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)

Coeliac disease is an immune-mediated disorder resulting in nutrient malabsorption now thought to have a prevalence of between 1:100 and 1:200 in the UK population. Symptoms can include diarrhoea, steatorrhoea, abdominal bloating, cramps, flatulence, weight loss, weakness and fatigue. In addition to the morbidity associated with presenting symptoms, patients are also at increased risk of metabolic bone disease, enteropathy-associated T-cell lymphoma and other malignancies (gastric, oesophageal, bladder, breast, brain). There appears to be a strong genetic component to this disease. This article provides a short review of the historical, clinical and genetic aspects of this disease and highlights several findings from recent structural and molecular immunology studies. A model of the pathogenesis is proposed where the contributions of innate and adaptive immune systems are delineated and the essential dual roles of gliadin (from ingested gluten) in the initiation and maintenance of this disease are summarised. Finally, potential future therapeutic options based on this new understanding are discussed.
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PMID:The molecular basis of coeliac disease. 1682 Sep 91

Metabolic bone disease is often silent, often undiagnosed, and occurs frequently in patients with chronic gastrointestinal illnesses. Potentially modifiable risk factors, such as malnutrition, malabsorption, prolonged use of glucocorticoids, and a sedentary lifestyle, can lead to low bone mass, an increased rate of bone loss, and debilitating bone disease. This article explores common gastrointestinal illnesses that place patients at risk for developing metabolic bone disease. Concepts are presented to assist the practitioner in identifying patients at risk; clinical evaluation and diagnostic test selection are discussed, and therapeutic options for the prevention and treatment of metabolic bone disease in gastrointestinal illness are presented.
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PMID:Metabolic bone disease in gastrointestinal illness. 1747 81

The availability of osteodensitometry has contributed significantly to increase the awareness of inflammatory bowel disease (IBD)-associated bone disease. Reported osteoporosis prevalence in patients with IBD range from 2% to 30%. The fractures risk varies between studies, influenced by demographic, clinical and genetic factors. The main pathogenetic factors involved are malabsorption, treatment with glucocorticoids, inflammation (increased cytokine production) and hypogonadism. A screening should be considered for all patients with small bowel Crohn's disease and especially for those with extensive disease, multiple resections, and malnutrition. Supplementation with both calcium and vitamin D is frequently the first step taken, but is insufficient to inhibit bone loss in many patients requiring use of glucocorticoids. Among available therapies, only biphosphonates are effective for treatment of glucocorticoid-induced osteoporosis.
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PMID:A 2008 panorama on osteoporosis and inflammatory bowel disease. 1829 97

Chronic vitamin D deficiency, inadequate calcium intake, and secondary hyperparathyroidism are common in obese individuals, placing them at risk for low bone mass and metabolic bone disease. After bariatric surgery, they are at even higher risk, owing to malabsorption and decreased oral intake. Meticulous preoperative screening, judicious use of vitamin and mineral supplements, addressing modifiable risk factors, and monitoring the absorption of key nutrients postoperatively are essential in preventing metabolic bone disease in bariatric surgery patients.
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PMID:Perioperative management of bariatric surgery patients: focus on metabolic bone disease. 1855 75

Osteomalacia is a metabolic bone disease associated with impaired mineralization of the bone due to Vitamin D and Calcium deficiency that can develop in gastrointestinal disorders. Gastrointestinal malabsorption after surgery, in disorders of the small bowl, in diseases of the hepatobiliary tree and in pancreatic insufficiency can lead to decreased enteral resorption of the fat-soluble Vitamin D and/or depletion of endogenous Vitamin D stores due to abnormal enterohepatic circulation. As a consequence of the Vitamin D deficiency in combination with the underlying condition patients develop an impaired calcium absorption resulting in hypocalcaemia, which leads to defective bone mineralization. Additionally chronic gastrointestinal inflammation and corticosteroid therapy - which is often needed in these patients - have a negative effect on bone metabolism as well. The therapy consists of oral substitution of Vitamin D and Calcium as well as sufficient sun light exposure or in severe cases the use of artificial UVB-radiation.
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PMID:[Gastrointestinal diseases and osteomalacia]. 1871 73

Osteomalacia (OM) is a condition that usually is overlooked and neglected when compared with other metabolic bone disease such as osteoporosis. Presenting with a wide spectrum of nonspecific clinical, radiographic, and biochemical manifestations, OM is a treatable metabolic disease that is precisely diagnosed by anterior iliac crest bone biopsy. Clinical clues to lead one to suspect OM in the context of a diffuse bone disease include the presence of generalized bone pain affecting mainly shoulders, hips and rib cage, proximal muscle weakness, low serum calcium x phosphorus product, increased serum alkaline phosphatase, low calcium in the 24-h urine test, and low serum 25 hydroxyvitamin D. Radiographic examination may show a characteristic "erased" or "fuzzy" type of demineralization, pseudofractures, or bone deformities. OM is confined usually to elderly individuals or to those patients with intestinal malabsorption and hypophosphatemia.
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PMID:Musculoskeletal manifestations of osteomalacia. 1907 64

