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)

A 78-year-old lady initially presented with painful hips, low back pain, lethargy and weight loss. She had a past history of osteomalacia. Investigations revealed evidence of malabsorption and jejunal biopsy revealed sub-total villous atrophy in keeping with coeliac disease. Peripheral blood film was within normal limits. She responded well clinically to a gluten-free diet and calcium and vitamin D supplementation. Four years after the initial diagnosis she presented acutely with vomiting, pleuritic chest pain, pyrexia and bronchospasm. Blood cultures confirmed the presence of Streptococcus pneumoniae and she was treated appropriately with ampicillin. Despite this she died shortly after admission. It is recognized that blood film examination alone cannot exclude hyposplenism complicating coeliac disease and it is presumed that this was the reason for the development of fatal pneumococcal septicaemia in this patient. Prophylactic vaccination may be appropriate in hyposplenism secondary to coeliac disease.
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PMID:Fatal pneumococcal septicaemia in a coeliac patient. 983 17

Gastrointestinal and hepatic diseases are frequently associated with metabolic bone disorders, especially osteoporosis and osteomalacia. Malabsorption of vitamin D and calcium are important aetiological factors, although other factors may contribute, like the use of glucocorticosteroids in the treatment of inflammatory bowel disease. Treatment is first of all focused on correction of calcium and vitamin D deficiency. In severe osteoporosis additional treatment with bisfosfonates needs serious consideration.
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PMID:[Disorders of bone metabolism in gastrointestinal and hepatic diseases]. 1072 54

A 52-yr-old white female presented with worsening low back and hip pain, associated with lower limb proximal muscle weakness and a waddling gait. Her laboratory evaluation revealed hypocalcemia, hypophosphatemia, a very low 25-hydroxyvitamin D level of less than 5 ng/mL, and a bone mineral density in the osteoporotic range. Her laboratory studies were consistent with osteomalacia, although this diagnosis was not established by histomorphometry. She avoided dairy products, spent little time outdoors, and when she went out, she covered her face, arms, and legs. She was on no medication. Her workup for malabsorption including sprue was negative. She was treated with calcium plus high-dose vitamin D 600,000 IU intramuscularly twice witihin 2 mo and had an impressive clinical improvement. Her difficulty with ambulation improved within 1 wk of start of therapy. Her bone mineral density increased by 40% at the spine and 35% at the hip at 4 mo of therapy, by 63% and 39% at 10 mo, and by 62% and 52% at 15 mo at these sites, respectively. Treatment of osteomalacia is extremely rewarding, with dramtic clinical improvement and normalization of bone mineral density.
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PMID:Nutritional osteomalacia: substantial clinical improvement and gain in bone density posttherapy. 1074 6

A 66-year-old man who underwent a total gastrectomy 13 years ago was admitted to our hospital complaining of severe low back pain and muscle weakness. Biochemical examinations revealed hypocalcemia, hypophosphathemia, low serum 25 (OH) vitamin D and hyperparathyroidism. A chest CT scan revealed pseudofractured ribs, whereas plain X-photography did not show any significant findings. We diagnosed the illness as osteomalacia due to malabsorption. The patient has been receiving oral active vitamin D and calcium, and the pain and serum calcium and phosphate values have improved to the point that he can receive out-patient treatment.
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PMID:Osteomalacia that became symptomatic 13 years after a total gastrectomy. 1083 Jan 80

Metabolic bone disease due to calcium and vitamin D malabsorption is a well-defined consequence of gastrectomy and to a lesser extent of pancreatic insufficiency. The diversity of its presentation, however, can be misleading, resulting in delayed diagnosis or a thorough investigation for possible underlying neoplasias being undertaken. We describe the case of a man with partial gastrectomy and pancreatectomy with osteomalacia and secondary hyperparathyroidism.
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PMID:Gastrectomy and osteomalacia: an association not to be forgotten. 1096 11

