然后将GDM组患者分为A、B两组,分别给予低、高两种不同剂量钙和维生素D干预至分娩前,比较两组治疗前后上述指标的差异。结果GDM组血钙、磷为（2．3±0．1）mmol／L、（1．3±0．2）mmol／L,NGT组血钙、磷分别为（2．2±0．1）mmol／L,（1．1±0．1）mmol／L（P〈0．05）;GDM组和NGT组24h尿钙均升高;GDMB组24h尿钙治疗前为（11．0±6．9）mmol／L,治疗后为（8．2±4．3）mmol／L,明显下降（P〈0．05）。结论GDM孕妇骨代谢特点和NGT孕妇基本相同,24h尿钙均显著增加。GDM可能导致血钙、磷轻度增加。补充足量的钙剂和维生素D可使尿钙丢失减少。     

注射维生素D治疗佝偻病可不用钙剂

传统观点认为,对佝偻病病儿注射维生素D前应先用3天钙剂,以免发生低钙抽搐。近来研究认为,维生素D进入人体后,不仅不会降低血钙,反而可升高血钙。1984年我们通过动物(鸡)实验发现,鸡注射维生素D后,其血清钙较注射前明显升高(均未用钙剂)。为此。我们对182例佝偻病病儿在施行维生素D_3突击治疗前,均未用钙     

40例氟骨症患者钙代谢的研究

本文报道了湖南省灰汤地区40例氟骨症患者的钙代谢研究的结果,表明氟骨症病人为负钙平衡(P<0.01),其主要机制为肠钙净吸收率降低,尿钙增加和饮食饮水内含钙不足。钙剂加维生素 D 治疗一月后病人的负钙平衡被纠正(P<0.01),血钙恢复到正常水平,(R<0.05),血氟下降(P<0.05),而安慰剂治疗一月后无上述作用。本研究说明钙剂对氟骨症的治疗和预防均是有益的。     

2型糖尿病患者尿白蛋白排泄量与尿电解质变化的关系(附80例分析)

目的:了解2型糖尿病(type 2 diabetes mellitus,T2DM)患者尿白蛋白排泄量不同时尿电解质的变化。方法:收集T2DM患者80例,根据24h尿白蛋白排泄量(24h urine albumin excretion,UAE)分为正常蛋白尿组(NA组,UAE<30mg/24h)、微量蛋白尿组(MA组,UAE30～300mg/24h)及大量蛋白尿组(PR组,UAE>300mg/24h),观察24h尿电解质(尿钠、钾、钙、磷、镁)排泄量,血电解质及反映肾功能的各生化指标水平。结果:PR组24h尿钠、钙、磷高于MA组和NA组,MA组高于NA组(均P<0.05)。PR组24h尿钾低于MA组和NA组,MA组低于NA组(均P<0.05)。PR组血浆钙、镁低于MA组和NA组(均P<0.05)。24h尿钠与24h尿钾、肌酐清除率(creatinine clearance,Ccr)负相关,与尿β2-MG、血肌酐(SCr)正相关;血25-(OH)D3与24h尿钙、磷、镁、SCr负相关,与血钙、血镁、Ccr正相关;24h尿钙与尿磷正相关,与血钙负相关;血钙与血磷、血镁正相关(均P<0.01)。结论:2型糖尿病患者尿电解质排泄量随尿白蛋白排泄量不同而改变。     

活性维生素D临床应用

活性维生素D在临床上应用广泛。对于肝、肾功能逐渐衰退,伴有肌少症和/或神经功能损害的老年骨质疏松症(osteoporosis,OP)患者,妊娠/哺乳相关的OP及骨密度(bone mineral density,BMD)下降患者,均可适当补充。活性维生素D联合钙剂是甲状旁腺功能减退症和骨软化症的首选治疗方案,同时也是慢性肾脏病-矿物质和骨异常患者预防和治疗继发性甲状旁腺功能亢进症的主要措施之一。活性维生素D治疗窗相对狭窄,用药期间需要定期监测安全性指标,如血钙磷、尿钙磷及全段甲状旁腺素等。     

