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PubMed1969

Bronchial carcinoma and hypercalcaemia.

Hypercalcaemia due to malignant disease, in the absence of bone metastases, is generally regarded as a rare event. It occurred in 16% of a series of cases of bronchial carcinoma coming to necropsy. Hypercalcaemia is a relatively common complication of bronchial carcinoma. The hypercalcaemia is usually accompanied by hypophosphataemia and, in this respect, must be distinguished from the hypercalcaemia that may be found with breast carcinoma. It is frequently accompanied by hypokalaemic alkalosis; this must not be confused with the metabolic disorder that results from the production of ectopic ;ACTH'. The bones sometimes show changes of osteitis fibrosa akin to those seen in hyperparathyroidism. Cystic disease of bone recognizable radiologically is rare, probably because of the relatively short duration of the metabolic disturbance. The parathyroids are usually mildly atrophic. There is no evidence that the main pathogenetic mechanism is stimulation of the parathyroids by the tumour. Acceptable instances of parathyroid hyperplasia are very rare: the significance of these exceptional cases awaits further study.Squamous carcinoma of the bronchus is the type mainly incriminated. Oat-cell carcinoma and bronchial adenocarcinoma are involved less frequently than expected by chance. The significance of the tumour types implicated is discussed in relation to the possible pathogenesis.

Adenocarcinoma↗

PubMed1975

Slipped epiphyses in renal osteodystrophy.

Clinical, biochemical, roentgenological, and histological features of slipped epiphyses (epiphysiolysis) in 11 out of 112 children with renal osteodystrophy have been analysed. Characteristic age-related patterns of involvement of different epiphyses are described. Quantitative measurements of iliac bone histology, serum parathyroid hormone levels, and clinical history show the presence of more advanced osteitis fibrosa in children with epiphysiolysis than in those without. A good correlation was found between serum parathormone levels and osteoclastic resorption, endosteal fibrosis as well as osteoid. Histological studies show that the radiolucent zone between the epiphyseal ossification centre and the metaphysis in x-rays is not caused by accumulation of cartilage and chondro-osteoid (as usually found in vitamin D deficiency rickets) but by the accumulation of woven bone and/or fibrous tissue. The response to vitamin D therapy in most cases was good. Parathyroidectomy was required in only one case.

Adolescent↗

PubMed2004

Oxyphil parathyroid adenoma: a malignant presentation of a benign disease.

Functioning parathyroid adenomas of the oxyphil cell type are rare, and the clinical characteristics of patients with these tumors have not been well defined. We describe two cases of severe primary hyperparathyroidism (PHPT) caused by benign oxyphil parathyroid adenomas. The patients' clinical presentations mimicked parathyroid carcinoma. Both had very large tumors associated with marked elevations in PTH and serum calcium levels. Skeletal manifestations were also atypical for benign PHPT, with severe osteoporosis in one patient and osteitis fibrosa cystica in the other. These cases also highlight the remarkable capacity of the skeleton to recover after successful parathyroidectomy, previously reported in other forms of severe PHPT. Bone mineral density improved dramatically 1 yr after parathyroidectomy, with increases of 51% at the lumbar spine, 36% at the total hip, and 11% at the distal one third radius. Most of the increases occurred in the first postoperative months. Consistent with this early and accelerated skeletal response, markers of bone turnover were increased 2 months after surgery and normalized by 8 months postoperatively. In patients with PHPT who present with severe or atypical clinical features, oxyphil adenoma should be considered.

Adenoma, Oxyphilic↗

PubMed1995

Direct effect of calcitriol on the regulation of parathyroid hormone secretion in a case of pseudo-hypoparathyroidism (a 24-month follow-up study).

The diagnosis of pseudohypoparathyroidism with osteitis fibrosa was made in a 51-year-old woman on the basis of hypocalcaemia, elevated plasma PTH (1-84) and blunted cAMP response to hPTH infusion. Radiologically, widespread signs of hyperparathyroidism were observed and quantitative histomorphometry confirmed the increased bone cellular turnover. Treatment with calcitriol (1,25 dihydroxyvitamin D3) induced a dramatic improvement of bone lesions. During treatment PTH (1-84) normalized with high dosage of calcitriol in spite of low or subnormal levels of serum calcium, and subsequently increased for each reduction of calcitriol dosage despite normal calcium levels. Our observations support a major and direct effect of 1,25 dihydroxyvitamin D3 on the regulation of parathyroid secretion of parathyroids glands.

