Outcomes linked to eligibility for stem cell transplantation trials in diffuse cutaneous systemic sclerosis.

OBJECTIVES: The aim of this study was to explore outcomes in a cohort of dcSSc patients fulfilling eligibility criteria for stem cell transplantation (SCT) studies but receiving standard immunosuppression. METHODS: From a large single-centre dcSSc cohort (n = 636), patients were identified using the published SCT trials' inclusion criteria. Patients meeting the trials' exclusion criteria were excluded. RESULTS: Of the 227 eligible patients, 214 met the inclusion criteria for ASTIS (Autologous Stem Cell Transplantation International Scleroderma), 82 for SCOT (Scleroderma: Cyclophosphamide Or Transplantation) and 185 for the UPSIDE (UPfront autologous haematopoietic Stem cell transplantation vs Immunosuppressive medication in early DiffusE cutaneous systemic sclerosis) trial, and 66 were excluded based on age >65 years, low diffusing capacity of the lungs for carbon monoxide (DLco), pulmonary hypertension or creatinine clearance <40 ml/min. The mean follow-up time was 12 years (s.d. 7). Among the eligible patients, 103 (45.4%) died. Survival was 96% at 2 years, 88% at 5 years, 73% at 10 years and 43% at 20 years. Compared with this 'SCT-eligible' cohort, those patients who would have been excluded from SCT trials had a worse long-term survival (97% at 2 years, 77% at 5 years, 52% at 10 years and 15% at 20 years, log rank P < 0.001). Excluded patients also had a significantly worse long-term event-free survival. Hazard of death was higher in patients with higher age at onset [hazard ratio (HR) 1.05, P < 0.001], higher ESR at baseline (HR 1.01, P = 0.025) and males (HR 2.12, P = 0.008). CONCLUSION: SCT inclusion criteria identify patients with poor outcome despite current best practice treatment. Patients meeting the inclusion criteria for SCT but who would have been excluded from the trials because of age, pulmonary hypertension, poor kidney function or DLco <40% had worse outcomes.

Evaluación de fugas extrarticulares del Fosfato crómico marcado con Fósforo-32 de producción nacional en pacientes hemofílicos / Evaluation of joint leakage of national Chromic Phosphate labeled with Phosphorus-32 in hemophilic patients

La radiosinoviortesis como tratamiento de la artropatía hemofílica, frecuentemente, ofrece excelentes resultados, al reducir grandemente el número de episodios de sangramiento y evitar daños ulteriores a las articulaciones. El Centro de Isótopos desarrolló el fosfato crómico coloidal marcado con Fósforo-32, producto listo para su empleo en pacientes hemofílicos. El objetivo de este trabajo fue evaluar la fuga extrarticular de este radiofármaco utilizado en la radiosinoviortesis en pacientes hemofílicos. Se determinó el porcentaje de fuga extrarticular del radiofármaco en 9 pacientes hemofílicos con sinovitis crónica, a los que se les realizó la radiosinoviortesis en la articulación de la rodilla. La radiactividad se midió, con un contador Geiger-Muller, sobre la rodilla tratada, en sus aspectos lateral, encima y medial; la rodilla contralateral; las cadenas linfáticas inguinales, de ambos lados, y el hígado. Los valores de fuga encontrados posteriormente a la inyección fueron 0,0046 por ciento a los 10 min; 0,0023 por ciento a las 24 horas; 0,1332 por ciento el día 7 y 4,0213 por ciento el día 30. Estos resultados coinciden con los valores comunicados por otros autores y con lo esperado de acuerdo a las características del producto, indican que se ejecutó el proceder adecuadamente y que los pacientes fueron seleccionados correctamente(AU)