两种维生素D防治SLE激素治疗期骨质疏松的对比研究

目的　比较维生素 D3与钙三醇治疗系统性红斑狼疮 (SL E)长期激素治疗并发骨质疏松的疗效 ,制定维生素 D3安全有效维持剂 量。方法　随机分组 ,维生素 D3组 (G1 ) 2 7例 ,给患者肌注维生素 D360万 U,每周 1次肌注 ,待血钙正常改为 2 w1次。对照组 (G2 ) 3 3例 ,给 患者口服钙三醇 0 . 2 5μg/日。两组用药 8w,分别于用药前及用药后 2、 4、 8w检测两组血 1 , 2 5(OH) 2 D3、甲状旁腺激素 (i PTH)、钙、磷、碱性磷酸酶 (A LP)的浓度。结果　血 1 , 2 5(OH) 2 D3浓度 :G1 用药 2 w时升高 ,未达正常水平 , G2 达正常水平 (P<0 . 0 5)。治疗 4w时 ,两组 均达正常水平。血 i PTH浓度 :两组治疗 2 w时开始下降 , 4w达正常水平 (P>0 . 0 5)。血钙、磷、AL P浓度的变化两组比较无明显差异。G2 3例 出现高钙血症 , 3例钙磷乘积 >70 , G1 无 (P<0 . 0 1 )。结论　两种药疗效相同。G1 未出现高钙血症及钙磷乘积升高而优于钙三醇 ,以其用药次数 少、价格低廉、安全有效的优势易于推广。     

140例移植肾受者骨质丢失原因分析

目的研究调查移植肾受者骨密度并分析其主要影响因素。方法选取移植肾功能正常的受者140例，其中50例患者移植前检测血钙、磷、甲状旁腺激素、骨钙素、活性维生素D、尿钙和尿吡啶啉，双能X线吸收法测定腰椎和股骨近端骨密度。结果移植前患者钙、磷代谢异常明显，移植后血钙、磷、甲状旁腺激素、骨钙素、活性维生素D等均有明显改善，但尿钙／肌酐和尿吡啶啉／肌酐有增高趋势，股骨骨密度明显下降。平均每日激素用量为移植后尿钙／肌酐的主要预测因素。每日环孢素用量、体重指数与移植受者各部位骨密度明显正相关。累计激素用量是肾移植绝经女性病人腰椎和股骨颈骨密度的不良预测因素。结论患者肾移植后骨量减少和骨质疏松的发生率较高。骨质吸收增加可能是其主要原因。激素是移植。肾受者尤其绝经女性骨质吸收增加的主要因素之一。     

1,25-二羟胆骨化醇与结节病高血钙症

已知结节病患者常产生高血钙症和高尿钙症,但其钙代谢异常的发病机理至今仍是一个谜。以往认为结节病钙代谢异常是对维生素 D 的敏感性异常,或维生素内源性产生过度与肠道吸收钙增加,高血钙症和/或高尿钙症,骨对维生素 D 作用的过度敏感和对甲状旁腺激素(PTH)过高的反应等均为有关因素。作者对1例36岁患结节病的男性患者进行7年连续观察。发现7年中出现4次自发的高血钙症,均发生在夏季月份。其间血清25-羟胆骨化醇(25-OHD_3)随高血钙症有轻度升高,但均在正常范围内(3～     

不同药物对糖尿病骨质疏松的短期疗效比较

把糖尿病事并骨质疏松而血糖控制满意的患者分为单纯加用钙剂组（组１）、钙剂加维生素Ｄ２组（组２）、钙剂加钙全组（组３）、钙剂加密息组（组４）及单纯尿治疗组为对照组（组５），治疗三个月后进行疗效比较。结果组１、组５治疗前后骨密度、骨代谢指标（血钙、血磷、碱性磷酸酶（ＡＫＰ）、血甲主腺激素（ＰＴＨ）、尿羟脯氨酸（均无明显变化）（Ｐ〉０．０５）。组２治疗后ＰＴＨ明显降低（Ｐ〈０．０５）。组３、组４血ＰＴＨ     

Prevalence of calcium sensing receptor autoantibodies in patients with sporadic idiopathic hypoparathyroidism

