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PubMed1977

Hypercalcemic hyperparathyroidism in hypophosphatemic rickets.

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.

Adolescent↗

PubMed1988

Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.

We studied the natural history of primary hyperparathyroidism in patients in whom the disease was discovered fortuitously by multichannel biochemical screening and who were selected for conservative management because they were asymptomatic, had no renal stone disease or radiographic osteitis fibrosa, and had serum calcium values below 3.00 mmol/L, serum creatinine levels below 133 mumol/L, and forearm bone density not more than 2.5 SD below the mean expected for age, sex, and race. One hundred and seventy-four patients meeting these criteria were encountered during a 10-yr period, of whom 80 (mean age, 61 yr) had adequate follow-up; they did not differ significantly in any initial characteristic from the remaining 94 patients. These 80 patients were followed for 1-11 yr (mean, 46 months; median, 38 months), during which there was no change, mean or individual, in any index of PTH secretion or any of its biochemical effects and no decline in forearm bone density apart from that expected from increased age. There were 4 deaths from causes unrelated to hyperparathyroidism, and the overall death rate was not increased. The data suggest that no change occurred in either the number of parathyroid cells or secretory set-point, the 2 principal determinants of basal PTH secretion. This implies a biphasic course, with a short period of disease progression followed by a long period of disease stability. Our data support the decision to withhold surgical intervention in such patients, but to establish this as the correct policy for all asymptomatic patients will require a controlled clinical trial.

Aged↗

PubMed1996

Hypercalcemia due to constitutive activity of the parathyroid hormone (PTH)/PTH-related peptide receptor: comparison with primary hyperparathyroidism.

In Jansen's disease (JD), the hypercalcemia found in about half the cases is the result of a mutant, constitutively overactive, form of the PTH/PTHrP receptor, which in these cases also causes the skeletal dysplasia. The subject of the present report was first seen in 1956 and is still under treatment at the same medical center. We report the clinical course and a detailed study of calcium and bone metabolism carried out in 1976 and compare the results with those of six typical patients with mild primary hyperparathyroidism in whom exactly the same studies were carried out. In the patient with JD, the hypercalcemia was of early onset; chronic and nonprogressive; refractory to the administration of phosphate, glucocorticoid, and calcitonin; and accompanied by suppressed PTH levels as determined by two different immunoassays, an undetectable PTHrP level, increased excretion of nephrogenous cAMP (an in vivo bioassay of endogenous PTH production), decreased tubular reabsorption of phosphate, increased tubular reabsorption of calcium, increased biochemical indexes of bone turnover, and increased histological indexes of bone turnover on iliac bone histomorphometry after double tetracycline labeling. There was exaggerated loss of cortical bone and preservation of cancellous bone. All the results in JD relating to renal or skeletal effects of PTH excess were within or close to the ranges found in the hyperparathyroid patients, except that tubular reabsorption of phosphate was more depressed. Because PTH secretion was suppressed, any effects mediated by putative alternative receptors would have been diminished. We conclude that 1) the hypercalcemia due to constitutive overactivity of the PTH/PTHrP receptor is indistinguishable from that of mild primary hyperparathyroidism in clinical characteristics and renal tubular and skeletal features; and 2) the classic laboratory manifestations of primary hyperparathyroidism, with the possible exception of osteitis fibrosa cystica, can all be accounted for by overactivity of a single receptor.

Bone Diseases, Developmental↗

PubMed2003

[Maxacalcitol, a medicine for secondary hyperparathyroidism (2 degrees HPT)].

Maxacalcitol (Oxarol) is a derivative of vitamin D compounds applied for the secondary hyperparathyroidism (2 degrees HPT) of hemodialysis (HD) patients as an injection and psoriasis as an ointment. 2 degrees HPT is one of the complications in HD patients with hyperplasia of parathyroid glands and elevated serum parathyroid hormone (PTH) levels. On the other hand, vitamin D compounds are known to have multiple actions in many organs (promotion of calcium absorption from the small intestine, induction of differentiation of leukemia cells, differentiation and proliferation of the chondrocyte, muscle cells and epidermal cells, immunosuppressive activities) and their activities on parathyroid glands seem to be mediated by the vitamin D receptor (genomic action). It was reported that both serum PTH and PTH mRNA levels were suppressed by Maxacalcitol with less calcemic action and also Maxacalcitol could ameliorate high-turnover bone and marked osteitis fibrosa in uremic rats. Here I review many reports focused on the effects of Maxacalcitol on the 2 degrees HPT.