Radiosynoviorthesis as a treatment for hemophilic arthropathy often offers excellent results, greatly reducing the number of bleeding episodes and avoiding further damage to the joints. The Isotope Center developed a product, Colloidal Chromic Phosphate labeled with Phosphorus-32, ready for use in hemophiliac patients. Our objective was to evaluate the joint leakage of this radiopharmaceutical use in radiosynoviorthesis in hemophilic patients. The percentage of radiopharmaceutical joint leakage was evaluated in 9 hemophilic patients with chronic synovitis, who underwent radiosynoviorthesis in the knee joint. The radioactivity was measured on the treated knee, in its lateral, above and medial aspects, the contralateral knee, the inguinal lymphatic chains of both sides and the liver, with a Geiger-Muller detector. The leakage values 8203;​found after the injection were 0.0046 percent at 10 minutes, 0.0023 percent at 24 hours, 0.1332 percent on day 7 and 4.0213 percent on day 30. These results are agreed with the values reported by other authors and with was expected according to the characteristics of the product, indicatate that the procedure was executed properly and that the patients were correctly selected(AU)

Suspected primary hypoparathyroidism in a domestic ferret (Mustela putorius furo).

CASE DESCRIPTION: A 4-year-old castrated male domestic ferret (Mustela putorius furo) was examined because of a 3-week history of intermittent seizures, signs of depression, hypocalcemia, and hyperphosphatemia. CLINICAL FINDINGS: Plasma biochemical analysis confirmed hyperphosphatemia (17.7 mg/dL) and low concentrations of total (4.3 mg/dL) and ionized (0.49 mmol/L) calcium. Serum parathyroid hormone concentration (2.30 pmol/L) was low or in the low part of the reference interval. TREATMENT AND OUTCOME: Calcium gluconate was administered (2.0 mg/kg/h [0.9 mg/lb/h], IV), followed by a transition to administration of calcium carbonate (53 mg/kg [24.1 mg/lb], PO, q 12 h) and dihydrotachysterol (0.02 mg/kg/d [0.009 mg/lb/d], PO). Attitude of the ferret improved and seizures ceased as blood calcium concentrations increased. The ferret was reexamined because of seizures approximately 1 year after oral maintenance administration of dihydrotachysterol and calcium was initiated. The ferret responded well to emergency and long-term treatment but then was lost to follow-up monitoring. The ferret died approximately 2 years after the initial evaluation and treatment. Hypertrophic cardiomyopathy was diagnosed during necropsy, but the parathyroid glands could not be identified. CLINICAL RELEVANCE: To the authors' knowledge, primary hypoparathyroidism has not previously been reported in a ferret. The condition should be considered for ferrets with hypocalcemia and hyperphosphatemia without azotemia. Treatment with dihydrotachysterol and oral supplementation of calcium appeared to be a viable option for long-term management.

Dihydrotachysterol therapy for hypoparathyroidism: consequences of inadequate monitoring. Five cases and a review.

BACKGROUND: The half synthetic Vitamin D analogue dihydrotachysterol (DHT) is widely used for hypocalcaemic hypoparathyroidism following surgical removal of parathyroids. Such treatment generally initiated by surgeons right after surgery has to be continued in clinical practice. Unfortunately, the required careful monitoring of calcium metabolism is often lacking and as demonstrated may lead to life-threatening conditions. PATIENTS AND METHODS: Here we report on five patients referred to our nephrology unit because of unknown impairment of renal function during therapy with DHT. All patients had clinical signs of hypercalcaemia. Since most symptoms are nonspecific they were not perceived by primary care physicians. In fact DHT treatment was continued for 4 - 50 years. In all cases calcium levels were determined after inadequate long intervals ranging from 3.08 to 4.97 mmol/l. Creatinine levels ranged from 277 to 365 micromol/l. All patients suffered from symptoms of severe hypercalcaemia, three of them needing intensive care unit treatment. RESULTS: All patients were treated effectively with a regimen consisting of intravenous saline, a loop diuretic, and application of bisphosphonates. As confirmed by renal biopsy persisting alleviation of renal function was due to calcifications. After discontinuation of DHT therapy patients were safely switched to shorter acting vitamin D derivates maintaining a normal calcium level. CONCLUSIONS: In comparison to short acting vitamin-D derivates hypercalcaemic episodes with DHT appear to last longer and may therefore occur with higher incidence. A future option could be the use of synthetic parathyroid hormone (s-PTH) recently shown to be safe and effective. Nevertheless a customized therapy and careful monitoring is indispensable in any case to prevent irreversible organ damage.