OBJECTIVE: The pathogenesis of sporadic idiopathic hypoparathyroidism is unclear. The calcium sensing receptor (CaSR) plays a pivotal role in extracellular calcium homeostasis and is the candidate autoantigen in hypoparathyroidism associated with autoimmune polyglandular endocrinopathy syndrome. We therefore looked for antibodies (Ab) against the CaSR in patients with sporadic idiopathic hypoparathyroidism and their association, if any, with the major histocompatibility complex (MHC) class II human leukocyte antigen (HLA)-DR haplotypes. METHODS: The subjects included 51 patients with sporadic idiopathic hypoparathyroidism and 45 healthy controls. Investigations included computerised tomography, serum calcium, phosphorus, thyroxine, TSH, cortisol, intact parathyroid hormone (iPTH), ACTH and thyroid peroxidase (TPO) and adrenal antibodies. The CaSRAb were assayed in patients' sera by Western blot. Genotyping of the HLA-DR locus was performed using PCR and sequence-specific oligonucleotide probes. RESULTS: Intracranial calcification and cataract were present in 76.5% and 41.1% of the patients respectively and 62.7% had convulsions. Autoantibodies against the 168 kDa CaSR protein were demonstrated in the serum of 49.0% of the patients and in 13.3% of the controls (P<0.001). Pre-incubating serum samples from the CaSRAb-positive patients with parathyroid membrane produced a 90% decrease in the band intensity. HLA-DRB1*01 and DRB1*09 alleles were significantly associated with idiopathic hypoparathyroidism (relative risk of 7.8, P=0.001). The frequency of HLA-DRB1*09 and DRB1*10 alleles tended to be higher in patients positive for the CaSRAb. There was no significant difference in the frequency of occurrence of convulsions, cataract, intracranial calcification, calcium:phosphorus ratio, and iPTH levels between patients with and without CaSRAb. CONCLUSION: 49.0% of the patients studied had serological evidence of organ-specific autoimmunity against the CaSR protein. The occurrence of CaSRAb and the HLA-DR associations imply an autoimmune component to the disease, but the primary role of the CaSRAb in the pathogenesis of the disease needs to be assessed further.     

Prevalence of clinical remission in patients with sporadic idiopathic hypoparathyroidism

Background Remission of disease activity is a characteristic feature of autoimmune endocrine disorders such as Graves’ disease, Addison’s disease and occasionally in patients with premature ovarian failure. Autoimmunity is also implicated in sporadic idiopathic hypoparathyroidism (SIH) with clinical remission of disease reported in three cases. Objective To assess the rate of remission in patients with sporadic idiopathic hypoparathyroidism and review the cases reported so far. Subjects and methods Subjects included 53 patients (M:F, 24:29) with SIH who had been symptomatic for at least 1 year (range 1–31 years). They were treated with calcium and 1‐α‐(OH)D₃/cholecalciferol therapy and had a mean duration of follow up of 5·0 ± 3·2 years. Treatment was withdrawn in two stages in the patients who maintained normal levels of serum total calcium during the preceding year of treatment. In stage‐1, the dose of therapy was reduced to half and subsequently all treatment was stopped (stage 2) in those patients who maintained normal serum total calcium levels on the reduced dose. Remission of SIH was defined as maintenance of normal serum total (≥2·12 mmol/l) and ionized calcium, inorganic phosphorus and serum intact parathyroid hormone (iPTH) for at least 3 months after withdrawal of calcium and 1‐α‐(OH)D₃/cholecalciferol therapy. Calcium sensing receptor autoantibodies (CaSRAb) were determined by Western blot. Results Two of the 53 patients (3·8%) with SIH stayed in remission for 1 year after complete withdrawal of therapy. CaSRAb was absent in both the cases. The clinical features, age at onset and duration of hypocalcaemic symptoms in cases with remission were comparable to those who did no show remission. Conclusion Sporadic idiopathic hypoparathyroidism is not irreversible as is widely believed and spontaneous remission of disease may occur in 3·8% of patients.     