Animals↗

PubMed2003

[Endocrine surgery: the tenth report. Diagnosis, surgical indications and operative strategy of renal hyperparathyroidism].

In Japan, there are many dialysis patients because of the successful development and wide application of dialysis techniques. Almost all patients require long-term hemodialysis treatment because kidney transplantation is performed rarely. Renal hyperparathyroidism is one of the serious complications for hemodialysis patients. According to the overview of regular dialysis treatment reported by the Japanese Society for Dialysis Therapy, parathyroidectomy is required in 9.2%of patients who remain on hemodialysis more than 10 years and in 33.5%of those who so remain for more than 25 years. In this paper, we will describe the diagnosis, surgical indications, and operative strategy of renal hyperparathyroidism. The symptoms and biochemical variables were high serum parathyroid hormone (PTH) level, hyperphosphatemia, bone and joints pain, itching, irritability, muscle weakness, severe skeletal deformity, progression of ectopic calcification, and anemia. The clinical indications for performing parathyroidectomy to treat renal hyperparathyroidism in our institute are based on the indications reported by Tominaga et al. These are 1) high serum PTH level, 2) detection of enlarged parathyroid glands, 3) detection of osteitis fibrosa cystica on radiography or detection of high bone turnover by bone metabolic markers or bone scintigram, 4) resistance of symptoms to medical treatment. The routine operative procedure for renal hyperparathyroidism is total parathyroidectomy with forearm autograft. For autotransplantation, 30 pieces sliced 1x1x3 mm of diffuse hyperplasia are implanted into 30 pockets in the forearm without arteriorvenous (A-V) fistula for hemodialysis. In any surgical procedure for renal hyperparathyroidism, it is crucial to identify all parathyroid glands, including supernumerary glands and ectopic glands. At the initial operation for renal hyperparathyroidism, the surgeon must remove all parathyroid glands to avoid persistent and recurrent hyperparathyroidism and choose proper and adequate parathyroid tissue for autograft.

Humans↗

PubMed1977

Maxillary giant cell reparative granuloma.

"Giant cell reparative granuloma" was introduced into medical literature by Jaffe in 1953. Prior to that time most authors considered this lesion to be a variant of the benign giant cell tumor of the long bones, or a giant cell variant of osteitis fibrosa. Bernier and Cahn established the subdivision between the rare central giant cell reparative granuloma and the common peripheral epulis. In the past, considerable emphasis has been placed on the importance of differentiating the true giant cell tumor from the giant cell reparative granuloma of the jaw bones. Most authors now believe the true giant cell tumor does not appear in the jaw bones except in rare cases associated with Paget's disease of the skull. Developing from membranous, rather than cartilaginous, ossification might account for this. Both peripheral and central intraosseous lesions, parathyroid osteopathy and the pathologic tissue of cherubism show no appreciable histologic difference. These tumefactions are histologically a proliferative fibroblastic lesion with multinucleated giant cells. The histopathology of the giant cell tumor of the long bones is probably identical to the histopathology of the giant cell reparative granuloma of the jaw bones. The diagnosis of giant cell reparative granuloma must be made by physical examination, history, laboratory, X-ray parameters and clinical follow-up. Localized maxillary swelling is the most important clinical feature. The swelling is smooth and palpation can reveal a rubbery, elastic sensation where bone has been thinned. There are no specific radiographic signs. Conservative surgical management is indicated and adequate for giant cell reparative granulomas. Radiation is not indicated because of long term risks. Steroids have not been proven useful.

Adult↗

PubMed1999

Primary hyperparathyroidism and the risk of fracture: a population-based study.