Impact of parathyroid status and Ca and vitamin-D supplementation on bone mass and muscle-bone relationships in 208 Belarussian children after thyroidectomy because of thyroid carcinoma.

This observational study analyzes Ca-P metabolism and its impact on bone mass accrual and density and the muscle-bone mass/mass relationships in male and female children and adolescents who were parathyroidectomized because of thyroid carcinoma. Two hundred and eight children and adolescents (119 girls and 89 boys) from Gomel city (Belarus) and its rural surroundings were referred to our institution after having undergone total thyroidectomy for the treatment of advanced papillary thyroid cancer. A subgroup of children with demonstrated primary hypoparathyroidism received dihydrotachysterol (AT-10) and/or Ca supplementation. Among routine procedures over a maximum follow-up period of 5 years (average 3.7 years, maximum 8 visits), whole-body scans were taken using dual energy X-ray absorptiometry (DXA) at each visit in order to determine whole-body bone mineral content (TBMC), projected "areal" bone mineral density (TBMD), total lean mass (TLM) and total fat mass (TFM). The average serum Ca, P and AP concentrations over the whole observation period were significantly different between the groups; however, TBMC z-scores for all studied children were statistically similar in all visits. In girls, no between-group differences in height- and weight-controlled TBMC and TBMD or the TBMC/TLM ratio were observed (ANCOVA) and supplementation exerted no effect on these data, suggesting that the total bone mass accrual was not impaired by PTH deficiency in the studied conditions. However, non-supplemented boys showed lower values of the TBMC/TLM ratio than girls, and supplementation normalized these values in direct correlation with the induced improvement in serum P availability to bone. Results indicate that the primary impairment in parathyroid function and bone metabolism indicators in the thyroidectomized children was unrelated to any measurable change in crude bone mass values. However, in boys this condition impaired the TBMC/TLM ratio in such a way that the administered supplementation could normalize it as a function of improved P availability. Girls' skeleton seemed to have been naturally protected against the negative metabolic effect of the studied condition. An estrogen-induced enhancement of the biomechanical impact of muscle contractions on bone mass and structure could not be excluded in this group.

Suspected pseudohypoparathyroidism in a domestic ferret.

A 1.5-year-old ferret examined because of seizures was found to have low serum calcium, high serum phosphorus, and extremely high serum parathyroid hormone concentrations. Common causes of these abnormalities, including nutritional secondary hyperparathyroidism, chronic renal secondary hyperparathyroidism, tumor lysis syndrome, and hypomagnesemia, were ruled out, and a tentative diagnosis of pseudohypoparathyroidism was made. Pseudohypoparathyroidism is a hereditary condition in people that, to our knowledge, has not been identified in ferrets previously and is caused by a lack of response to high serum parathyroid hormone concentrations, rather than a deficiency of this hormone. The ferret improved after treatment with dihydrotachysterol (a vitamin D analog) and calcium carbonate. It was still doing well after 3.5 years of continued treatment.

Hypercalcemia-induced renal insufficiency during therapy with dihydrotachysterol.

During vitamin-D therapy drug accumulation and intoxication should be considered. In the present study we report on five patients with renal insufficiency during therapy with dihydrotachysterol or calcitriol. Four patients received dihydrotachysterol for 29 (7-44) years and one patient received calcitriol for 4 years to treat hypoparathyroidism after thyroid surgery. As confirmed by renal biopsy impairment of renal function was due to calcifications as a consequence of prolonged hypercalcemia. The effective duration of dihydrotachysterol is ten days as compared with five days for calcitriol. Severe hypercalcemic episodes with dihydrotachysterol are longer-lasting than those with the shorter acting vitamin-D derivatives. Further, they occur with higher incidence as was shown by our own observations and previously published data by other workers. Hence, impairment of renal function during therapy with dihydrotachysterol should be considered as being due to hypercalcemia and hypercalciuria.

