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)

Chronic pancreatitis is a longlasting inflammatory disease manifested clinically in the advanced stage by malabsorption syndrome. Its manifestations include also changes in the calcium metabolism and the occurrence of osteoporosis and osteomalacia or their combination. The objective of the study was to assess the vitamin D3 blood concentration in patients with chronic pancreatitis. The group comprised 15 patients (8 men and 7 women), median age 45.0 years. The authors found a significantly reduced serum concentration of vitamin D3 (p < 0.01) in patients with chronic pancreatitis. They assume that vitamin D deficiency is one of the decisive causes of bone complications in prolonged pancreatitis. Supplementation with vitamin D or its metabolites is then a necessary part of preventive and therapeutic provisions.
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PMID:[Vitamin D deficiency as one of the causes of bone changes in chronic pancreatitis]. 1564 Dec 50

A 78 year old woman had suffered ten spontaneous bone fractures, the first occurring when she was 57 years old. She is now wheel-chair bound. After 21 years, the underlying osteomalacia due to oligosymptomatic celiac disease with malabsorption was diagnosed. The treatment consists of a gluten free diet and substitution of calcium and vitamin D until there is a normalisation of calcium, vitamin D and alkaline phosphatase. Any spontaneous fracture deserves a careful search for metabolic bone disease. An elevation of alkaline phosphatase indicates osteomalacia rather than osteoporosis.
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PMID:[Ten fractures in 21 years]. 1592 67

Vitamin D3 is synthesized in the skin during summer under the influence of ultraviolet light of the sun, or it is obtained from food, especially fatty fish. After hydroxylation in the liver into 25-hydroxyvitamin D (25(OH)D) and kidney into 1,25-dihydroxyvitamin D (1,25(OH)2D), the active metabolite can enter the cell, bind to the vitamin D-receptor and subsequently to a responsive gene such as that of calcium binding protein. After transcription and translation the protein is formed, e.g. osteocalcin or calcium binding protein. The calcium binding protein mediates calcium absorption from the gut. The production of 1,25(OH)2D is stimulated by parathyroid hormone (PTH) and decreased by calcium. Risk factors for vitamin D deficiency are premature birth, skin pigmentation, low sunshine exposure, obesity, malabsorption and advanced age. Risk groups are immigrants and the elderly. Vitamin D status is dependent upon sunshine exposure but within Europe, serum 25(OH)D levels are higher in Northern than in Southern European countries. Severe vitamin D deficiency causes rickets or osteomalacia, where the new bone, the osteoid, is not mineralized. Less severe vitamin D deficiency causes an increase of serum PTH leading to bone resorption, osteoporosis and fractures. A negative relationship exists between serum 25(OH)D and serum PTH. The threshold of serum 25(OH)D, where serum PTH starts to rise is about 75nmol/l according to most surveys. Vitamin D supplementation to vitamin D-deficient elderly suppresses serum PTH, increases bone mineral density and may decrease fracture incidence especially in nursing home residents. The effects of 1,25(OH)2D and the vitamin D receptor have been investigated in patients with genetic defects of vitamin D metabolism and in knock-out mouse models. These experiments have demonstrated that for active calcium absorption, longitudinal bone growth and the activity of osteoblasts and osteoclasts both 1,25(OH)2D and the vitamin D receptor are essential. On the other side, bone mineralization can occur by high ambient calcium concentration, so by high doses of oral calcium or calcium infusion. The active metabolite 1,25(OH)2D has its effects through the vitamin D receptor leading to gene expression, e.g. the calcium binding protein or osteocalcin or through a plasma membrane receptor and second messengers such as cyclic AMP. The latter responses are very rapid and include the effects on the pancreas, vascular smooth muscle and monocytes. Muscle cells contain vitamin D receptor and several studies have demonstrated that serum 25(OH)D is related to physical performance. The active metabolite 1,25(OH)2D has an antiproliferative effect and downregulates inflammatory markers. Extrarenal synthesis of 1,25(OH)2D occurs under the influence of cytokines and is important for the paracrine regulation of cell differentiation and function. This may explain that vitamin D deficiency can play a role in the pathogenesis of auto-immune diseases such as multiple sclerosis and diabetes type 1, and cancer. In conclusion, the active metabolite 1,25(OH)2D has pleiotropic effects through the vitamin D receptor and vitamin D responsive elements of many genes and on the other side rapid non-genomic effects through a membrane receptor and second messengers. Active calcium absorption from the gut depends on adequate formation of 1,25(OH)2D and an intact vitamin D receptor. Bone mineralization mainly depends on ambient calcium concentration. Vitamin D metabolites may play a role in the prevention of auto-immune disease and cancer.
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PMID:Vitamin D physiology. 1656 71