While severe primary hyperparathyroidism (HPT) is clearly associated with osteitis fibrosa cystica, it remains uncertain whether mild, asymptomatic primary HPT adversely affects the skeleton. Thus, we assessed the incidence of age-related fractures in a large, population-based inception cohort of 407 cases of primary HPT (93 men and 314 women) recognized during the 28-year period, 1965-1992. Fracture risk was assessed by comparing new fractures at each site to the number expected from gender- and age-specific fracture incidence rates for the general population (standardized incidence ratios, SIRs). These community patients with primary HPT mostly had mild disease (mean +/- SD serum calcium, 10.9 +/- 0.6 mg/dl). Altogether, 471 fractures occurred during 5766 person-years of follow-up. Overall fracture risk was significantly increased in these patients (SIR 1.3, 95% confidence interval [CI] 1.1-1.5). Primary HPT was associated with an increased risk of vertebral (SIR 3.2, 95% CI 2.5-4.0), distal forearm (SIR 2.2, 95% CI 1.6-2.9), rib (SIR 2.7, 95% CI 2.1-3.5), and pelvic fractures (SIR 2.1, 95% CI 1. 1-3.5). The risk of proximal femur fractures was only marginally increased (SIR 1.4, 95% CI 1.0-2.0). By univariate analysis, increasing age and female gender were significant predictors of fracture risk, although higher serum calcium levels were also associated with increased fracture risk, and parathyroid surgery may have had a protective effect. By multivariate analysis, however, only age (relative hazard [RH] per 10-year increase, 1.6, 95% CI 1. 4-1.9) and female gender (RH 2.3, 95% CI 1.2-4.1) remained significant independent predictors of fracture risk. Thus, primary HPT among unselected patients in the community is associated with a significant increase in the risk of vertebral, Colles', rib, and pelvic fractures. These data have important implications for the current trend to recommend nonsurgical management for patients with mild primary HPT.

Adolescent↗

PubMed2002

Differential effects of intermittent and continuous administration of parathyroid hormone on bone histomorphometry and gene expression.

A mechanism explaining the differential skeletal effects of intermittent and continuous elevation of serum parathyroid hormone (PTH) remains elusive. Intermittent PTH increases bone formation and bone mass and is being investigated as a therapy for osteoporosis. By contrast, chronic hyperparathyroidism results in the metabolic bone disease osteitis fibrosa characterized by osteomalacia, focal bone resorption, and peritrabecular bone marrow fibrosis. Intermittent and continuous PTH have similar effects on the number of osteoblasts and bone-forming activity. Many of the beneficial as well as detrimental effects of the hormone appear to be mediated by osteoblast-derived growth factors. This hypothesis was tested using cDNA microgene arrays to compare gene expression in tibia of rats treated with continuous and pulsatile administration of PTH. These treatments result in differential expression of many genes, including growth factors. One of the genes whose steady-state mRNA levels was increased by continuous but not pulsatile administration was platelet-derived growth factor-A (PDGF-A). Administration of a PDGF-A antagonist greatly reduced bone resorption, osteomalacia, and bone marrow fibrosis in a rat model for hyperparathyroidism, suggesting that PDGF-A is a causative agent for this disease. These findings suggest that profiling changes in gene expression can help identify the metabolic pathways responsible for the skeletal responses to the hormone.

Animals↗

PubMed1991

[Clinical characteristics in multiple endocrine neoplasia type 1 in Japan: a review of 106 patients].