Biopsy↗

PubMed1983

The effects of calciferol and its metabolites on patients with chronic renal failure. II. Calcitriol, 1 alpha-hydroxyvitamin D3, and 24,25-dihydroxyvitamin D3.

The available data with regard to the use of calcitriol, 1 alpha-hydroxyvitamin D3 (1 alpha-OH D3), and 24,25-dihydroxyvitamin D3 (24,25-[OH]2D3) in the management of chronic renal insufficiency are reviewed. Patients with mild to moderate osteitis fibrosa experience substantial improvement with either calcitriol or 1 alpha-OH D3 therapy. However, few patients experience a reversal to normal in histologic characteristics of bone. The conditions of patients with osteomalacia do not respond to either calcitriol or 1 alpha-OH D3 therapy. The bone lesion appearing in these patients is most likely a toxic effect of aluminum. The prognosis is usually poor, but the conditions of some patients may respond to administration of 24,25-(OH)2D3 together with calcitriol. Preliminary data suggest that use of chelating agents may be beneficial. In this group of patients, 24,25-(OH)2D3 administration together with calcitriol may be beneficial.

24,25-Dihydroxyvitamin D 3↗

PubMed1984

Renal osteodystrophy.

As is apparent from the preceding discussion, renal osteodystrophy is a complex entity with multiple causes and many manifestations. Significant problems have included the identification and management of the various forms of bone disease seen in uremia. The prevention and therapy of osteitis fibrosa and secondary hyperparathyroidism have been significantly improved as a result of adequate phosphate restriction and the use of active forms of vitamin D (primarily calcitriol in the U.S., dihydrotachysterol and 1 alpha-hydroxyvitamin D in Europe). Recently, a major problem has been the recognition of bone disease due to aluminum accumulation. The therapy of this bone disease was generally unsuccessful until recent preliminary data suggested that deferoxamine therapy may be useful in these patients. The study of renal osteodystrophy has certainly advanced our knowledge of mineral metabolism, with clarification of the metabolism and action of PTH and vitamin D metabolism and identification of the pathogenic role for aluminum. In the future, most manifestations of renal osteodystrophy may be preventable or adequately treated.

Alkaline Phosphatase↗

PubMed1986

Clinical features of aluminum-associated bone disease in long-term hemodialysis patients.

We encountered 11 patients with aluminum-associated bone disease (AABD), and treated them with deferoxamine (DFO). In 3 patients, a second bone biopsy was done during DFO treatment. Clinical features of AABD were compared with surgically proven secondary hyperparathyroidism (2 degrees HPT) with osteitis fibrosa on X-ray. Patients with AABD had disabling bone pain. This disease showed radiological signs ranging from normal, localized bone atrophy, to multiple fractures. It was characterized by increased soft tissue activity and localized abnormal uptake of 99mTc-MDP, detected by skeletal scintigrams. Patients with AABD had low levels of parathyroid hormone and alkaline phosphatase, but high aluminum (Al) levels compared to those with 2 degrees HPT. Serum Al increased after DFO administration, and the patients improved both clinically and histologically. 1-alpha-Hydroxyvitamin D3 (1-alpha-OH D3) was not effective for AABD. We concluded that the administration of antacids containing Al should be minimized in dialysis patients.

Adult↗

PubMed2006

From mild to severe primary hyperparathyroidism: The Brazilian experience.

Primary hyperparathyroidism often presents as an asymptomatic disorder. In our institution, routine serum calcium measurements have now been used as part of medical examination for 23 years. Out of 124 patients consecutively seen at our institution, 47% presented with no symptoms related to the disease, while 25% presented with severe skeletal involvement and osteitis fibrosa cystica, 25% with renal stone disease without overt bone involvement, and 2% with the typical neuropsychiatric syndrome. This same pattern is seen in the city of São Paulo. In severe disease pathological fractures are frequently seen, especially in long bones of the lower extremities, and also loss of lamina dura of the teeth and salt-and-pepper appearance of the skull. Bone mineral density is extremely low in these patients but usually show remarkable recovery following surgical cure. Serum PTH and bone markers are considerable higher in severely affected patients, who also have a high rate of vitamin D deficiency, and the parathyroid lesion is easier located compared with asymptomatic patients. From pathological specimens 87% had histological confirmation of a single adenoma, 6.4% multiple gland hyperplasia and 3.8% carcinoma.