Osteomalacia is characterized by defective mineralization and low bone mineral density (BMD). Clinical and biochemical improvements typically occur within a few weeks of starting treatment, though the bone mineral deficits may take longer to correct. We report a case series of 26 patients with frank osteomalacia (pseudo fractures on X-rays, elevated serum total alkaline phosphatase and parathyroid hormone, normal/low serum calcium and phosphorus, and low serum 25-hydroxy vitamin D) who were followed-up for changes in BMD during treatment using dual- energy X-ray absorptiometry (DXA). There were 23 patients with nutritional vitamin D deficiency, 2 with malabsorption syndrome, and 1 with renal tubular acidosis. All patients were treated with vitamin D and calcium; the 3 patients with associated disorders were treated accordingly. At baseline, there was low BMD at all sites tested. The rate of increase in vertebral and hip BMD was rapid in the initial few months, which subsequently slowed down. In contrast to the large increases in BMD at the femoral neck and lumbar spine, the radial BMD did not recover. At the time when most patients had marked clinical and biochemical improvement (2.8+/-1.4 mo), the vertebral and hip BMD, although improved from baseline, had not completely recovered. Bone loss at the forearm (cortical site) appears to be largely irreversible. Although the clinical correlates of these changes are presently unclear, BMD measurements are useful in assessing the initial severity of bone loss as well as the response to therapy.
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PMID:Changes in bone mineral density following treatment of osteomalacia. 1673 41

Non-prescribed antacid drugs that contain magnesium and aluminum are widely used in the treatment of gastritis and peptic ulcer. One of the side effects of these antacid drugs is that they bind phosphate in the gut and result in its malabsorption. In this paper, a 42-year-old female patient who used magnesium hydroxide (Magnesie calcinee powder 100 g) to benefit from its laxative feature, and developed osteomalacia after losing 90 kg in 2 years will be presented by going through the related literature. She had widespread joint pain and could hardly walk without the help. Ca, P and vitamin D were at lower limit of normal, ALP, Mg and PTH were increased in her laboratory tests. There were stress fractures at the femur neck and at the upper part of the tibia in plane radiographies. The patient was hospitalized with the diagnosis of osteomalacia and she was treated successfully.
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PMID:Osteomalacia from Mg-containing antacid: a case report of bilateral hip fracture. 1717 47

Coeliac disease is a malabsorption syndrome in which dietary gluten damages the small bowel mucosa. Gluten contains gliadin, the primary toxic component that is primarily found in wheat, barley and rye products. The initial diagnosis of coeliac disease is usually made by endoscopic biopsy of the jejunum although sometimes imaging features can suggest the diagnosis. Once a diagnosis is made, patients need to be diet compliant and monitored for potential complications. Many complications are more common when dietary compliance is poor. Complications include intussusception (usually intermittent), ulcerative jejunitis, osteomalacia, cavitating lymph node syndrome and an increased risk of malignancies such as lymphoma, adenocarcinoma and squamous cell carcinoma. Radiological evaluation is central in the evaluation of these complications. Imaging may assist both in the diagnosis and staging of complications as well as enabling radiological guided percutaneous biopsy for complications of coeliac disease such as lymphoma. As coeliac disease is a relatively common disorder, it is likely that most radiologists will encounter the disease and its potential complications. The aim of this review article is to discuss and illustrate the role of modern radiology in evaluating the many presentations of this complex disease.
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PMID:The imaging of coeliac disease and its complications. 1753 15