A review of 106 patients with multiple endocrine neoplasia (MEN) type 1 reported between 1966-1989 in Japan was conducted in order to clarify the natural history of this disease. Sporadic MEN 1 was found in 61 patients, and familial MEN 1 was found in 45 patients from 15 families. The mean ages at diagnosis of the two groups were 46.2 and 41.3 years, respectively, and the male to female ratio was 3:4. With regards to the involvement of the pituitary, parathyroid and endocrine pancreas, the combination of three endocrine glands was 31%, and that of two was 48%, in which the pituitary, parathyroid and endocrine pancreas had tumorous lesions in 60%, 88% and 63%, respectively. The first clinical manifestations of MEN 1 were the symptoms of hyperparathyroidism (32%), pituitary tumors (26%), peptic ulcer (28%) and hypoglycemia (13%). These symptoms appeared between 6 and 57 years of age (mean 34 years). The main clinical symptoms of the pituitary tumors were acromegaly and gigantism (37%), galactorrhea-amenorrhea syndrome (20%), Cushing's disease (10%) and visual disturbance due to compression of the tumor (20%). The clinical manifestations of hyperparathyroidism were mainly asymptomatic hypercalcemia (41%), nephrolithiasis (42%) and osteitis fibrosa (5%). In the patients with pancreatic tumor, Zollinger-Ellison syndrome (52%) and hypoglycemic symptoms (42%) were found. Tumors in the adrenal cortex, thyroid, carcinoid and lipoma were detected in association with MEN 1 in the frequencies of 28%, 21%, 9% and 5%, respectively. Death was reported in 37 patients between 9 and 86 years of age (mean 50.0 years). The cause of death was gastrointestinal bleeding and perforation (45%), surgery (24%) and disseminated carcinomatosis (18%). Recently, the gene predisposing to this syndrome has been assigned to chromosome 11 (11q13) in non-Japanese cases but not yet in Japanese MEN 1 patients.

Adolescent↗

PubMed1997

Psychiatric symptoms, bone density and non-specific symptoms in patients with mild hypercalcemia due to primary hyperparathyroidism: a systematic overview of the literature.

To determine (1) the relationship between primary hyperparathyroidism with mild hypercalcemia and psychiatric disturbances, bone density, or non-specific symptoms, and (2) the effect of parathyroidectomy on these outcomes, a systematic and critical review of the literature was conducted. Relevant citations were identified using MEDLINE (1966 to August, 1995) and PsycINFO (1967 to August, 1995). Studies were included for the overview if they described patients with mild hypercalcemia (< 12 mg/dl), and if they dealt with at least one of the following outcomes: psychiatric disturbances, bone density, joint pain, constipation, polyuria/nocturia or weight loss. Either a calculated effect size or Z score was used to estimate the effect of the disease or parathyroidectomy on these outcomes. Seven studies met the inclusion criteria for this overview. Two out of three case-control studies on psychiatric symptoms found a significant association between primary hyperparathyroidism with mild hypercalcemia and psychiatric disturbances (effect sizes; 0.17, 1.2 and 1.6). One of the three studies also examined the effect of parathyroidectomy on psychiatric symptoms, and found an effect size of 1.5. All four cross-sectional studies that measured bone mass showed significantly reduced bone density in the forearm and the lumbar spine. The bone loss ranged from 0.9 to 1.4 standard deviation below the age- and sex-adjusted mean value in the forearm, and was 0.5 in the spine. There was no relevant study regarding non-specific symptoms. Among the seven studies, five did not explicitly indicate whether the patients had classical symptoms of either osteitis fibrosa cystica or renal stones. Primary hyperparathyroidism with mild hypercalcemia is associated with psychiatric disturbances and reduced bone density. Nevertheless, further research is needed to determine the symptoms, particularly for a group of patients without either classical bone disease or renal stones. The effects of parathyroidectomy on these outcomes also remain to be determined.

Bone Density↗

PubMed1998

Hypocalcemia due to spontaneous infarction of parathyroid adenoma and osteomalacia in a patient with primary hyperparathyroidism.

A 49 year-old Japanese woman had subjected enlargement of a cervical tumor, and also suffered two bone fractures in 2 years. The cervical tumor had enlarged further in the month prior to admission, becoming warm and tender. Endocrinological examination revealed that the serum intact PTH concentration was remarkably high at 400 pg/mL despite the low serum calcium concentration, and that the serum vitamin Ds concentration was decreased. Bone roentgenograms revealed severe osteolytic changes compatible with osteitis fibrosa cystica and a pathologic fracture of the humerus. Under a diagnosis of primary hyperparathyroidism, parathyroidectomy was performed, followed by fixation surgery for the pathologic fracture. Histologically, the cervical tumor was a parathyroid chief-cell adenoma with massive necrosis, and the bone pathology by iliac bone biopsy revealed the existence of osteomalacia. She was treated with calcium, vitamins D and K2 and calcitonin after the surgery. This case is a rare condition manifesting hypocalcemia with catastrophic osteoporosis under the coexistence of spontaneous infarction of parathyroid adenoma with osteomalacia, suggesting that the clinical features of hyperparathyroidism are modified by both the autoparathyroidiectomy and the existence of osteomalacia due to vitamin D deficiency.

