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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Typical features of hereditary vitamin D-dependent (pseudovitamin D-deficient) rickets were observed beginning at ages 20 and 5 months in a brother and sister. Both had calcium malabsorption correctable with high doses of 25-hydroxyvitamin D. During periods of hypocalcemia they both manifested secondary hyperparathyroidism with hypophosphatemia and high serum concentrations of endogenously produced 1,25-dihydroxyvitamin D. In each, normalization of serum calcium concentration and resolution of osteomalacia were obtained with continuous administration of high doses of ergocalciferol or high doses of 1,25-dihydroxycholecalciferol. Chemical features of vitamin D deficiency were corrected in the presence of high circulating concentrations of 1,25-dihydroxyvitamin D2, produced endogenously, or of 1,25-dihydroxyvitamin D3, administered by mouth. Serum concentrations of 25-hydroxyvitamin D2, 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal in five first degree relatives. We conclude that in these five first degree relatives. We conclude that in these siblings, rickets and osteomalacia resulted from a hereditary decreased sensitivity to 1,25-dihydroxyvitamin D at the intestine and perhaps other vitamin D target tissues.
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PMID:A familial syndrome of decrease in sensitivity to 1,25-dihydroxyvitamin D. 23 95

In 6 groups of peri- and post-menopausal women, there was an inverse relation between the urinary sediment smear maturation value and the fasting urinary hydroxyproline/creatinine ratio. Administration of ethinyloestradiol and Progynova both reduced urinary hydroxyproline into the pre-menopausal range, the fall being proportional to the starting value. Oestrogen therapy also produced a significant fall in plasma ionised calcium. In a prospective trial, oestrogen therapy prevented post-menopausal bone loss but calcium therapy was less effective. It is suggested that a high fasting urinary hydroxyproline/creatinine ratio might be taken as an indication for oestrogen therapy in post-menopausal women. In established post-menopausal osteoporosis, pre-disposing risk factors appear to be low calcium intake, malabsorption of calcium and low oestrogen status. These patients appear to represent the fast bone-losers in the post-menopausal population. The accelerated bone loss can be wholly or partially corrected by hormone replacement therapy and by calcium supplements given to those with normal absorption only. These therapies also prevent loss of height due to further crush fractures. The malabsorption of calcium is very resistant to vitamin D therapy but responds to 1alpha-OHD3. Balance data suggest that the most effective therapy may be a combination of 1alpha-OHD3 with oestrogen.
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PMID:The prevention and management of post-menopausal osteoporosis. 26 26

Using a 2-hour 47Ca absorption test, significant depression of active calcium absorption was demonstrated in 48 vitamin D untreated haemodialysis patients. This malabsorption of calcium could be corrected by the daily oral administration of 1--2 microgram of 1alphaOHD3 and 1--1.5 microgram of 1,25(OH)2D3. 5 microgram daily for 2 weeks of 3-deoxy-1alphaOHD3 AND 16 and 64 microgram daily for 1 week of 24R,25(OH)2D3 proved ineffective. In 32 successfully transplanted patients, restoration of normal or near normal renal function (serum creatinine less than 1.9 mg/100 ml) was not always followed by an immediate improvement in active calcium absorption. Calcium absorption, especially in female patients, was adversely affected by the required immunosuppressive prednisone therapy and improvement was slow.
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PMID:Effect of 1alpha-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, 3 deoxy-1alpha-hydroxycholecalciferol, 24R, 25-dihydroxycholecalciferol and successful renal transplantation on calcium absorption in haemodialysis patients. 34 40

Intestinal malabsorption of calcium and the development of osteomalacia in conservatively treated renal failure is explained by a quantitative deficiency of 1,25-dihydroxycholecalciferol, which also contributes to the development of hypocalcaemia. Excess of 25-hydroxycholecalciferol can substitute for this deficiency. The presence and healing of azotaemic osteomalacia is unrelated to the prevailing plasma [Ca] x [P] product. The data suggest that "vitamin D" acts directly on bone mineralisation, but the claim that this apparent effect is normally due to 25-hydroxycholecalciferol is considered unproven. Most of the phenomena of azotaemic osteodystrophy are encountered in simple vitamin D deficiency; as in that condition, deficiency of 1,25-dihydroxycholecalciferol may be of primary significance in causing secondary hyperparathyroidism in renal failure.
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PMID:Vitamin D and the syndromes of azotaemic osteodystrophy. 36 40

Calcium and phosphate absorptions were studied by radiotracer techniques in 30 patients after successful cadaveric renal transplantation, and results were compared with those in a group of normal subjects and in groups of patients with chronic renal failure (CRF). Both calcium and phosphate absorptions were impared in patients with CRF, including those receiving haemodialysis. Abnormalities of calcium absorption, however, seemed to occur earlier in the course of advanced renal failure than abnormalities in phosphate absorption. Calcium absorption improved dramatically after successful renal transplantation, while phosphate absorption remained the same. A dissociation between calcium and phosphate absorptions is not often seen clinically, and the mechanisms for it are unknown. Phosphate malabsorption may be a further contributing factor in the development of persistent hypophosphataemia after transplantation.
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PMID:Dissociation of absorptions of calcium and phosphate after successful cadaveric renal transplantation. 37 43