Adenoma↗

PubMed1975

Calcium metabolism in renal failure.

Osteodystrophy is almost universally present in chronic renal failure. Mild, but detectable, abnormalities--especially in parathyroid hormone (PTH) secretion--occur even when the glomerular filtration rate is greater than 30 cc/min. Osteomalacia is common in areas in which vitamin D intake and exposure to sunlight are minimal; when these factors are plentiful, osteitis fibrosa predominates. Osteoporosis is seen with increasing frequency in hemodialyzed patients. Nonosseous complications of secondary hyper-parathyroidism include hypercalcemia, metastatic calcification and pruritus. The most important factor in the medical therapy of osteodystrophy is control of serum phosphate levels. Next, a positive calcium balance must be provided either by giving vitamin D as dihyrdotachysterol, raising dialysate calcium or administering calcium orally. Parathyroidectomy is sometimes indicated, especially when the patients are transplant candidates and manifest hypercalcemia. Whether or not transplant is contemplated, patients with persistently high calcium-phosphate products, severe metastatic calcification or rapidly progressive osteodystrophy should be considered for parathyroidectomy. Newer, experimental vitamin D preparations, such as 1,25-dihydroxycholecalciferol or 1-alpha-hydroxycholecalciferol, should improve the managemet of patients with renal osteodystrophy and decrease the need for parathyroidectomies.

Bone and Bones↗

PubMed1983

Parathyroid hormone response to hypocalcemia in hemodialysis patients with osteomalacia.

The parathyroid hormone response to hypocalcemia was investigated in hemodialysis patients with osteomalacia and compared to those with osteitis fibrosa. Hypocalcemia was induced during hemodialysis by employing a dialysate devoid of calcium. Patients with osteomalacia had a blunted maximum amino terminal parathyroid hormone response (+/- SD) (0.39 +/- 0.33 vs. 0.87 +/- 0.53 ng/ml, P less than 0.05) and maximum carboxy terminal parathyroid hormone response (+/- SD) (0.36 +/- 0.20 vs. 0.84 +/- 0.47, P less than 0.02) to hypocalcemia. The decline in plasma calcium was greater in patients with osteomalacia at 90 (P less than 0.05), 120 (P less than 0.01), and 150 min (P less than 0.01). In osteomalacia patients the surface density of histologically detectable trabecular bone aluminum correlated directly with the percent relative osteoid volume (P less than 0.005) and inversely with the maximum amino terminal parathyroid hormone response to hypocalcemia (P less than 0.025). These results suggest that hemodialysis patients with osteomalacia have diminished secretion of parathyroid hormone and a decreased ability to restore plasma calcium homeostasis during hypocalcemia.

Bone and Bones↗

PubMed1982

Deterioration of renal bone disease in patients treated with salmon calcitonin.

Twelve patients with chronic renal failure and osteitis fibrosa were treated for periods of 1-9 months with thrice-weekly injections of 10-200 iu salmon calcitonin. Treatment had no significant effects on symptoms of bone disease and side effects were common. A transient fall in plasma alkaline phosphatase levels occurred in only three patients, and both plasma alkaline phosphatase and hydroxyproline levels rose in the majority of patients. Radiographic signs of hyperparathyroidism increased in seven of the nine patients treated for longer than 3 months. Paired bone biopsy specimens in nine patients showed significant increases in osteoblast counts, but no changes in the indices of resorption. These treatment-induced changes were reversed when treatment with 1,25-dihydroxyvitamin D3 was substituted for calcitonin. The use of this regimen of salmon calcitonin is not recommended in the long-term management of hyperparathyroid bone disease in chronic renal failure.

Adult↗

PubMed2005

Significance of minimodeling in dialysis patients with adynamic bone disease.