1,25-Dihydroxyvitamin D3 corrects insulin and lipid abnormalities in uremia.

The effect of intravenous 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] therapy on insulin and lipid metabolism was examined in patients on maintenance hemodialysis (HD). Eight patients (Group I, 19 +/- 1 years old) were studied before and after four weeks of intravenous 1,25 (OH)2D3 therapy (1.8 +/- 0.3 micrograms), during which time the serum parathyroid hormone (PTH) concentrations did not change. Another eight patients (Group II, 18 +/- 1 years old) were studied before and after four weeks of oral dihydrotachysterol (0.8 +/- 0.1 mg). Serum PTH also did not change in Group II. Serum glucose concentrations during an oral glucose tolerance test (OGTT) were higher in Group I before 1,25(OH)2D3 compared with controls and these normalized following four weeks of intravenous 1,25(OH)2D3. Serum glucose concentrations during OGTT were also higher in Group II before DHT compared with controls and did not change following four weeks of oral DHT. Insulin sensitivity during euglycemic clamp studies in Group I before 1,25(OH)2D3 (223 +/- 20 mg/m2/min; P < 0.01) was low compared with controls (320 +/- 26 mg/m2/min) and was normalized following therapy (315 +/- 25 mg/m2/min). Insulin sensitivity was also low in Group II at the beginning of the study and did not change at the end of the four week period. Both early-phase and late-phase insulin secretion were low in Group I before 1,25(OH)2D3 compared with controls and normalized following intravenous 1,25(OH)2D3 therapy. Both early-phase and late-phase insulin secretion were also low in Group II at the beginning of the study and did not change at the end of the four week period of DHT treatment. Plasma triglycerides were elevated in Group I patients before treatment (198 +/- 16 mg/dl; P < 0.01) compared with controls (139 +/- 12 mg/dl) and were normalized (148 +/- 13 mg/dl) following intravenous 1,25(OH)2D3 therapy. Plasma total cholesterol and high density lipoprotein cholesterol were normal before treatment compared with controls and did not change following Intravenous 1,25(OH)2D3 therapy. Plasma triglycerides, total cholesterol and high density lipoprotein cholesterol did not change in Group II during the study period. Thus, intravenous 1,25(OH)2D3 therapy corrected glucose intolerance, insulin resistance, hypoinsulinemia as well as hypertriglyceridemia in patients on HD, in the absence of PTH suppression.

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.

The effect of phosphate supplementation on linear growth in children with X-linked hypophosphatemia.

BACKGROUND: X-linked hypophosphatemia is the most common inherited cause of rickets. Current therapy for this disorder includes vitamin D and phosphate supplementation; however, phosphate therapy has been associated with nephrocalcinosis. The purpose of this study is to evaluate the effect of oral phosphate therapy on growth in patients with X-linked hypophosphatemia treated with either calcitriol or dihydrotachysterol (vitamin D). METHODS: We retrospectively evaluated the prepubertal growth of 36 children with X-linked hypophosphatemia. The height standard deviation score (Z-score) of patients initially treated with vitamin D alone and the Z-scores of patients treated with vitamin D and phosphate therapy were compared. In addition, the growth of therapy were compared. In addition, the growth of patients treated with vitamin D was compared with that of patients treated with vitamin D and phosphate from the outset of therapy. RESULTS: Patients treated with vitamin D alone for 5.36 +/- 2.18 years had an improvement in Z-score from -3.1 +/- 1.10 to -2.49 +/- 0.66 SDS, P < .05. Adding phosphate therapy for patients initially treated with vitamin D alone for 4.83 +/- 2.99 years did not further improve Z-score (-2.49 +/- 0.66 vs -2.35 +/- 0.83). Initial therapy with vitamin D and phosphate for 4.33 +/- 2.19 years also improved Z-score, (-2.84 +/- 1.02 vs -1.98 +/- 0.82, P < .05). The change in Z-score was similar to the group treated with vitamin D alone compared with the group treated initially with vitamin D and phosphate (0.65 +/- 0.54 vs 0.85 +/- 0.65, respectively). CONCLUSION: These data demonstrate that both vitamin D alone and in combination with phosphate improved linear growth. Adding oral phosphate for children initially treated with vitamin D alone did not improve Z-score. Initial therapy with vitamin D and vitamin D plus phosphate produced similar changes in linear growth.