Rickets and fractures have been reported in captive polar bears. Taurine (TAU) is key for the conjugation of ursodeoxycholic acid (UDCA), a bile acid unique to bears. Since TAU-conjugated UDCA optimizes fat and fat-soluble vitamin absorption, we asked if TAU deficiency could cause vitamin D malabsorption and lead to metabolic bone disease in captive polar bears. We measured TAU levels in plasma (P) and whole blood (WB) from captive and free-ranging cubs and adults, and vitamin D3 and TAU concentrations in milk samples from lactating sows. Plasma and WB TAU levels were significantly higher in cubs vs captive and free-ranging adult bears. Vitamin D in polar bear milk was 649.2 +/- 569.2 IU/L, similar to that found in formula. The amount of TAU in polar bear milk is 3166.4 +/- 771 nmol/ml, 26-fold higher than in formula. Levels of vitamin D in bear milk and formula as well as in plasma do not indicate classical nutritional vitamin D deficiency. Higher dietary intake of TAU by free-ranging cubs may influence bile acid conjugation and improve vitamin D absorption.
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PMID:Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? 1923 63

Lung transplantation has become a viable option for those cystic fibrosis (CF) patients with end-stage lung disease. Despite the challenges that the CF patients present, the survival seen after lung transplantation is more favorable than seen in patients with chronic obstructive pulmonary disease and pulmonary fibrosis. Although the CF patients with severe respiratory disease usually are infected with organisms that display in vitro resistance to the commonly used antibiotics, these patients usually have successful outcomes with transplantation. The other challenges include the presence of nontuberculous mycobacteria, the significant incidence of liver involvement, the development of an ileus or the development of the distal intestinal obstruction syndrome, and the presence of gastroesophageal reflux. Most of the patients have metabolic bone disease, even preoperatively, that warrants treatment, especially with the significant loss of bone density seen in the first year after transplant, thought to be related, in part, to the high dose of corticosteroids. Diabetes mellitus and its consequences are not uncommon. The malabsorption of fat seen in the pancreatic-insufficient patients complicates the absorption kinetics of the anti-rejection drugs. In May 2005 the United Network of Organ Sharing instituted a lung-allocation score to better distribute the donated lungs to those patients who would achieve the most benefit. This score uses several variables to balance the likelihood of the patients living one year with a transplant versus one year without a transplant. With this change in the allocation of organs, the median waiting times have significantly decreased, the mortality on the waiting list has decreased, and the number of CF patients transplanted has not changed. With substantial experience, more programs are now transplanting patients who require constant mechanical ventilation or patients who have undergone previous pleural procedures, especially in the treatment of a pneumothorax. The limiting factor now in lung transplantation is the number of organs available. Efforts to increase the donor pool, such as alveolar recruitment strategies to improve gas exchange, have been effective in allowing more patients to be transplanted. Lung transplantation is now an accepted form of therapy in those patients who are developing progressive respiratory failure.
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PMID:Lung transplantation in cystic fibrosis. 1946 64

Osteomalacia is an end-stage bone disease of chronic and severe vitamin D or phosphate depletion of any cause. Its importance has increased because of the rising incidence of vitamin D deficiency. Yet, not all cases of osteomalacia are cured by vitamin D replacement, and furthermore, not all individuals with vitamin D deficiency develop osteomalacia. Although in the past osteomalacia was commonly caused by malabsorption, nutritional deficiency now is more common. In addition, recent literature suggests that nutritional vitamin D deficiency osteomalacia follows various bariatric surgeries for morbid obesity. Bone pain, tenderness, muscle weakness, and difficulty walking are all common clinical manifestations of osteomalacia. Diagnostic work-up involves biochemical assessment of vitamin D status and may also include a transiliac bone biopsy. Treatment is based on aggressive vitamin D repletion in most cases with follow-up biopsies if patients are started on antiresorptive or anabolic agents.
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PMID:Osteomalacia as a result of vitamin D deficiency. 2252 44

Cystic fibrosis (CF) is the most common autosomal recessive disease among Caucasians. It is due to a mutation in the cftr gene, which encodes the CF transmembrane conductance regulator (CFTR), a chloride channel located in the plasma membrane of mucus-secreting epithelial cells. Numerous other functions of the CFTR protein were identified recently. The survival gains achieved in CF patients over the last 30 years have led to the emergence of delayed complications, one of which is bone disease. The fracture risk is increased from late adolescence onward. Vertebral fractures have an estimated prevalence of 14% among CF patients and can cause severe respiratory complications. Bone mineral density (BMD) is below the age-specific range. Among young adults with CF, 23.5% have BMD values below the cutoff for osteoporosis. Z-scores, which are decreased in children with CF compared to healthy controls, diminish further in adolescence as a result of inadequate peak bone mass accumulation. Studies have shown increased bone resorption, most notably during infectious episodes, and disturbances in bone formation. The numerous pathophysiological mechanisms that contribute to diminish bone strength in CF patients include exocrine pancreatic failure with malabsorption, protein-calorie malnutrition, inflammation related to recurrent infection, and deficiencies in vitamins D and K. In addition, many recent studies support a role for abnormal CFTR function in the osteoblast dysfunction seen in CF. Appropriate diagnostic and therapeutic management of osteoporosis in CF patients is crucial. Risk factors for osteoporosis should be corrected to the extent possible. Oral bisphosphonate therapy may deserve consideration, particularly in adults.
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PMID:Bone disease in cystic fibrosis: what's new? 2123


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