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At least 19 recordsLinked to original sources
PubMed1991

Partial hypoparathyroidism. A variant of transient congenital hypoparathyroidism.

We encountered three children who had neonatal hypocalcemia followed by a period of normocalcemia and recurrence of hypocalcemia later in childhood. They were full-term infants with normal birth weights who developed hypocalcemia within the first 48 hours after birth. The hypocalcemia resolved in 1 week, 3 months, and 14 months in the three patients. The recurrences of hypocalcemia occurred at 4, 7, and 12 years of age. Their plasma parathyroid hormone concentrations were consistently low but detectable. We suggest that partial hypoparathyroidism is the underlying abnormality in these patients and that neonatal hypocalcemia in otherwise healthy infants indicates the need for calcium measurements during childhood and adolescence.

Calcitriol↗
PubMed1982

Comparative efficacy of various vitamin D metabolites in the treatment of various types of hypoparathyroidism.

Fourteen patients with pseudohypoparathyroidism, 17 with idiopathic hypoparathyroidism, and 12 with postoperative hypoparathyroidism were treated with vitamin D2, dihydrotachysterol, 1 alpha-hydroxyvitamin D3)1 alpha-OHD3), and 1,25-dihydroxyvitamin D3 for 6-18 months. The optimal maintenance dose or minimum daily dose of 1,25-dihydroxyvitamin D3 to maintain serum calcium at approximately 8.5 mg/100 ml and control all the clinical symptoms was 1.3 +/- 0.16 micrograms/day (mean +/- SE) in pseudohypoparathyroidism, 1.5 +/- 0.18 micrograms/day in idiopathic hypoparathyroidism, and 1.9 +/- 0.50 micrograms/day in postoperative hypoparathyroidism. There was no significant difference in the optimal maintenance dose among the 3 groups. The optimal maintenance dose of 1 alpha-OHD3, however, was 2.0 +/- 0.12 micrograms/day in pseudohypoparathyroidism, significantly lower than that in idiopathic hypoparathyroidism (3.5 +/-0.29 micrograms/day; P less than 0.001) and in postoperative hypoparathyroidism (4.89 +/- 0.54 micrograms/day; P less than 0.001). Significantly lower doses were required in the treatment of idiopathic hypoparathyroidism than in postoperative hypoparathyroidism (P less than 0.05). No significant difference was found in the optimal maintenance dose of dihydrotachysterol and vitamin D2 among the 3 groups. The average pretreatment serum calcium levels and clinical manifestations were indistinguishable among the 3 groups of patients. This suggests that such a difference in the optimal maintenance dose of 1 alpha-OHD3 is ascribed not to the difference in the severity of hypoparathyroidism, but most probably to differences in the pathophysiological processes in pseudohypoparathyroidism and idiopathic or postoperative hypoparathyroidism. The excess parathyroid hormone levels in blood of patients with pseudohypoparathyroidism (and not in other types of hypoparathyroidism) may explain such a difference.

Adolescent↗
PubMed2006

Hypoparathyroidism in transfusion-dependent patients with beta-thalassemia.

Hypoparathyroidism is thought to be a rare consequence of iron overload seen in beta-thalassemic transfused patients. This study was conducted to determine the prevalence of hypoparathyroidism in a large number of beta-thalassemic patients, and its potential correlation with the presence of other endocrinopathies caused by iron overload. Serum and urine biochemical parameters were measured in 243 thalassemic patients (136 females and 107 males) in order to determine the prevalence of hypoparathyroidism and evaluate bone turnover. The patients were divided into two groups according to the presence of hypoparathyroidism. We compared the prevalence of other endocrinopathies and disease complications in the two groups. Hypoparathyroidism was detected in 13.5% of the patients (33 subjects; 17 males and 16 females). Serum-intact parathyroid hormone, and total and ionized calcium were significantly lower, while phosphorus was significantly higher in thalassemic patients with hypoparathyroidism. The reduction in BMD was more prominent in normal thalassemic patients (Z score = -2.246 +/- 0.97) compared with those with hypoparathyroidism (Z score = -1.975 +/- 0.89), although the difference was not statistically significant. Disturbed glucose metabolism was more common in patients with hypoparathyroidism (P < 0.05). In addition, heart dysfunction was statistically more frequent in this group (odds ratio = 2.51, P < 0.05). Hypoparathyroidism is a not infrequently observed complication in thalassemic patients. Since the concentration of ferritin is not a valuable tool in the prediction of the development of hypoparathyroidism, parathyroid function should be tested periodically, particularly when other iron overload-associated complications occur.

