Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a four-year period, 27 patients underwent total parathyroidectomy with autotransplantation of parathyroid tissue to the forearm. In order to minimize the risk of persistent or recurrent hyperparathyroidism (HPT), a routine thymic resection and a wide excision of fat tissue around the parathyroids was performed to ensure excision of possible supernumerary glands or rudimentary parathyroid tissue. The indications for operation were HPT secondary to chronic renal failure in 24 patients (22 of whom had hypercalcaemia) and persistent or recurrent primary HPT in 2 cases. One further patient, who had a multiple endocrine neoplasia syndrome type I, underwent this procedure at the primary parathyroid operation. Preoperative hypercalcaemia was reversed in all patients but three during the first postoperative days, concomitantly with a fall in the parathyroid hormone (PTH) level. Fourteen patients showed marked hypocalcaemia postoperatively, necessitating calcium or vitamin D supplementation. This medication could later be discontinued in all of them. Thirteen patients, including two of those with primary HPT, never required any supplemental therapy. Survival of the grafts was documented by several observations. In all patients normal serum calcium values were being maintained without supplemental therapy at follow-up. During induced hypocalcaemia a PTH secretory response was demonstrated in all eight studied patients with a gradient between the grafted and non-grafted arm. In two patients in whom the grafts were examined histologically 19 and 28 months after the transplantation, viable parathyroid tissue was observed. In the initial part of the study excised tissue was cryopreserved. Since persistent hypocalcaemia did not occur in our patients, we have now abandoned this safety precaution. Thus, total parathyroidectomy with autotransplantation of parathyroid tissue is a valuable method for restoring long-term parathyroid function in patients with secondary HPT and uraemia. It also appears of value in selected cases of primary HPT.
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PMID:Parathyroid autotransplantation. An investigation of parathyroid autograft function. 665 65

Nitrogen balance was studied in 4 patients with uremia during treatment with a protein-reduced diet (20 g) supplemented with either essential amino acids and histidine or a mixture of keto analogues of five of the essential amino acids and essential amino acids. 3 patients completed the study. Nitrogen balance was negative on the diet only and was improved with both forms of supplementation. However, supplementation with the keto acids did not offer any advantage over the conventional essential amino acid supplementation. 1 patient developed serious hypercalcemia during treatment with the keto acid supplementation.
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PMID:Nitrogen balance studies in patients with uremia during treatment with protein-reduced diet and supplementation with essential amino acids or keto acids. 670 48

A 50-year-old carpenter with stable pulmonary sarcoidosis for nine years underwent uneventful right total hip replacement. Four months later he developed nausea, renal failure, and hypercalcemia. The hypercalcemia and uremia promptly subsided with corticosteroid therapy and no other etiology except sarcoidosis could be established to explain the hypercalcemia. Hypercalcemia did not recur following discontinuation of corticosteroid therapy. These events suggest trauma to bone can precipitate hypercalcemia in patients with stable sarcoidosis, and serum calcium levels should be monitored for three-six months following trauma to bone from surgery or accidents in these patients.
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PMID:Hypercalcemia following bone surgery in a patient with stable pulmonary sarcoidosis. 688 6

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
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PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

The contribution of bone scintigraphy to the diagnosis of skeletal involvement in multiple myeloma was evaluated in a consecutive, unselected series of 25 previously untreated patients. Definite scintigraphic abnormalities were found in 11 patients (localized in 4, generalized in 7) (44%). In the majority of patients the clinical value of the information gained from scintigraphy was roughly equal to that found by radiography. However, 2 patients with normal and 2 with questionable bone scans had X-ray evidence of skeletal involvement, and the extent of bone destruction in 4 cases was seriously underestimated in the bone scans. Small osteolytic lesions were as a rule not detected by scintigraphy. On the other hand, in 8 patients the bone scan added information of involvement of ribs, pelvis and vertebrae, not clearly visualized by X-ray. In 2 patients, both with IgA myeloma, hypercalcemia and uremia, a massive extraskeletal uptake of the bone-seeking isotope was observed. Autopsy verified in one case the presence of a disseminated metastatic calcification.
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PMID:Bone scintigraphy in the diagnosis of skeletal involvement and metastatic calcification in multiple myeloma. 711 58

A model of chronic renal failure was created in nine adult sheep by two-stage, subtotal nephrectomy. Carotid-jugular cannulas provided clot-free access for 72 to 274 days without exit-site infections. All sheep became uremic and anemic. Median survival, while uremic, was 145 days (72 to 327 days), although three were sacrificed. Five required dialysis within the first week of uremia, and median survival on dialysis was 70 days (41 to 177 days). Sheep that maintained adequate nutrition survived the longest on dialysis. Mean creatinine and BUN levels in the stable uremic and dialyzed sheep were 4.8/95 and 7.8/59 mg/dl, respectively. The other serum chemistries remained unchanged (mean values) from normal, although one sheep died of hypercalcemia (17.8 mg/dl). Renal blood flow correlated to GFR in both normal and uremic states. GFR fell more than serum creatinine rose, suggesting extrarenal excretion of creatinine.
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PMID:Physiologic studies in normal and uremic sheep: I. The experimental model. 720 57