Malabsorption (M) is characterized by absorption defect of one or several nutriments in small bowel. Its clinical expression is rarely obvious and biological signs are: anaemia, low serum protein, albumin and lipid rates, low serum calcium, phosphorus and potassium level, and hypoprothrombinaemia. But only 4 simple and reliable tests are needed for diagnosis: i. e.: daily faecal fat amount measurement, daily faecal nitrogen excretion, the xylose test and the Schilling's test. This syndrome is related to many conditions which can be divided into 2 groups with and without intestinal abnormalities. The relationships between M and skin diseases belong to 4 types (J. Marks and S. Shuster): 1) M is responsible for the cutaneous signs, 2) M is caused by a skin disease, 3) both M and skin disease are the result of a same cause, 4) M and skin disease are associated in an indirect way. Only the two first types are dealt with in this report. Skin manifestations occur as a complication in 10 p. 100 to 20 p. 100 of cases of M. They are mostly polymorphous or non-specific, as they are related to multiple vitamin or essential amino acid deficiencies and heal with the treatment of M. The main conditions encountered are diffuse pigmentation, acquired ichthyosis, follicular keratosis, nail brittleness and hair loss. Mucous membrane lesions, purpura and eczematoid or psoriasis-like dermatitis have also been described. More uncommon are clubbing of fingers, finger print abnormalities, kwashiorkor or acrodermatitis enteropathica-like eruptions. The dermatogenic enteropathy, i. e. a M syndrome due to a skin disease, occurs as a result of widespread involvement of the body for instance in psoriasis or eczema; its clinical expression is rarely obvious, the histological record of gut biopsy usually normal and the results of biological tests often dissociated, but steatorrhoea is frequently found. The pathogenesis of the condition is still unknown but its importance is related to the extent of the skin disease and it only improves with the treatment of the latter. All these features and others are discussed in the report with a comprehensive review of the literature.
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PMID:[Cutaneous manifestations of malabsorption diseases (author's transl)]. 38 Apr 45

Bone loss can be prevented by standard oestrogen replacement therapy and delayed by the administration of calcium supplements. The most suitable patients to treat are those with a raised urinary hydroxyproline or other evidence of rapid bone loss. Patients aged below 65 years with established osteoporosis, and in whom oestrogens are not contraindicated, will derive some benefit from oestrogen therapy. In those with malabsorption of calcium, vitamin D may be added to oestrogen therapy in a dose not exceeding 10,000 units daily or alternatively, small doses of one of the vitamin D metabolites, e.g. 1 alpha OHD3 (alfacalcidol) 1 microgram daily, or 1,25(OH)2D3 (calcitriol) 0.5 microgram daily. In patients aged over 65 years, supplementary calcium (not less than 1000 mg daily) is recommended.
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PMID:Treatment of postmenopausal osteoporosis. 39 32

The early and late effects of a single high-dose irradiation (100 rad) in the pig small intestine have been studied by histoenzymology and electron microscopy and related to some functional data. 1) The initial atrophy induced by the irradiation appears late (on the 6th day), compared to other species. This is due to the fairly long regeneration time of the villi epithelium in the pig. 2) The initial lesions are similar to those observed in different experimental models (nuclear alterations, karyolytic bodies, etc.). They particularly involve the crypts, and are specially focused in the undifferentiated cells of GS phase or mitosis, but also in goblet and Paneth's cells. 3) The villi regeneration, over on the 23rd day, is preceeded by an active mitotic phase which first renews the undifferentiated cells. This mitotic activity, reaching its highest value on the 16th day, goes on during the whole regeneration period itself. 4) At the beginning, this regeneration is denoted by the high esterase activity of the crypt collar. It appears in many goblet cells and also in some absorptive cells which show, at once, some of the enzymatic activities of the striated border. However, for a short period, lipid absorption is quantitatively reduced. This is connected with the temporary cell immaturity (up to the 20th day) and to the poorly developed rough endoplasmic reticulum and Golgi apparatus. 5) Further on, the persistence of a malabsorption syndrome (lipids, calcium) is not connected, for the main point, with modifications of the morphology or the cytology of the villi (in spite of the abnormally high number of goblet cells and the presence of few pathologic absorptive cells). It is, in fact, related to the persistence of an inflammatory state of the lamina propria associated with an exudative enteropathy. The meaning of this last finding is not clear: it could depend on a primary infectious state due to the modifications of the endoluminal intestinal flora, or, rather, on a secondary infection supported by the trophic epithelial disturbances induced by a continuous vascular dyshoria due to the irradiation.
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PMID:High-dose irradiation in the pig small intestine. Histoenzymology and electron microscopic study. 40 73

Five years following jejunoileal intestinal bypass surgery for obesity, a patient developed debilitating weakness and muscle pain. Osteomalacia was suspected clinically by radiographic and laboratory abnormalities and confirmed by bone biopsy. Malabsorption was documented as well as secondary hyperparathyroidism. Successful treatment of this syndrome with vitamin D and calcium identified a medically reversible disorder which obviated the need for surgical reanastomosis.
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PMID:Osteomalacia and weakness complicating jejunoileal bypass. 43 11

To investigate whether hepatobiliary rickets is caused by defective intestinal absorption of vitamin D or by impaired hepatic hydroxylation of the vitamin, we studied three children who developed severe rickets, hypocalcemia, and hypophosphatemia, two despite having received 400 to 800 IU vitamin D per day by mouth, and one despite prolonged treatment with 10,000 IU daily. On oral vitamin D therapy, plasma vitamin D and 25-hydroxyvitamin D levels were low. When two children were treated with weekly intravenous doses of 3,000 IU vitamin D to approximate the recommended prophylactic allowance, their plasma calcium and phosphate values improved promptly, the radiographic lesions healed, and the plasma concentrations of vitamin D and 25-hydroxyvitamin D became normal. Our studies indicate that the primary cause of hepatobiliary rickets is intestinal malabsorption of vitamin D, not impairment of the hepatic metabolism of the vitamin.
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PMID:Pathogenesis of rickets in chronic hepatobiliary disease in children. 44 26


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