FGF-23 is elevated by chronic hyperphosphatemia

The Identification and characterization of FGF-23 has provided an opportunity to gain new insight into phosphorus metabolism. Circulating FGF-23 promotes renal excretion of phosphorus, and FGF-23 is measurable in the serum of normal subjects. Serum levels of FGF-23 are elevated in patients with renal phosphate wasting disorders such as tumor induced osteomalacia, X-linked hypophosphatemia and fibrous dysplasia. However, the factors that alter its serum concentration are not known. The study of serum FGF-23 is confounded by the fact that high serum calcium, PTH, and any other putative phosphotonins, have similar effects on serum and urine phosphorus. To circumvent the confounding effect of serum PTH and calcium, we studied serum FGF-23 and phosphate levels in patients with chronic hypoparathyroidism and hyperphosphatemia. Serum was collected in the morning after an overnight fast from three groups: 1) 9 patients with chronic hypoparathyroidism on stable treatment with calcium and calcitriol, 2) 9 patients with primary hyperparathyroidism, and 3) 77 normal controls. Patients with hypoparathyroidism had predictably higher levels of serum phosphorus than patients with hyperparathyroidism or normal controls (5.6 +/- 1.1, 3.1 +/- 0.6, and 3.1 +/- 0.5 mg/dL, mean +/- 1 SD, respectively (p < 0.01 for hypoparathyroid vs. either group)). They also had higher levels of FGF-23 (150 +/- 120 vs. 70 +/- 60, or 55 +/- 20 RIU/ml, respectively (p < 0.05 vs. either group)). In conclusion, serum FGF-23 levels are elevated in patients with hyperphosphatemia and chronic hypoparathyroidism, suggesting a feedback system in which serum FGF-23 responds to serum phosphorus and regulates it. However, in the setting of chronic hypoparathyroidism, the degree of elevation of FGF-23 is insufficient to normalize serum phosphorus.     

Effects of endogenous and exogenous parathyroid hormone on tubular reabsorption of calcium in pseudohypoparathyroidism

Resistance to the proximal tubular actions of PTH is a well defined feature in patients with pseudohypoparathyroidism type I (PsH). However, it is less clear whether there also is resistance to the distal tubular effect of PTH on calcium reabsorption in these patients. Thus, we examined the effects of endogenous and exogenous PTH on calcium reabsorption in seven patients with PsH before and during treatment with 1 alpha-hydroxyvitamin D3 (1 alpha OHD3). Eleven patients with idiopathic hypoparathyroidism served as controls. Before treatment, urinary calcium excretion was comparable in the two groups and did not decrease significantly after PTH infusion in either group. During treatment with 1 alpha OHD3, in contrast, steady state urinary calcium excretion in patients with PsH was much lower than that in patients with idiopathic hypoparathyroidism at comparable serum calcium concentrations and did not exceed the upper limit of the normal range when PsH patients were normocalcemic. Infusion of PTH into 1 alpha OHD3-treated PsH patients led to a significant reduction in urinary calcium excretion, even though PTH had no effect on their urinary cAMP or phosphate excretion. These findings suggest that the renal resistance to PTH in patients with PsH is confined to its proximal tubular actions and does not include its distal tubular effect on calcium reabsorption, at least during treatment with active vitamin D metabolites.     

Long-term treatment of hypoparathyroidism: a randomized controlled study comparing parathyroid hormone-(1-34) versus calcitriol and calcium

Hypoparathyroidism is one of the few remaining hormonal insufficiency states for which replacement therapy is unavailable. Previous short-term controlled trials have shown PTH to be a safe and effective treatment of hypoparathyroidism. In this randomized, parallel group, open-label trial, we compared synthetic human PTH-(1-34) (PTH) with conventional therapy, calcitriol and calcium, over a 3-yr period. Twenty-seven patients with confirmed hypoparathyroidism, aged 18-70 yr, were randomized to either twice daily sc PTH or oral calcitriol and calcium. The primary end points were calcium levels in serum and urine. Secondary end points were creatinine clearance, markers of bone turnover, and bone mineral density. Throughout the 3-yr study period, serum calcium levels were similar in both treatment groups within or just below the normal range. Mean urinary calcium excretion was within the normal range from 1-3 yr in PTH-treated patients, but remained above normal in the calcitriol group. Bone mineral content and bone mineral density showed no significant between-group differences over the 3-yr study period. We conclude that treatment with twice daily sc PTH provides a safe and effective alternative to calcitriol therapy and is able to maintain normal serum calcium levels without hypercalciuria for at least 3 yr in patients with hypoparathyroidism.     

