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)

Intestinal calcium malabsorption in postmenopausal osteoporotic women is often linked indirectly to decreased serum 1,25(OH)2 vitamin D or to intestinal resistance to its action, rather than directly to the low circulating estrogen that results following menopause. The studies presented indicate that the intestinal mucosal cells of rats contain estrogen receptor immunoreactivity, express the mRNA for estrogen receptors, and respond directly to 17 beta-estradiol with enhanced calcium transport that is suppressed by gene transcription and protein synthesis inhibitors. These findings suggest that estrogen has a physiological role in the regulation of intestinal calcium absorption and that its deficiency in postmenopausal osteoporosis, and following therapeutic oophorectomy, may result directly in calcium malabsorption that is believed to be an important factor in the bone loss that occurs in these conditions.
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PMID:Evidence for estrogen receptor-linked calcium transport in the intestine. 832 21

Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.
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PMID:Osteoporosis in men. New insights into aetiology, pathogenesis, prevention and management. 988 98

To our knowledge, raloxifene hydrochloride, a selective estrogen receptor modulator, has never been reported to interfere with absorption of levothyroxine. We describe a 79-year-old woman with chronic, treated primary hypothyroidism, presenting with increasing levothyroxine requirement while taking raloxifene at the same time as levothyroxine. For two 6- to 8-week periods, we separated the ingestion of raloxifene and levothyroxine by about 12 hours. In addition, we tested the absorption of 1.0 mg of levothyroxine sodium with and without the coadministration of 60 mg of raloxifene hydrochloride on 2 separate occasions by collecting serial blood samples for 6 hours. Hypothyroidism occurred in a reproducible fashion whenever levothyroxine and raloxifene were administered together and improved whenever they were taken separately. Combined administration of levothyroxine and raloxifene resulted in lower levels of serum thyroxine compared with administration of levothyroxine alone. By a yet unknown mechanism, raloxifene caused malabsorption of levothyroxine in our patient when coadministered.
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PMID:Raloxifene causing malabsorption of levothyroxine. 1279 75

Inflammatory bowel diseases, most frequently Crohn's disease, are frequently accompanied by decreased bone mineral content (30-70%). The osteopenia is not explained by the side effects of treatment or the secondary malabsorption. There must be a common pathological pathway in the background. The mineral content of bones is most easily measured by dual-ray absorptiometry. The measurement should be performed at the time of the diagnosis of bowel disease. It is useful to perform some routine laboratory examinations (serum calcium and phosphate, urinary calcium excretion level, etc.) and some special tests (serum osteocalcin and crosslaps) to exclude some other pathological pathways as well as to plan the anti-osteoporotic therapy. Appropriate calcium and vitamin-D supplementation is essential in prevention and therapy as well. Several drug-classes have proven useful in the therapy of severe osteoporosis associated with inflammatory bowel diseases such as bisphosphonates, hormone replacement therapy, selective estrogen receptor modulators and calcitonin. The authors provide an algorithm for the therapy of metabolic bone disease in inflammatory bowel disease.
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PMID:[Osteoporosis associated with inflammatory bowel diseases]. 1520 26

Roux-en-Y gastric bypass is a gastric reduction duodenal switch with a combination of restrictive and malabsorptive procedures. It is the most common gastric bypass procedure performed in the United States. Malabsorption causing nutritional deficiencies does occur, yet a PubMed literature search (1955-2009) returned no reports of malabsorption of anticancer agents after gastric bypass. To our knowledge, this is the first report of three cases of malabsorption of the anticancer agent tamoxifen after this procedure. The first patient was a 58-year-old woman who underwent Roux-en-Y bypass for morbid obesity. Two years later, she developed estrogen receptor-positive ductal carcinoma in situ of the breast, underwent lumpectomy and irradiation, and tamoxifen was started. Two years after that, she presented with concerns of potential malabsorption of the drug. Her plasma tamoxifen level was 28 ng/ml, which was below the lower limit of the therapeutic range (77-274 ng/ml for 10-30-mg/day regimens). The second patient was a 51-year-old woman who sought medical advice on risk reduction for breast cancer after receiving a diagnosis of atypical ductal hyperplasia of the breast. She also had a history of morbid obesity and underwent Roux-en-Y bypass. Tamoxifen was started to reduce her risk of breast cancer; her plasma tamoxifen level was subtherapeutic at 14 ng/ml. The third patient was a 53-year-old woman with estrogen receptor-positive breast cancer who underwent lumpectomy and was prescribed anastrozole, an aromatase inhibitor. She also underwent Roux-en-Y bypass for morbid obesity. As she experienced adverse effects while receiving anastrozole, the drug was discontinued, and tamoxifen 20 mg/day was started. Her tamoxifen plasma level was 52 ng/ml. Therefore, her tamoxifen dosage was increased to 20 mg twice/day. Six weeks later, her tamoxifen level was 120 ng/ml (therapeutic range 95-520 ng/ml for the increased dosage). These three cases suggest that steady-state serum tamoxifen levels should be evaluated in patients who have undergone Roux-en-Y gastric bypass. Until adequate data suggest otherwise, parenteral anticancer alternatives should be considered when systemic therapy is needed in a patient with malabsorption.
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PMID:Tamoxifen malabsorption after Roux-en-Y gastric bypass surgery: case series and review of the literature. 2009 95