Fanconi's syndrome in a dog with primary hypoparathyroidism.

An 11-year-old castrated male mixed breed dog was referred for evaluation of muscle twitching, polyuria, polydipsia, anorexia, and periocular alopecia. Primary hypoparathyroidism was diagnosed by documenting decreased serum concentrations of parathyroid hormone and ionized calcium. Neurological, gastrointestinal, and dermatological signs resolved after calcium repletion. Initially, 1,25-dihydroxycholecalciferol PO was required to correct the hypocalcemia. Dihydrotachysterol, in combination with oral calcium supplementation, was used for long-term maintenance of normal serum calcium concentration. Aminoaciduria, glucosuria, and hyperchloremic metabolic acidosis were consistent with a diagnosis of Fanconi's syndrome. This diagnosis was further supported by the presence of hypokalemia and increased urinary fractional excretion of sodium, potassium, calcium, phosphorus, and magnesium. Renal tubular dysfunction resolved after oral supplementation with calcium and vitamin D3. Fanconi's syndrome in this dog may have been caused by decreased serum concentration of 1,25-dihydroxycholecalciferol, which was secondary to decreased parathyroid hormone production.

Parathyroid autotransplantation in patients undergoing a total thyroidectomy: a review of 261 patients.

Parathyroid autotransplantation was first described in 1907 by Halsted. However, this simple and effective method of preserving parathyroid function has been used with increasing frequency only during the past 25 years. Beginning in the late 1960s, our group has transplanted normal parathyroid tissue into the ipsilateral sternocleidomastoid muscle whenever these glands could not be preserved in situ with adequate blood supply. In addition, if the blood supply of all four parathyroid glands appeared compromised, cryopreservation of parathyroid tissue was performed in case the autotransplanted tissue did not function after surgery. Since 1970, 393 patients underwent a total thyroidectomy. Parathyroid glands that could not be saved in situ were biopsied to confirm their identity by frozen section and then autotransplanted. Of the 393 patients who underwent a total thyroidectomy, 261 patients required transplantation of one or more glands. Among those 261 patients who underwent selective parathyroid autotransplantation, 33 (13%) required temporary calcium and vitamin D supplementation. Of these 33 patients, 2 (less than 1%) had permanent hypoparathyroidism and are receiving long-term vitamin D therapy.

A prospective, double-blind study of growth failure in children with chronic renal insufficiency and the effectiveness of treatment with calcitriol versus dihydrotachysterol. The Growth Failure in Children with Renal Diseases Investigators.

Because controlled trials in adults have shown accelerated deterioration of renal function in a small number of patients receiving calcitriol for renal osteodystrophy, we initiated a prospective, randomized, double-blind study of the use of calcitriol versus dihydrotachysterol in children with chronic renal insufficiency. We studied children aged 1 1/2 through 10 years, with a calculated glomerular filtration rate between 20 and 75 ml/min per 1.73 m2, and with elevated serum parathyroid hormone concentrations. Ninety-four patients completed a mean of 8.0 months of control observations and were randomly assigned to a treatment period; 82 completed the treatment period of at least 6 months while receiving a calcitriol dosage (mean +/- SD) of 17.1 +/- 5.9 ng/kg per day or a dihydrotachysterol dosage of 13.8 +/- 3.3 micrograms/kg per day. With treatment the height z scores for both calcitriol- and dihydrotachysterol-treated groups showed no differences between the two groups. In relation to cumulative dose, there was a significant decrease in glomerular filtration rate for both calcitriol and dihydrotachysterol; for calcitriol the rate of decline was significantly steeper (p = 0.0026). The treatment groups did not differ significantly with respect to the incidence of hypercalcemia (serum calcium concentration > 2.7 mmol/L (> 11 mg/dl)). We conclude that careful follow-up of renal function is mandatory during the use of either calcitriol or dihydrotachysterol because both agents were associated with significant declines in renal function. There was no significant difference between calcitriol and dihydrotachysterol in promoting linear growth or causing hypercalcemia in children with chronic renal insufficiency. Dihydrotachysterol, the less costly agent, can be used with equal efficacy.