Development of systemic lupus erythematosus in a patient with hypoparathyroidism: a case report and review of the literature

Systemic lupus erythematosus (SLE) is an autoimmune disease in which organs undergo damage. Hypoparathyroidism is a rare disease, which presents in two forms: hereditary and acquired. Cases of hypoparathyroidism and SLE rarely co‐exist. Only six cases have been reported; five of them first presented with lupus and then hypoparathyroidism or simultaneously. We present here developing lupus disease in a woman who had idiopathic hypoparathyroidism. According to increasing data about the autoimmune origin of idiopathic hypoparathyroidism, these case reports suggest that there may be an autoimmune process linking these diseases.     

Ⅱ型糖尿病肾病和非肾病患者甲状旁腺激素和钙磷代谢关系的初步探讨

测定４６例Ⅱ型糖尿病患者（肾病２５例，非肾病２１例）和２４例正常人血清甲状旁腺激素（ＰＴＨ）、钙（Ｃａ）、磷（Ｐ）、碱性磷酸酶（ＡＫＰ）、肌酐（Ｃｒ）和尿白蛋白（Ａｌｂ），发现糖尿病患者血ＰＴＨ、ＡＫＰ和尿Ｐ浓度较正常人增高，血Ｃａ、Ｐ浓度较正常人降低，其中肾病患者ＰＴＨ值又较非肾病组增高，差异有显著性。相关分析示糖尿病肾病的ＰＴＨ值与血Ｃｒ、ＡＫＰ和尿Ｐ有较好的相关性。作者认为糖尿病患者存在钙、磷代谢异常，体钙缺乏，这种代谢异常在糖尿病肾病患者尤为明显，血清ＰＴＨ值、ＡＫＰ和尿Ｐ浓度是反映糖尿病肾病钙、磷代谢异常的有意义指标。     

Pattern of bone mineral density in patients with sporadic idiopathic hypoparathyroidism

OBJECTIVE: Measurement of bone mineral density (BMD) in patients with hypoparathyroidism directly addresses the effect of chronic under-exposure of bone to PTH. Because post-thyroidectomy hypoparathyroidism is potentially complicated by the pre-existence of thyrotoxicosis and the need for postoperative thyroxine replacement, we have studied a large group of patients with sporadic hypoparathyroidism who have been followed up in our endocrine clinic. Studies conducted in limited number of patients with sporadic idiopathic hypoparathyroidism (SIH) have suggested an increase in BMD in such patients. In this current study, we have measured BMD in a large cohort of patients with SIH and have assessed the relationship of BMD with duration of disease and with the adequacy of treatment, as indicated by follow-up serum calcium, phosphate and alkaline phosphatase levels. DESIGN: Case control study and intra-group comparison. SUBJECTS: Forty-seven patients (M : F ratio 23 : 24) with SIH who had been reviewed during 2003-2004 in our endocrine clinic were recruited for this study. Their mean age (+/- SD) was 34.6 +/- 13.6 years and the duration from the time of initial diagnosis was 9.6 +/- 8.5 years. Forty-eight match healthy volunteers were recruited from hospital staff and from normocalcaemic relatives. METHODS: Bone mineral density was measured at total lumbar spine (L1-L4), hip and forearm by dual energy X-ray absorptiometry (DXA). The relationship of BMD was analysed with duration of disease symptoms (group I, < or = 1 year, group II, > 1 and < 5 years and group III, > or = 5 years) and mean serum total calcium observed during follow-up (group A, calcium < or = 1.79 mmol/l and group B, > or = 1.80 mmol/l). RESULTS: Patients with SIH showed significantly higher BMD at total lumbar spine and hip when compared to controls (1.098 +/- 0.187 vs. 0.936 +/- 0.131 g/cm2 and 0.967 +/- 0.141 vs. 0.882 +/- 0.149 g/cm2, P < 0.001 for both). BMD in the forearm was not significantly different in patients and controls. The age- and BMI-adjusted lumbar spine BMD showed correlation with duration of disease (r = 0.348 and P = 0.019). Patients with longer duration of hypoparathyroidism had higher BMD at lumbar spine (group I vs. group III, 0.951 +/- 0.132 vs. 1.156 +/- 0.180 g/cm2, P < 0.05). There was no significant correlation between BMD values in patients with SIH and their mean serum total calcium levels during the period of follow-up (r = 0.192, P = 0.206). Neither was the mean BMD significantly different between group A and B. Serum total alkaline phosphatase showed a significant negative correlation with BMD at lumbar spine (r = -0.445, P = 0.012). CONCLUSIONS: Patients with sporadic idiopathic hypoparathyroidism have increased mean BMD in the lumbar spine and hip but not in the forearm, compared to normal matched healthy controls. The increase in BMD is related to the duration of the disease rather than the serum calcium levels.     