Adult↗
PubMed2003

Increased bone mineral density in patients with chronic hypoparathyroidism.

Bone mineral density (BMD) has been shown to be increased in postmenopausal females with postthyroidectomy hypoparathyroidism, but it is not known whether similar gains occur in patients with idiopathic hypoparathyroidism. In this study, we measured the BMD of lumbar spine and proximal femur in 14 patients, 8 with idiopathic hypoparathyroidism and 6 with postthyroidectomy hypoparathyroidism, using dual-energy x-ray absorptiometry. Their age ranged from 23-57 yr old, with a mean of 42.5 yr. The results showed that patients with hypoparathyroidism had a higher BMD than the normal age- and sex-matched population. This was particularly evident at the lumbar spine (L2-L4), with positive Z-score of 1.93 +/- 1.03, whereas Z-score at the femoral neck was 1.14 +/- 0.62 SD. Subgroup analysis showed that those with postthyroidectomy hypoparathyroidism had a mean lumbar spine BMD of 1.434 g/cm(2) and femoral neck BMD of 1.026 g/cm(2), compared with a mean BMD of 1.364 g/cm(2) and 1.022 g/cm(2) at spine and hip, respectively, for those with idiopathic hypoparathyroidism. Statistical analysis did not reveal any significant difference in the BMD, T-score, and Z-score of the bone, at these two sites, between the two groups. In conclusion, the state of chronic hypoparathyroidism is associated with increased BMD, especially at the lumbar spine. Those with idiopathic hypoparathyroidism have a similar degree of increase in BMD as those with postthyroidectomy hypoparathyroidism.

Absorptiometry, Photon↗
PubMed1999

Cognitive impairment and intracranial calcification in chronic hypoparathyroidism.

BACKGROUND: Intracranial calcification is associated with chronic hypoparathyroidism. The relationship between intracranial calcification, neurological abnormalities and cognitive deficits in this disorder is unknown. The purpose of this study was to determine whether chronic hypoparathyroidism is associated with cognitive impairment. METHODS: We studied 11 hypoparathyroid patients and compared them with a sex-, age-, and education-matched control group. The hypoparathyroidism was postsurgical in nine and idiopathic in two. All patients underwent nonenhanced head computed tomography, detailed neurological examinations, and a battery of cognitive tests. These tests were performed separately and individual examiners were blinded to the results of the other components of the study. RESULTS: The mean age of the patients was 55 years; the duration of hypoparathyroidism was at least 9 years. Neuropsychological testing revealed cognitive impairment in 65% of hypoparathyroid subjects, and the presence of significant differences between the hypoparathyroid and control groups. Computed tomography showed intracranial calcification in 6 of 10 hypoparathyroid subjects tested, and neurological (motor) examination revealed 5 of 11 with abnormal findings. There were positive correlations between the presence of cognitive deficits and cerebral calcification (r = 0.59, P = 0.07), between abnormal motor findings and cerebral calcification (r = 0.77, P < 0.01) and between abnormal motor findings and the degree of cognitive deficit (r = 0.83, P < 0.01). CONCLUSIONS: We conclude that cognitive and neurological deficits commonly occur in patients with chronic hypoparathyroidism and may be pathophysiologically related to the presence of intracranial calcification.

Adult↗
PubMed2002

Well-being, mood and calcium homeostasis in patients with hypoparathyroidism receiving standard treatment with calcium and vitamin D.