Calcitonin-secreting cells, 'C cells', have specific receptors for calcitriol, thus the calcitriol deficiency in uraemia may affect calcitonin secretion and/or production. The aim of the present study was to evaluate in CAPD patients the effect of calcitriol replacement (4 weeks of oral calcitriol, 0.5 micrograms/day) on both, basal calcitonin concentration and calcitonin response to calcium infusion (calcium gluconate, 3 mg/kg/h). Calcitriol replacement produced a normalization of serum calcitriol level without a significant change in serum calcium concentration. After calcitriol replacement, basal calcitonin increased from 78 +/- 15 to 101 +/- 13 pg/ml, P < 0.05. The increment in calcitonin induced by a calcium infusion was lower after (15 +/- 4 pg/ml) than before (29 +/- 4 pg/ml) calcitriol replacement. In addition, calcitriol administration induced a decrease in serum PTH level. Replacement of calcitriol in CAPD patients produced an increase in serum calcitonin concentration and a decrease in the calcitonin response to hypercalcaemia.
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PMID:Effect of calcitriol replacement on serum calcitonin and parathyroid hormone levels in CAPD patients. 772 33

Nonmedullary thyroid carcinoma is known to occur in association with primary hyperparathyroidism. A combination of secondary, uremic, hyperparathyroidism and non-medullary thyroid carcinoma is rare and was hitherto reported in only 12 cases. We report another three patients with this parathyroid/thyroid disease combination, suggesting that it may represent not merely a coincidence. A number of factors active in secondary hyperparathyroidism may play a role in the induction and/or promotion of the thyroid cancer. These include parathyroid endocrinopathy, goiterogenic effect of prolonged hypercalcemia, and uremia. During surgery on the parathyroid glands, associated thyroid lesions demand special considerations.
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PMID:Secondary hyperparathyroidism and nonmedullary thyroid cancer. 774 92

Adynamic (or aplastic) bone disease is a bone histologic pattern characterized by decreased bone formation rate, low cellularity, and normal or decreased osteoid thickness. It was first described in symptomatic patients undergoing dialysis who were overloaded with aluminum because of contaminated dialysate or chronic ingestion of aluminic phosphate binders; the evidence of the overload was extensive coloration (more than 25%) with aurin tricarboxylic acid, whereas the Perls stain coloration for iron was negative. We have, however, reported these histologic changes in asymptomatic patients with uremia who were never exposed to aluminum, in two patients before end-stage renal failure and in six patients undergoing dialysis. The main step in the prevention of adynamic bone disease is the absolute exclusion of aluminum exposition even by so-called "safe doses" of aluminum phosphate binders because in the long term they are never actually safe. Because idiopathic adynamic bone disease may nevertheless occur, parathyroid hormone suppressive treatment by oral calcium taken with meals as phosphate binders (+/- 1 alpha-hydroxyvitamin D3 derivatives) should be carefully monitored by measurements of plasma concentrations of not only calcium and phosphate but also of intact parathyroid hormone levels. In order to have normal bone formation rate levels, patient intact parathyroid hormone levels should be between one and three times the upper limit of the normal level. Although adynamic bone disease may not be a true bone disease when not due to aluminum, it is a risk factor for increased incidence of hypercalcemia and hyperphosphatemia and therefore for metastatic calcifications. Therefore, when hypercalcemia occurs with hyperphosphatemia and normal intact parathyroid hormone in patients treated with 1 alpha-hydroxyvitamin D3, it is proposed that the latter drug should be discontinued first, whereas oral calcium is increased to correct hyperphosphatemia, and calcium concentration is decreased in the dialysate to prevent hypercalcemia, even though plasma parathyroid hormone may increase up to three times the upper limit of the normal level. In patients previously exposed to aluminum, a deferoxamine test should be performed and a deferoxamine treatment started if the test is positive.
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PMID:Adynamic bone disease in patients with uremia. 807 43

The renal concern in a multiple myeloma (MM) case has a frequency of 50% and causes a worsening of the disease with a survival average of about 12 months. The monoclonal light free chains (CLL) produced in excess by the plasmacytes are present in the urine as proteinuria of Bence Jones (PBJ) in 60-70% of patients affected by MM. They represent the major pathogenetic factor of the nephropathy in course of MM as they can deposit in shape of intratubular "casts" in the myeloma casts nephropathy (MCN). In some worse cases, dehydration or hypercalcaemia can cause an irreversible acute renal insufficiency (RI). It is therefore important in a patient affected with MM with PBJ to prevent, locate and opportunely treat these situations which worsen the nephropathy. Beside the tubular cast nephropathy, the CLL "accumulate" in the kidney even though with a lower frequency compared to MCN, in the light chains deposition disease (LCDD) and in the amyloidosis AL (AL). LCDD is characterized by a deposit of nodular amorphous materials PAS positive in the glomerulus and sometimes even in the tubulus. It usually presents itself as a chronic RI and a proteinuria causing nephrotic syndrome (NS). This quickly evolves into uraemia and its evolution can be lessened by the MM treatment. AL in course of MM also reveals with a chronic RI and NS. CLLs deposit in the typical fibrillar structure, on the vessel walls, in the glomerulus, in the mesangium and can be marked out with the Congo red colouring and the subsequent green birefringence through microscope with polarized light. Prognosis of AL is extremely severe and no benefit is given by the treatment of the hematological illness. It is therefore absolutely necessary to study the renal histology through biopsy when MM is grade B, that is, with serumal creatinine above 2 mg/dl as: MCN imposes the MM treatment programme in order to reduce the tubular excess of PBJ and to attempt to make RI reversible; MCN with tubular atrophy and interstitial fibrosis results in an unfavourable prognosis as it expresses a nephropathic irreversibility due to the loss nephrons. It will therefore necessary to start on a renal substitutional treatment programme. Renal damage in course of MM is not always tubular, rather an unexpected glomerular damage of LCDD or amyloidosis AL type can be found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The kidney in multiple myeloma. The physiopathological and clinical aspects]. 818 90


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