Adenoma↗

PubMed2001

Effects of in-center daily hemodialysis upon mineral metabolism and bone disease in end-stage renal disease patients.

CONTEXT: Alternative hemodialysis schedules have been proposed to improve the quality of the dialysis. Nonetheless, their influence upon mineral and bone disorders is unknown. OBJECTIVE: To report the impact of a daily hemodialysis schedule upon the lesions of renal osteodystrophy. TYPE OF STUDY: Prospective non-controlled study. SETTING: Public University Hospital. PARTICIPANTS: Five patients treated by daily hemodialysis for at least 24 months. INTERVENTION: Daily dialysis sessions were accomplished with non-proportional dialysis machines without an ultrafiltration control device, with blood flow of 300 ml/min, bicarbonate dialysate ([Ca]=3.5 mEq/L) at 500 ml/min, and low-flux membrane dialyzers. Sessions were started at 6:00 p.m. (except Sundays) and lasted 2 hours. MAIN MEASUREMENTS: Serum levels of Ca and P from the last 6 months on conventional hemodialysis for the same patients were used for comparison with each semester of daily hemodialysis. Bone biopsies and PTH levels were obtained at the end of the conventional hemodialysis period and then again after 2 years of daily hemodialysis. RESULTS: Mean serum calcium was significantly higher during the second and third semesters of daily dialysis [10.0 mg% (SD 0.6), and 10.0 mg% (SD 0.8), respectively] compared to standard dialysis [9.4 mg% (SD 0.8)], p < 0.05. Mean values for phosphorus were significantly lower during every semester of daily hemodialysis [6.3 mg% (SD 1.8), 5.8 mg% (SD 1.7), 6.0 mg% (SD 1.7), and 6.0 mg% (SD 1.8)] compared to standard dialysis [7.2 mg% (SD 2.7)], P < 0.05. Variations in mean Ca x P product followed the same pattern as for phosphorus [59.5 (SD 16.0), 57.1 (SD 16.3), 59.8 (SD 17.7), and 58.31 (SD 20.9) vs. 68.6 (SD 27.3), P < 0.05]. After 2 years on daily hemodialysis, 2 patients who had aplastic lesion were found to have mild bone disorder. In addition, one patient with mixed bone lesion and moderate bone aluminum accumulation had osteitis fibrosa with no aluminum. Intact PTH values at the beginning of study and after 2 years on daily hemodialysis did not differ [134 pg/ml (SD 66) vs. 109 pg/ml (SD 26), P = 0.60, respectively]. CONCLUSIONS: Patients treated using daily hemodialysis had better control of serum phosphorus and perhaps a lower risk of metastatic calcifications. Daily hemodialysis also seemed to be beneficial to low turnover bone disease and bone aluminum deposition.

Adult↗

PubMed2005

Bone disease in patients with chronic kidney disease under conservative management.

CONTEXT AND OBJECTIVE: Few studies have focused on bone disease in patients with chronic kidney disease under conservative treatment. The objective was to evaluate bone disease in patients with chronic kidney disease. DESIGN AND SETTING: Case series, at the Nephrology Division, Hospital Universitário Pedro Ernesto. METHODS: 131 patients with creatinine clearance from 10 to 60 ml/min/1.73 m(2) were followed up for at least one year. Serum creatinine, albumin, calcium, phosphorus, alkaline phosphatase, total CO2 (tCO2), intact parathyroid hormone (iPTH), and alkaline phosphatase were measured. Creatinine clearance was calculated from 24-hour urine creatinine measurements and protein ingestion estimates from urea assays. RESULTS: Patients presenting creatinine clearance < 30 ml/min/1.73 m(2) had higher iPTH values, but normal serum levels for calcium, phosphorus, alkaline phosphatase and tCO2. Patients presenting iPTH values of twice the normal upper limit (144 pg/ml) showed lower tCO2 values. Bone alkaline phosphatase was evaluated in 37 patients with creatinine clearance < 30 ml/min/1.73 m(2), showing correlation with alkaline phosphatase but not with parathyroid hormone. Bone biopsy on nine patients with creatinine clearance < 30 ml/min/1.73 m(2) and iPTH > 144 pg/ml showed osteitis fibrosa (4), mild lesion (4) and high turnover (1). CONCLUSION: The present data suggest the importance of early control for iPTH and metabolic acidosis, among patients under conservative management for chronic kidney disease, in order to prevent complications related to bone disease.