OBJECTIVE: Standard treatment in hypoparathyroidism consists of calcium and vitamin D (or vitamin D analogs) but does not employ replacement of the actual missing hormone. Only few studies have evaluated the efficacy of calcium/vitamin D treatment in hypoparathyroidism; the impact of chronic hypoparathyroid disease on well-being has not been investigated previously. DESIGN: Cross-sectional, controlled study in 25 unselected women with postsurgical hypoparathyroidism since 6.4plus minus8.0 years (s.d.) on stable treatment with calcium and vitamin D (or analogs) and in 25 controls with a history of thyroid surgery but intact parathyroid function, who were matched for sex, age and time since surgery. METHODS: Assessment of well-being and mood using validated questionnaires (the revised version Symptom Checklist 90 (SCL-90-R); the Giessen Complaint List (GBB-24); and the von Zerssen Symptom List (B-L Zerssen)), serum and urinary calcium/phosphorus homeostasis, and in the hypoparathyroid patients also screening for secondary disease by kidney ultrasound, ophthalmological split lamp examination, and measurement of bone mineral density. RESULTS: Serum calcium was in the accepted therapeutic range in the majority of hypoparathyroid patients. However, calcium/phosphorus homeostasis as a whole was clearly non-physiological. Nephrolithiasis was detected in 2 and cataracts in 11 of 25 hypoparathyroid patients. As compared with controls, hypoparathyroid patients had significantly higher global complaint scores in GBB-24 (P=0.036), B-L Zerssen (P=0.002) and SCL-90-R (P=0.020) with predominant increases in the subscale scores for anxiety, phobic anxiety and their physical equivalents. CONCLUSIONS: Current standard treatment in hypoparathyroidism is not only associated with an altered calcium/phosphorus homeostasis but also fails to restore well-being in these patients. Future studies need to address the impact of more physiological treatment options like parathyroid hormone(1-34) or parathyroid transplantation on well-being and mood in these patients.

Adult↗
PubMed1995

[Idiopathic hypoparathyroidism (isolated)].

X-linked recessive, autosomal dominant and autosomal recessive types of familial isolated hypoparathyroidism have been reported, and there are a variety of syndromes of isolated hypoparathyroidism in association with other developmental anomalies involving dwarfism, cortical thickening of tubular bones, nephropathy, sensoryneural deafness and lymphedema. The molecular genetic basis of these forms of idiopathic hypoparathyroidism has been investigated recently. Several genetic abnormalities were elucidated; mutations of the parathyroid hormone gene in some families of autosomal dominant and autosomal recessive familial isolated hypoparathyroidism, a defect at the Xq 26-q 27 region on the long arm of the X chromosome in X-linked recessive familial isolated hypoparathyroidism, and chromosomal deletions at 22q 11 in DiGeorge syndrome. Although adult onset idiopathic hypoparathyroidism may be caused by autoimmune mechanism as a part of polyglandular autoimmune syndrome or as isolated hypoparathyroidism, this type of idiopathic hypoparathyroidism is relatively rare in Japan. Etiology of sporadic cases of adult onset idiopathic hypoparathyroidism still remains to be elucidated.

Animals↗
PubMed1997

Current therapy of hypoparathyroidism--a survey of German endocrinology centers.

Hypoparathyroidism is a rare disease with hypocalcemia as the leading symptom. In adults, hypocalcemia is mainly due to postoperative hypoparathyroidism. Hypoparathyroidism requires lifelong therapy with vitamin D or metabolites. Genuine vitamin D3 (Vigantol) is the most economic treatment of hypoparathyroidism; however, vitamin D3 has a very long biologic half life with the subsequent danger of chronic vitamin D intoxication. Dihydrotachysterol (A.T.10), an analogue of vitamin D, acts similarly and can be used alternatively. 1,25-dihydroxyvitamin D3 (Rocaltrol), the biologically active metabolite of vitamin D3, is very potent, but bears the danger of causing acute intoxication; it has a short half life and is more expensive than vitamin D3. A further metabolite, 1-hydroxy-vitamin D3 (alfacalcidol, Doss, EinsAlpha) is available for therapeutic use. Clinical intervention trials concerning the best therapy and management of hypoparathyroidism are lacking. We therefore surveyed German physicians treating hypoparathyroidism. Furthermore, we carried out a retrospective study of 45 patients treated in our endocrinology department during the last 8 years and examined whether measurement of 25(OH)-vitamin D3 is helpful in managing hypoparathyroidism. The data from 59 children and 270 adults could be completed in the survey. 1,25-dihydroxyvitamin D3 was the only vitamin D agent that was administered in the treatment of children, whereas in adults 52% were treated with dihydrotachysterol, 28% with genuine vitamin D3, and 20% with 1,25-dihydroxyvitamin D3. There was a positive correlation between serum 25(OH)-vitamin D3 levels and administered vitamin D3 doses. In patients treated with vitamin D3, serum calcium levels correlated significantly with serum 25(OH)-vitamin D3 levels whereas they did not correlate with administered calcium doses. Thus: (1) in Germany dihydrotachysterol is preferred for therapy of hypoparathyroidism in adults and (2) measurement of serum 25(OH)-vitamin D3 may be helpful in assessing efficacy of therapy and compliance in patients treated with vitamin D3.

Adult↗