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)

Wasting occurs in approximately 20 percent of people with AIDS and is associated with higher mortality rates and diminished quality of life. Weight loss in HIV-positive patients targets lean body mass or muscle rather than fat. Wasting syndrome is currently defined as a 10 percent loss in body weight accompanied by 30 days of fever and/or diarrhea. Many physicians find the definition too limiting and are modifying the criteria to make it more inclusive of earlier forms of the disease. Wasting is caused by inadequate calorie intake, malabsorption of nutrients, an altered metabolic rate, and hormone deficiency. Physicians need to monitor body composition of people with HIV to prevent and reverse the loss of lean body mass.
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PMID:How to recognize wasting syndrome. 1136 21

During growth, estrogen deficiency in females may produce increased bone size as a result of removal of inhibition of periosteal apposition, while failed endosteal apposition produces thin cortices and trabeculae in the smaller bone. In males, androgen deficiency produces reduced periosteal and endosteal apposition, reduced bone size, and cortical and trabecular thickness. At completion of longitudinal growth, advancing age is associated with emergence of a negative bone balance in each basic multicellular unit (BMU) because of reduced bone formation. Bone loss occurs, but slowly because the remodeling rate is slow. In midlife, in females, estrogen deficiency increases remodeling rate, increases the volume of bone resorbed, and decreases the volume of bone formed in each of the numerous BMUs remodeling bone on its endosteal (endocortical, trabecular, intracortical) surfaces so bone loss accelerates. In males, remodeling rate remains slow and is driven largely by reduced bone formation in the BMU. Hypogonadism in 20% to 30% of elderly men contributes to bone loss. In both sexes, calcium malabsorption and secondary hyperparathyroidism may partly be sex-hormone dependent and contributes to cortical bone loss. Concurrent periosteal apposition partly offsets endosteal bone loss, but less so in women than in men. More women than men fracture because their smaller skeleton incurs greater architectural damage and adapts less by periosteal apposition. Sex hormone deficiency during growth and aging is pivotal in the pathogenesis of bone fragility.
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PMID:Estrogen, androgen, and the pathogenesis of bone fragility in women and men. 1603 88

Patients with inflammatory bowel disease (IBD) are at increased risk for osteoporotic fracture. Bone density testing and osteoporosis management are recommended for IBD patients at greater risk for fracture (ie, postmenopausal women, men aged . 60 years, and those with low body mass indices, glucocorticoid use, family history of osteoporosis, and malabsorption). Patient management includes modification of osteoporosis risk factors, such as calcium and vitamin D supplementation, hormone deficiency correction, and smoking cessation. When indicated, bisphosphonates, such as risedronate and alendronate, have been shown to increase bone mass and reduce fracture risk in patients with glucocorticoid-induced osteoporosis. Infliximab, an anti-tumor necrosis factor a antibody, increases bone mineral density, but this effect has not as yet translated into reduced fracture risk.
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PMID:Osteoporosis in patients with inflammatory bowel disease: risk factors, prevention, and treatment. 1669 75