Absorptiometry, Photon↗

PubMed2004

Management of hyperphosphataemia in dialysis patients: role of phosphate binders in the elderly.

Phosphorus control remains a relevant clinical problem in dialysis patients. With age, however, serum phosphorus level decreases significantly because of a spontaneous decrease in protein intake. Older patients usually need lower doses of phosphorus binders. Nevertheless, hyperphosphataemia is observed in a quarter of patients aged >65 years. Phosphorus retention is related to an imbalance between phosphorus intake and removal by dialysis, and is usually aggravated when vitamin D analogues are employed. Hyperphosphataemia induces secondary hyperparathyroidism and the development of osteitis fibrosa. Recent publications describe an association between phosphorus retention and increased calcium and phosphorus product (Ca2+ x P), with significant progression of tissue calcification and higher mortality risk. Dietary intervention, phosphorus removal during dialysis and phosphorus binders are current methods for the management of hyperphosphataemia. However, the phosphorus removed by standard haemodialysis is insufficient to achieve a neutral phosphorus balance when protein intake is >50 g/day. Additional protein restriction may impose the risk of a negative protein balance. More frequent dialysis may help to control resistant hyperphosphataemia. Phosphorus binders constitute the mainstay of serum phosphorus level control in end-stage renal disease patients. Aluminium-based phosphorus binders, associated with toxic effects, have largely been substituted by calcium-based phosphorus binders. However, widespread use of calcium-based phosphorus binders has evidenced the frequent appearance of hypercalcaemia and long-term progressive cardiovascular calcification. Sevelamer, a relatively new phosphorus binder, has proved efficacious in lowering serum phosphorus and parathyroid hormone (PTH) levels without inducing hypercalcaemia. Furthermore, several investigators have reported that sevelamer may prevent progression of coronary calcification. However, its efficacy in severe cases of hyperphosphataemia remains to be confirmed in large series. There are no specific guidelines for phosphorus control in the elderly. Until more information is available, levels of mineral metabolites should be targeted in the same range as those recommended for the general population on dialysis (calcium 8.7-10.2 mg/dL, phosphorus 3.5-5.5 mg/dL and Ca2+ x P 50-55 mg2/dL2). PTH values over 120 ng/L help to avoid adynamic bone disease. Since elderly patients have a higher incidence of adynamic bone (which buffers less calcium) and vascular calcification, sevelamer should be the phosphorus binder of choice in this population; but sevelamer is costly and its long-term efficacy has not been definitively validated. Patients with low normal levels of calcium may receive calcium-based phosphorus binders with little risk. Patients with low values of PTH and high normal calcium should receive sevelamer. Tailored combinations of calcium-based phosphorus binders and sevelamer should be considered, and calcium dialysate concentration adjusted accordingly.

Adult↗

PubMed2001

Parathyroid hormone in the treatment of osteoporosis.

Parathyroid hormone (PTH), especially intact human PTH [hPTH(1-84)] and its various fragments [hPTH(1-31), (1-34), (1-36), (1-38) and their modifications], has been used for the treatment of osteoporosis over the last 10 years. Although chronic continuous excess of PTH markedly increases bone resorption, as seen in the typical example of primary hyperparathyroidism and osteitis fibrosa generalisata, intermittent PTH administration has been found to stimulate bone formation in animals, providing a basis for the use of PTH as a therapeutic agent for osteoporosis. In addition to dramatically increasing trabecular bone density and also sustaining cortical bone density, PTH administration increases bone strength and reduces the fracture rate, despite occasional increases in cortical porosity. Administration of PTH in combination with antiresorptive agents such as estrogen, calcitonin, vitamin D and bisphosphonates augments its effect. Because of its bone anabolic action, PTH is expected to be effective for osteoporosis in those of advanced age with suppressed bone remodelling, which might not respond favourably to antiresorptive agents.