Effect of daily oral vitamin D and calcium therapy, hypophosphatemia, and endogenous 1-25 dihydroxycholecalciferol on parathyroid hormone and phosphate wasting in renal transplant recipients.

Ten stable, normocalcemic renal transplant patients with good allograft function, hyperparathyroidism, and variable hypophosphatemia were treated for 2 to 9 months with oral calcium carbonate and replacement doses of vitamin D analogues. Parathyroid hormone levels (PTH) and renal phosphate wasting were not autonomous or fixed but decreased with therapy. Although serum 1-25(OH)2D3 levels could be shown to rise appropriately during oral vitamin D therapy and fall afterwards, a separate study in a larger group of patients showed no effect of elevated parathyroid hormone or hypophosphatemia to increase endogenous 1-25(OH)2D3 levels. Some 42% of patients with elevated carboxy-terminal PTH, had elevated N-terminal PTH, which was closely associated with more severe phosphate wasting. Aggressive oral calcium and vitamin D supplementation in certain normocalcemic renal transplant patients may decrease endogenous PTH levels, improve hypophosphatemia, and provide a physiologic increase in levels of 1-25(OH)2D3.

Masking of physicians in the Growth Failure in Children with Renal Diseases Clinical Trial.

Masking--hiding identities of treatments from the patient, physician and/or statistician--is a critical element in clinical trials. Wherever possible, masking is implemented to eliminate observational bias or systematic error. In this paper, general concepts of masking in clinical trials are examined. Specific masking procedures used in the "Growth Failure in Children with Renal Diseases" (GFRD) Clinical Trial are described. A method to evaluate the "success" of this masking procedure for physicians is introduced. For each randomized patient at each clinical center, the clinic director was asked to predict which treatment (1,25-dihydroxyvitamin D3 or dihydrotachysterol) was assigned. Results showed that 72% of responses initially indicated "absolutely no idea" of treatment. Additional analyses revealed that the number and percentage of "correct" guesses were essentially equal for the two treatment groups and that a patient's time on treatment did not affect the mask. We conclude that the mask of physicians in the GFRD Clinical Trial was well maintained.

Hypercalciuria in parathyroid disorders: effect of dietary sodium control.

Moderate dietary Na restriction (80 mmol/d for 7 days) during constant Ca intake can reduce high urinary Ca excretion to normal levels in idiopathic hypercalciuria (IH). A similar protocol was used to test its effect in primary hyperparathyroidism (PHPT) and also in hypoparathyroid subjects (HOPT) during treatment with dihydrotachysterol (DHT). Nine subjects with PHPT, 10 with HOPT, and one with pseudo-HOPT were evaluated after Na-restricted (80 mmol/d) and Na-supplemented (200 mmol/d) diets for 7 days each with dietary Ca constant. Na restriction resulted in a decrease in mean urinary 24-hour Ca excretion in PHPT subjects (10.6 v 7.6 mmol/d [424 v 304 mg], P less than 0.0001) and in one pseudo-HOPT subject, similar to the pattern seen previously in IH subjects. In contrast, Na restriction was not accompanied by significant change in Ca excretion in HOPT. There was no change in serum immunoreactive PTH (iPTH) or 1,25(OH)2 vitamin D levels in either group when Na intake was altered. Thus, the presence of parathyroid hormone (PTH) is necessary for sodium-related alterations in urinary Ca to occur. The effect of PTH appears to be "permissive" rather than "active." Dietary Na restriction may have a role in the management of hypercalciuria in mild PHPT cases when parathyroidectomy is contraindicated.