Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe osteomalacia due to causes other than malabsorption and, where renal function was impaired, disproportionate to the degree of renal failure, is described in 15 adults. Only one was younger than 46 years, the median age being 59 years. The diagnosis was not made for months in most patients. After investigation, the patients were grouped as follows: nutritional three cases, "renal" six cases, hypophosphataemia three cases, neurofibromatosis and primary hyperparathyroidism one each. The last patient was poorly nourished and had taken anticonvulsants and analgesics. Most patients responded well to treatment with calciferol. These cases indicate the need to be aware that osteomalacia may occur in previously healthy middle-aged or elderly subjects.
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PMID:Osteomalacia due to unusual causes presenting in adults. 28 91

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
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PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.
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PMID:Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism. 231 Dec 30

For years, brown tumors have been considered to be a characteristic of primary hyperparathyroidism. However, since 1963 several reports indicate the incidence of brown tumors in patients with renal secondary hyperparathyroidism to be 1.5%-1.7%. The appearance of multiple brown tumor lesions is rather uncommon in secondary hyperparathyroidism which is also true for malabsorption as its cause. We report on a 56-year-old man presenting with pain in the bones and multiple osteolyses. A bone biopsy specimen and the laboratory examinations were indicative of secondary hyperparathyroidism caused by malabsorption most likely due to Billroth's II/I gastric resection. Thus, the patient's osteolyses represent brown tumors which have been induced by nutritional secondary hyperparathyroidism.
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PMID:Multiple brown tumors in a patient with nutritional secondary hyperparathyroidism. 292 41

In our first 200 cases of primary hyperparathyroidism confirmed by operation 12 were also shown to have a long history either of a malabsorption syndrome or of chronic renal-glomerular failure. We consider that they first went through a phase of secondary hyperparathyroidism, during which one or more of the glands became autonomous adenamata. This then produced the biochemical changes of "primary" hyperparathyroidism, necessitating excision of the adenoma. This condition is best described as "tertiary" hyperparathyroidism. The transition from secondary to tertiary hyperparathyroidism occurred in four of the 12 patients while under our observation. We think the same process can be traced retrospectively in the other eight cases. The concept of tertiary hyperparathyroidism may help to explain the high incidence of other diseases in association with primary hyperparathyroidism.The behaviour of the parathyroid glands provides a valuable model for the investigation of tumour formation in man. All states occurred in our patients with primary hyperparathyroidism, from normal through hyperplasia to adenoma formation and finally to parathyroid carcinoma.
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PMID:Tertiary hyperparathyroidism. 569 Dec

In the present case a primary hyperparathyroidism was aggravated by postgastrectomy bone disease and led to a spontaneous fracture of the left femur and to a pseudofracture of the right femur. Renal symptoms like concrements or nephrocalcinosis were based on the intestinal conditioned malabsorption of vitamin-D and calcium not evident. Radiologically there was a mixed pattern of ostitis fibrosa cystica generalisata von Recklinghausen and osteomalacia respectively osteoporosis based on postgastrectomy bone disease. Treatment was fully effective consisting of exstirpation of the adenoma and substitution of calcium and vitamin-D and ingestion of digestive enzymes and many little meals corresponding to the prescriptions of nutrition for partially gastrectomised patients.
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PMID:[Left spontaneous femoral fracture in primary hyperparathyroidism and postgastrectomy bone disease following a Billroth II stomach resection]. 662 60

Secondary osteoporosis may be associated with a number of endocrine dysfunctions and metabolic disorders. In this paper, osteoporosis in patients with Cushing's syndrome, hyperthyroidism, primary hyperparathyroidism, acromegaly, hypogonadism and some metabolic disorders such as diabetes mellitus, chronic renal failure and malabsorption syndrome are described. While the major manifestation of bone in these conditions is a reduction of bone mass and may be somewhat different from bone loss in primary osteoporosis histologically or radiologically, it is considered to be the same bone loss as primary osteoporosis in the present paper. In some conditions, for example, Cushing's syndrome, diabetes mellitus etc, factors responsible for bone loss are demonstrated.
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PMID:[Osteoporosis associated with endocrine dysfunctions or metabolic disorders]. 796 90

The effects of endocrine disease on bone mass continue to attract attention. Investigations include the effects on the skeleton of thyroid disease, primary hyperparathyroidism, and their treatment. The effect of growth hormone replacement in adults with panhypopituitarism has also been investigated; children with treated growth hormone deficiency appear to reach adulthood with low bone mass. The indications for surgery in asymptomatic primary hyperparathyroidism have recently been reviewed. The associations between autoimmune thyroid disease and connective tissue disease have been investigated. Although patients with Graves' disease are frequently positive for antinuclear antibodies, there appears to be no increased risk of systemic autoimmune disease. The possible pathogenesis of diabetic bone disease via calcium malabsorption, hypercalciuria, reduced bone formation, and collagen abnormalities has been reviewed. A long-term study has clarified the links among diabetic control, limited joint mobility, nephropathy, and retinopathy. The possible mechanisms by which pregnancy may induce remission in rheumatoid arthritis have been discussed.
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PMID:Endocrine disease. 843 94

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40


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