BACKGROUND: We previously concluded from histomorphometric analysis that minimodeling contributes to bone formation in adynamic bone disease in patients with primary hypoparathyroidism. Presently we investigated whether this mechanism might be peculiar to adynamic bone disease. METHODS: We histomorphometrically analyzed bone specimens obtained at biopsy or autopsy from 26 maintenance hemodialysis patients with hyperparathyroidism necessitating parathyroidectomy (group A) and from 27 dialysis patients with hypoparathyroidism (group B); respective mean ages were 60 +/- 7 years vs. 64 +/- 8 years; dialysis duration 14 +/- 6 years vs. 11 +/- 9 years; and serum intact parathyroid hormone (PTH) 1205 +/- 439 pg/mL vs. 41 +/- 27 pg/mL. Group B was divided further into outpatient and inpatient subgroups. RESULTS: By histomorphometry, group A patients were diagnosed with osteitis fibrosa, and those in group B with adynamic bone disease. Minimodeling bone volume and minimodeling bone number were significantly greater in group B than group A (P= 0.0028 and P= 0.0008, respectively). Minimodeling bone volume correlated significantly and positively correlated with total bone volume in group B (P= 0.0016), but not in group A. In group B, minimodeling bone volume and total bone voluem were greater in outpatients than inpatients (P < 0.0001 and P= 0. 025, respectively). Minimodeling bone volume and total bone volume showed significant negative correlation with age in group B (P < 0.001 and P= 0.005, respectively). CONCLUSION: Minimodeling might contribute to bone formation in dialysis patients with adynamic bone disease, in the absence of remodeling stimulated by parathyroid hormone (PTH), especially in relatively young patients with good activities of daily living.

Aged↗

PubMed1975

Management of primary hyperparathyroidism in the elderly.

Of 166 surgical patients for whom the diagnosis of primary hyperparathyroidism was established over a 20-year period, about one-third were over 60 years of age. For an additional 9 patients, or operation was advised, usually because of other life-endangering disease and the presence of only a mild degree of hypercalcemia without complications. In recent years, nearly 50 per cent of the patients did not have renal calculi or osteitis fibrosa cystica; this was unrelated to age. Most of the patients with management problems were seen since 1965. Age alone was not a dominant factor in relation to serious complications from hypercalcemia, the presence of other critical disease increasing the risk of operation, or the development of major postoperative complications. The only death from primary hyperparathyroidism occurred in a 74-year old patient who refused re-operation and died from an acute hypercalcemic crisis. A liberal, but selective, policy of surgical treatment is justified for primary hyperparathyroidism in the elderly. Patients for whom the diagnosis of primary hyperparathyroidism is established may be separated into three groups: those for whom early operation is indicated, those for whom operation should be delayed to permit recovery from other life-endangering acute disease, and those for whom operation is unjustified because of minimal uncomplicated hypercalcemia and other serious disease greatly limiting life expectancy. These categories encompass all age groups and are not restricted to the elderly. All patients require periodic re-evaluation.

Adult↗

PubMed2006

Development of renal bone disease.

Renal osteodystrophy (ROD) develops as the early stages of chronic renal failure (CRF) and covers a spectrum of bone changes observed in the uraemic patient, which extend from high remodelling bone disease (frequently known as osteitis fibrosa) to low turnover, or adynamic disease. Between these two extremes there are also cases of bone mineralization compromised in variable degrees, as is the case of 'mixed bone disease' and osteomalacia. The dynamic process of bone remodelling is compromised in CRF, and a positive or negative bone balance can be observed in uraemic patients. In addition to the classic modulators of bone remodelling, like parathyroid hormone, calcitriol and calcitonin, other factors were recently identified as significant modulators of osteoblast and osteoclast activation in uraemic patients. In fact, different cytokines and growth factors, acting at an autocrine or paracrine level, seem to play a relevant role in the bone and mineral changes observed in uraemia. Recently, observations have been made of the development of more sensitive and specific techniques to assay different biochemical markers of bone turnover and mineral metabolism. Analogously, new contributions of conventional bone histology, bone immunocytochemistry and molecular biology, which enabled the understanding of some etiopathogenic mechanisms of ROD, were observed.

Bone and Bones↗

PubMed1986

Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations.

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.

Adolescent↗

PubMed1979

Serum alkaline phosphatase in azotemic and hemodialysis osteodystrophy: a study of isoenzyme patterns, their correlation with bone histology, and their changes in response to treatment with 1alphaOHD3 and 1,25(OH)2D3.