A case of idiopathic hypoparathyroidism complicated with chronic thyroiditis]

It has been suggested that autoimmunity and genetic factors may play a specific role in the development of idiopathic hypoparathyroidism. We reported a case of idiopathic hypoparathyroidism complicated with chronic thyroiditis. The patient, a woman 40 years old, visited our clinic because of tetany of both hands and dizziness. She was of short stature with a round face. She also had a goiter, hypocalcemia, hyperphosphatemia and decreased parathyroidal function, but renal function was normal. Her TSH level was slightly high with a positive microsome test (x 1600), and the levels of thyroid hormones tended to be low. Based on Ellsworth-Howard test findings, a diagnosis of idiopathic hypoparathyroidism was made, with the complication of chronic thyroiditis confirmed by the thyroidal biopsy. Administration of l alpha-OH-D3 normalized the level of serum calcium. No special treatment was given for the chronic thyroiditis in order to observe its natural course. Her TSH returned to normal, and the level of thyroid hormones was increased to normal ranges. Tests were positive for anti-adrenal antibody and anti-gastric antibody. The complication of chronic thyroiditis, an autoimmune disease, and a positive finding for every antibody suggested the possible involvement of autoimmunity in the mechanism of development of idiopathic hypoparathyroidism. The administration of 1 alpha-OH-D3 resulted in an increase in the serum calcium level and also normalization of levels of TSH and thyroid hormones. Thus, it is likely that the elevation of the calcium ion or immunoregulation by active vitamin D may have induced the increase in thyroid hormone secretion.     

Moderate hypocalcemia due to normal serum 1,25-dihydroxyvitamin D levels in an asymptomatic kindred with familial hypoparathyroidism

Hypoparathyroidism was diagnosed in nine members of a kindred of three generations. This study investigated why these persons were asymptomatic and without developmental abnormalities, in contrast to the common presentation of idiopathic hypoparathyroidism. In the hypocalcemic subjects, serum calcium level was 7.4 +/- 0.8 mg/dl (mean +/- SD) and ionized serum calcium level was 3.48 +/- 0.21 mg/dl. Immunoreactive parathyroid hormone values were inappropriately low. Injection of EDTA in one patient lowered ionized calcium levels, but immunoreactive parathyroid hormone values did not rise. Serum levels of 1,25-dihydroxyvitamin D and other vitamin D metabolites were normal or elevated and substantially higher than in other hypoparathyroid states. The normally observed positive correlation between the fasting urinary calcium/creatinine ratio and serum 1,25-dihydroxyvitamin D that reflects the dependence of net bone resorption on 1,25-dihydroxyvitamin D was upheld in hypoparathyroid patients. It is proposed that the subjects with familial hypoparathyroidism in this kindred had moderate asymptomatic hypocalcemia without developmental abnormalities because normal or elevated serum 1,25-dihydroxyvitamin D levels enhanced intestinal calcium absorption. This may represent one point in the spectrum of idiopathic hypoparathyroidism. Alternately, both the moderate degree of hypocalcemia and the normal serum calcitriol values could have been related to mild, partial hypoparathyroidism, which could have been inherited in this kindred.