Animals↗

PubMed2003

Chinese herbs and bone disease.

We treated a patient with an unusual bone disease at least partly associated with Chinese herbs. Seven years after 65-year-old man had begun to consume Chinese herbs, multifocal osteoarthralgias were noted, and the patient was hospitalized for renal dysfunction (serum creatinine, 2.8 mg/dl; urea nitrogen, 19 mg/dl). Fanconi syndrome also was apparent. A renal biopsy specimen showed tubulo-interstitial fibrosis. Chinese herbs were discontinued and prednisolone was started, but bone and joint pain as well as renal function gradually worsened. Four years later, creatinine was 9.0 mg/dl and alkaline phosphatase was 571 IU/l. As bone scintigraphy revealed localized asymmetric lesions, Paget's disease of bone was suspected at first. However, neither osteosclerosis nor hypertrophy was seen in radiographs. Based on a bone specimen histology we diagnosed as mixed-type renal osteodystrophy including osteomalacia and osteitis fibrosa. Mosaic pattern of cement lines was not present. This case was not compatible with either Paget's disease or typical renal osteodystrophy as seen in dialysis patients. Etidronate disodium was effective in alleviating bone symptoms. The patient's bone disorder may be a new disease at least partly related to Chinese herbs independently of nephropathy.

Aged↗

PubMedDate not supplied

Parathyroid glands in chronic aluminum intoxication.

In chronic renal failure, aluminum overload may influence parathyroid function. In a study of possible aluminum-induced parathyroid abnormalities, parathyroid glands from nine parathyroidectomized patients on hemodialysis were examined by light and electron microscopy and by X-ray microanalysis. Aluminum overload was assessed by the presence of stainable aluminum (aluminum surface, 23.3% +/- 11% of total surface) in bone biopsy specimens. The mean plasma aluminum concentration was 7.7 +/- 1.9 mumol/L. All patients but one had elevated plasma concentrations of immunoreactive parathyroid hormone as well as osteitis fibrosa. The aluminum concentrations in bone and parathyroid gland from these patients were significantly higher than those in tissue from patients on hemodialysis without stainable bone aluminum. Abundant aluminum deposits were present in parathyroid chief cell cytoplasm in lipoid bodies, lipofuscin granules, and mitochondria. These cells exhibited features of active hormonal synthesis and contained numerous secretory granules. The data show that in the parathyroid glands of these aluminum-intoxicated patients the presence of aluminum deposits neither induced cellular damage or chief cell necrosis nor interfered with the production of parathyroid hormone.

Adult↗

PubMedDate not supplied

Effect of calcitonin on hemodialysis patients with hypercalcemia and renal osteodystrophy.

Because calcitonin administration has been shown to decrease the serum calcium level in certain hypercalcemic conditions, 10 patients on maintenance dialysis with renal osteodystrophy and persistent hypercalcemia were treated with salmon calcitonin for 3 months. While plasma calcium concentrations were reduced by calcitonin therapy in four patients, therapy was ceased in two patients due to a worsening of their hypercalcemia, although in another two patients the initial worsening of the hypercalcemia settled with continued therapy. No significant changes in calcium levels occurred in the remaining two patients. Analysis of the data suggests that a hypocalcemic effect of calcitonin was most likely in the presence of osteomalacia, while predominant osteitis fibrosa favored a hypercalcemic response. Calcitonin administration caused a mean increase in parathyroid hormone (PTH) secretion 3.6 +/- 1.5 to 6.5 +/- 1.7 ng/ml; p less than 0.05) after 6 weeks of therapy. Three patients reported improvement in their bone pain. These studies show that despite possible symptomatic and morphological effects of calcitonin, its hypocalcemic effect in patients with renal osteodystrophy and hypercalcemia is inconsistent.

Alkaline Phosphatase↗