One hundren seventy-eight azotemic patients, 114 on hemodialysis, had measurements of total serum ALP, and definition of isoenzyme patterns on acrylamide gel electrophoresis. In addition, bone histomorphometry was defined in all of the patients by means of transiliac bone biopsies. Serial estimations over 2 years were carried out on several patients, including some being treated with vitamin D2, 1alphaOHD3, and 1,25(OH)2D3. (1) In both nondialyzed and dialyzed patients, serum ALP showed a significant positive correlation with osteitis fibrosa due to secondary hyperparathyroidism irrespective of the presence or absence of concurrent osteomalacia. Increases in the bone isoenzyme were largely responsible for the rise in total ALP. (2) A higher incidence of osteomalacia (p less than 0.001) was observed in patients on hemodialysis in Newcastle Upon Tyne. In hemodialyzed patients where osteomalacia was accompanied by either no secondary hyperparathyroidism (21 patients) or minimal secondary hyperparathyroidism (14 patients), serum ALP remained within normal limits, giving no indication of the existing osteomalacic bone disease. Isoenzyme studies revealed a high prevalence of the intestinal type and also varied combinations of hepatic, intestinal, and bone types. (3) Good response to vitamin D depended on the presence of significant amounts of the bone isoenzyme. Azotemic osteodystrophy characterized by a raised serum ALP and a prominent bone isoenzyme predicted a good response to vitamin D, and the decrease in serum ALP following vitamin D was the result of a reduction in the bone isoenzyme. Patients with symptomatic dialysis osteomalacic bone disease, accompanied by normal total serum ALP and no elevation of the bone isoenzyme, responded less well.

Alkaline Phosphatase↗

PubMed2004

[Brown tumor in hyperparathyroidism secondary to chronic renal failure].

Brown tumor (BT) is an uncommon condition that represents the terminal stage of the cystic osteitis fibrosa and have been increasingly reported in hyperparathyroidism secondary to renal failure, due to the increase of survival in patient with hemodialysis. The fine needle aspiration diagnosis is of great importance in the recognition of the BT, although it can be difficult to distinguish it of lesions as the aneurysmal bone cyst and giant-cell tumor. We describe the case of 20-year-old female with chronic renal failure undergoing hemodialysis during six years. Both x-rays and computer tomography revealed a tumor in head of right humerus and lytic images in scapula of the same side, clavicles and ribs. The patient was subjected to a fine needle aspiration biopsy of the tumor of humerus head and the sample was processed with the habitual technique of inclusion in paraffin and stained with hematoxilina and eosina. Histological preparations showed several multinucleate giant cells and spindly or fibrillary cells, feature that was pointed out as compatible, in a context of secondary hyperparathyroidism to chronic renal failure, with a BT. We consider that the radiological and tomographyc finds, besides the history of chronic renal failure with a long history of hemodialysis, were enough to link, with great approach, the histopathology with the diagnosis of BT.

Adult↗

PubMed1988

Renal osteodystrophy: some new questions on an old disorder.

The two major lesions of renal osteodystrophy are osteitis fibrosa cystica (OFC) and osteomalacia (OM). OFC is the characteristic bone lesion of uremic hyperparathyroidism. Although renal failure causes predictable parathyroid hyperplasia, the precise pathogenetic mechanism is still not defined. The "hyperphosphatemia-hypocalcemia-parathyroid hormone (PTH) hypersecretion" sequence of events is no longer an adequate model for the pathogenesis of uremic hyperparathyroidism. Other abnormalities associated with uremia include reduced 1,25-dihydroxyvitamin D (1,25D) synthesis, changes in intracellular phosphorus content or transcellular phosphate fluxes, or alteration in PTH metabolism, eg, change in set-point for PTH secretion. Each abnormality interacts with others and contributes to PTH hypersecretion, but none can completely account for the development and persistence of hyperparathyroidism in renal failure. The possibility that uremia may directly cause parathyroid hyperplasia remains open. It is also possible that factor(s) that initiate hyperparathyroidism may turn out to be quite different from that which sustains the hyperparathyroid state. Although both vitamin D-deficient and vitamin D-resistant OM may develop in patients with renal failure, the majority of uremic OM seen currently is "vitamin D-refractory." Although now there is persuasive evidence implicating aluminum (Al) accumulation as the major pathogenetic cause for the mineralization defect seen in this disorder, additional disturbances may play important contributory roles. Such factors would include extraskeletal effects of Al, differences in host-susceptibility to this element, the localization of Al within bone, uremia per se, and the participation of other metals and toxins. Finally, possible interactions between hyperparathyroidism and OM of uremia are speculated on.

Aluminum↗