Long-term total parenteral nutrition (TPN) is a procedure commonly applied to patients with advanced forms of intestinal malabsorption. Among TPN complications, bone metabolic diseases, such as osteoporosis and osteomalacia, are a common finding. Initially considered to be a manifestation of aluminium toxicity which followed massive contamination with the element of the solutions used in TPN, metabolic osteopathy during TPN is currently considered a multiform syndrome, with a multifactorial pathogenesis, which may manifest itself with vague or clear clinical pictures. In this review, we analyse clinical, pathogenetic, and therapeutic aspects of the most common bone metabolic diseases in patients undergoing long-term TPN.
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PMID:Metabolic bone diseases during long-term total parenteral nutrition. 1772 Oct 75

Osteomalacia is caused by impaired vitamin D receptor (VDR) signaling, calcium deficiency, and altered bone mineralization. This can be due to insufficient sunlight exposure, malabsorption, reduced D hormone activation in chronic kidney disease, and rare alterations of VDR signaling and phosphate metabolism. Leading symptoms are bone pain, muscular cramps, and increased incidence of falls in the elderly. The adequate respective countermeasures are to optimize the daily intake of calcium and vitamin D3 and to replace active D hormone and phosphate if deficient. Osteoporosis is characterized by bone fragility fractures upon minor physical impact. Indications for diagnosis and treatment can be established by estimating the absolute fracture risk, taking into account bone mineral density, age, gender, and individual risk factors. Exercise, intervention programs to avoid falls, and specific drugs are capable of substantially reducing fracture risk even in the elderly. Secondary osteoporosis primarily requires both bone-altering medications and effective treatment of underlying diseases.
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PMID:[Metabolic bone diseases]. 1788 94

Primary intestinal lymphangiectasis (PIL), also known as Waldmann's disease, is a rare protein-losing enteropathy characterized by abnormal enlargement of the lymphatic ducts in the bowel wall. The symptoms usually start in early infancy. We report a case of osteomalacia in a 63-year-old patient with delayed-onset of PIL, for which she was on dietary treatment. She presented with a 3-year history of mechanical pain in the back and pelvis. Mild ascites and edema with functional impairment of the lower limbs were noted. The neurological evaluation was normal. Blood tests showed hypocalcemia, hypophosphatemia, alkaline phosphatase elevation, and evidence of intestinal malabsorption. Radiographs of the pelvis disclosed a fracture, Looser's zones in the iliopubic rami and left femoral neck, and a washed-out appearance of the vertebras. Dual-energy X-ray absorptiometry showed bone loss with T-score values of -1.2SD at the lumbar spine and -2.5SD at the femoral necks. A diagnosis of osteomalacia related to vitamin D deficiency was given. Serum 25-OH-vitamin D was 18.2ng/ml (normal, 20-40ng/ml) and serum parathyroid hormone was 620pg/ml (normal, 15-65pg/ml), suggesting secondary hyperparathyroidism. Intramuscular vitamin D was given, together with oral calcium and an adequate diet. At follow-up 8 months later, small improvements were noted in the symptoms and absorptiometry findings.
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PMID:Osteomalacia in a patient with primary intestinal lymphangiectasis (Waldmann's disease). 1790 Sep 62

Systemic sclerosis (SSc) may affect the gastrointestinal tract and cause very rarely malabsorption syndrome related to bacterial overgrowth. Malabsorption syndrome may be responsible for weight loss, diarrhea, osteomalacia, and iron and vitamins deficiency. We report the case of a SSc patient who developed osteomalacia caused by the combination of two exceptional conditions in the setting of SSc: celiac disease (CD) and primary biliary cirrhosis (PBC)-related Fanconi syndrome. Oral prednisone with angiotensin-converting enzyme inhibitors, was initiated because of active lesions of tubulitis, and led to the complete regression of bone pains, and by the improvement of renal function and regression of the features of proximal tubulopathy. Thus, in the presence of vitamin deficiencies in a patient with SSc, together with a search for malabsorption syndrome secondary to bacterial overgrowth, CD and/or PBC-associated Fanconi syndrome should be investigated.
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PMID:Osteomalacia revealing celiac disease and primary biliary cirrhosis-related Fanconi syndrome in a patient with systemic sclerosis. 1857 72


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