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

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

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 authors discuss the main features of the complex pathophysiology of patients subjected to duodenocephalopancreatectomy, and particularly the difficulties inherent in clinical assessment of the digestive and metabolic impairment consequent upon the duodeno-gastro-pancreatic mutilation. Out of a total of 57 cases of this description, they singled out for recheck 23 patients who had undergone duodenocephalopancreatectomy not less than six months and not more than seven years before (chronic pancreatitis, 11 cases; various malignancies of the periampullar area, 10 cases; Zollinger-Ellison syndrome, 1 case; retroperitoneal lymphoma, 1 case). Seventy-six per cent of patients who had been gainfully employed were able to resume their jobs after surgery. Steatorrhea, assessed in terms of fecal fats, was present in all cases; notwithstanding, 70% of the patients gained weight (average increase 7 kg). All patients were on enzyme replacement therapy. Only 4% developed diabetes, and none developed postoperative peptic ulcers. Conversely there was a high incidence (65%) of bone structure reshuffling, signally osteoporosis, probably imputable to steatorrhea and vitamin D malabsorption, plus the often associated increase of serum alkaline phosphatase activity.
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PMID:[The biological results of duodenocephalopancreatectomy. Clinical evaluations based on a long-term follow-up]. 53 2

Balance studies were performed in thirty-three post-menopausal women (all but five having vertebral crush fractures or femoral neck fractures) in the basal state and on treatment with 1alpha-hydroxyvitamin D3 and/or oestrogenic hormones. The results suggest that the effectiveness of oestrogen therapy is limited by calcium malabsorption and the effectiveness of 1alpha-hydroxyvitamin D3 is limited by oestrogen deficiency. The best results were obtained with combined therapy to remedy what appears to be two distinct deficiencies. To minimize the risks of hypercalcaemia and the possible risks of hormone therapy, we suggest that the treatment of choice in post-menopausal osteoporosis may be 1alpha-hydroxyvitamin D3 1microgram daily and ethinyloestrodiol 25 microgram daily for 3 weeks in every 4. Patients on a low dietary intake of calcium should probably be given calcium supplements. With this regimen, it should not be necessary to screen patients initially for calcium malabsorption or oestrogen deficiency because the majority of patients present with a combination of the two factors.
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PMID:The effect of 1alpha-hydroxyvitamin D3 with and without oestrogens on calcium balance in post-menopausal women. 60 14

Hepatic osteodystrophy consists of three types: osteomalacia, osteoporosis, and periosteal reaction with new bone formation. Secondary hyperparathyroidism is very rare, if it occurs at all. The cause of osteomalacia appears to be vitamin D deficiency due to a lack of vitamin D substrate. In the presence of adequate substrates, 25-OHD and dihydroxy vitamin D metabolites are formed. The vitamin D deficiency results in osteomalacia and malabsorption of calcium and phosphorus. The osteomalacia can be treated successfully with vitamin D supplements. In some patients calcium, phosphorus, and magnesium supplements may be required. The aetiology and treatment of the osteoporosis and the periosteal reactions remain obscure.
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PMID:Hepatic osteodystrophy. 70 74

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.
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PMID:Senile and postmenopausal osteoporosis. 76 91

Calcium metabolism was studied in a 12-year-old girl preseting with idiopathic juvenile osteoporosis. Absorption of orally administered 47-Ca was high. Serum calcium and phosphorus, serum immunoreactive PTH and CT and tubular phosphate reabsorption were found to be within normal limits. The data suggest that calcium malabsorption, nutritional calcium deficiency, hyperparathyroidism, a dysfunction related to sex hormones, and Cushing's syndrome cannot be implicated in the aetiology of the osteoporosis in this case who recovered spontaneously with sexual maturation.
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PMID:A case-report of idiopathic juvenile osteoporosis with particular reference to 47-calcium absorption. 89 71

The records of a series of 700 patients with inflammatory bowel disease, 498 with Crohn's disease and 202 with ulcerative colitis, have been analyzed to determine the relative incidence and characteristic features of their extra-intestinal manifestations. The group with Crohn's disease included 62 with colitis, 223 with ileocolitis, and 213 with regional enteritis. A consideration of the clinical patterns and an understanding of their pathophysiology suggested a subdivision into two main groups: one "colitis related" and one related to the pathophysiology of the small nonspecific third group. Group A, colitis related, comprises joint, skin, mouth, and eye disease. The complications might be immunologically determined, were closely associated with active inflammation, and often responded to medical or surgical treatment of the underlying bowel disease. They occurred in 36% of the entire series of patients: joints were involved in 23%, skin in 15%, and mouth and eye each in 4%. Pyoderma gangrenosum was observed most often in ulcerative colitis and erythema nodosum most often in granulomatous colitis. The incidence of Group A complications was higher in disease involving the colon (42%) than in disease restricted exclusively to the small bowel (23%). There were interrelationships among the various members of Group A, with multiple manifestations occurring in a third of affected patients. Group B, related to small bowel pathophysiology, includes malabsorption, gallstones, kidney stones, and non-calculous hydronephrosis and hydroureter. Disorders in this group were generally related to the severity of the disease in the small bowel and tended to persist even in the absence of active inflammation. In contrast to Group A, this group occurred most frequently in small bowel disease, and least in colonic disease. Malabsorption was virtually confined to the patients with small bowel disease (10% incidence), while gallstones and renal stones were also both more frequent in Crohn's disease (11% and 9% respectively), the latter usually in association with small bowel resection or ileostomy. Group C, found in a small percentage of patients, consists of nonspecific complications, including osteoporosis (3%), liver disease (5%), peptic ulcer (10%), and amyloidosis (1%).
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PMID:The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients. 95 99

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.
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PMID:Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone. 97 17

Presenile mandibular atrophy has been regarded as a bony condition in isolation. Direct vision of the mandible at the lower border and ascending rami at augmentation procedures in two cases clearly showed that the condition had affected the whole bone in all dimensions. A suggestion is made that mandibular atrophy arises as a result of many contributory factors, some local, but usually based on generalised undisclosed malabsorption states or osteoporosis.
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PMID:Presenile mandibular atrophy: its aetiology, clinical evaluation and treatment by jaw augmentation. 106 56


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