A component of ATP, phosphate is at the hub of the energy-related mechanisms operative in muscle cells. Together with calcium, phosphate is involved in bone tissue mineralization: thus, a chronic alteration in the metabolism of phosphate can induce bone and joint disorders. Diagnosis of chronic hypophosphatemia. Serum phosphate, calcium, and creatinine should be assayed simultaneously. Serum calcium is increased in hypophosphatemia caused by hyperparathyroidism and decreased in osteomalacia. Urinary phosphate excretion should be measured in patients with a normal serum calcium level and a serum phosphate level lower than 0.80 mmol/L. A decrease in urinary phosphate excretion to less than 10 mmol/24 h strongly suggests a gastrointestinal disorder, such as malabsorption, antacid use, or chronic alcohol abuse. In patients with a urinary phosphate excretion greater than 20 mmol/24 h, the maximal rate of tubular reabsorption of phosphate (TmPO4) and the ratio of TmPO4 over glomerular filtration rate (GFR) should be determined to look for phosphate diabetes. Manifestations and causes of phosphate diabetes in adults. Moderately severe phosphate diabetes in adults manifests as chronic fatigue, depression, spinal pain, and polyarthralgia, with osteoporosis ascribable to increased bone resorption. Although many cases are idiopathic, investigations should be done to look for X-linked vitamin D-resistant rickets missed during childhood, a mesenchymatous tumor, or Fanconi's syndrome with renal wasting of phosphate, glucose, and amino acids. Management of phosphate diabetes. Phosphate supplementation and, in patients with normal urinary calcium excretion, calcitriol produce some improvement in the symptoms and increase the bone mineral density. Whether dipyramidole is clinically effective remains unclear.
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PMID:Phosphate, the renal tubule, and the musculoskeletal system. 1139 20

The consequences of vitamin D deficiency upon the skeleton are well known and management in the absence of renal failure is relatively straightforward. Vitamin D, either by mouth or parenterally will correct the deficiency and heal the osteomalacia. The mechanisms underlying the causation of vitamin D deficiency are now better understood and indicate the importance of underlying calcium malabsorption and secondary hyperparathyroidism leading to 1,25(OH)2D-induced catabolism of 25(OH)D and possibly also of vitamin D itself. In such situations, e.g., gastrointestinal and pancreaticobiliary disease, calcium supplementation in addition to vitamin D is indicated. The reasons behind nutritional vitamin D deficiency and the possible role of meat in protecting from osteomalacia await further elucidation, but from epidemiological studies, calcium deficiency, per se, is not implicated in the etiopathogenesis. The concept of vitamin D insufficiency is poorly understood, and difficult to define since a single value or close range of serum 25(OH)D values is unlikely to predict the needs of all subjects. Oral calcium intake and renal function are also likely to be relevant to the level of 25(OH)D which is found to be sufficient or insufficient for any given individual to maintain a normal serum calcium level without secondary hyperparathyroidism. There is increasing evidence that vitamin D insufficiency, by leading to sustained hyperparathyroidism, is prejudicial to the skeleton, particularly cortical bone. Since it is without symptoms until fractures occur, it should be actively sought in those clinical situations now recognized as contributing to risk. It can only be identified by the periodic measurement of serum 25(OH)D and the calcitropic hormones PTH and 1,25(OH)2D. In addition, BMD should be measured in a predominantly cortical site such as the proximal forearm, as well as the more conventional sites of spine and hip. The implications of these recommendations are an increase in the use of assays for PTH and vitamin D metabolites in the groups of subjects discussed in this review. Patients with chronic malabsorption states might reasonably be expected to have measurements performed twice-yearly. When vitamin D insufficiency is found, treatment with either vitamin D, calcium or both will be necessary, depending on the etiology of the insufficiency state in the inividual. In some malabsorptive states, calcium malabsorption is the cause of hyperparathyroidism and oral calcium alone can be used to reverse excess PTH activity in those with an adequate state of vitamin D nutrition. However, even in those vitamin D replete individuals, vitamin D catabolism will be enhanced and a small additional oral dose of vitamin D can do no harm. Regular monitoring of PTH and vitamin D metabolites will remain a necessity to ensure continued efficacy of treatment. Current recommendations for dietary supplements of vitamin D are clearly inadequate [61]. There is compelling evidence for supplements of 800 IU per day in the elderly and other high risk populations. Such a dose is safe and without side effects. The available evidence suggests that this should be combined with calcium supplements of 1200 mg/day [19] and that the current UK recommendations for a daily calcium intake of 700 mg contrast with those from the USA at 1,200 mg for people over 50 years old. Physicians need to be aware of both the small but important problem of vitamin D depletion and osteomalacia with its sometimes ambiguous presentation, and the more common but covert vitamin D (and calcium) insufficiency with its widespread and varied clinical associations.
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PMID:Vitamin D nutrition and bone disease in adults. 1170 21

Children with cholestatic liver disease have been thought to develop hepatic osteodystrophy resulting from vitamin D and calcium malabsorption, resulting in secondary hyperparathyroidism and osteomalacia or rickets. However, treatment with vitamin D has not always proven successful in improving the bone disturbance. The aim of our study was to determine the role of vitamin D deficiency in the pathogenesis of hepatic osteodystrophy. We studied five patients, three female and two male, ages 0.9-19 yr, with biopsy-proven chronic cholestatic liver disease and previously low serum levels of vitamin D despite oral intake of vitamin D preparations. Patients were admitted to the Clinical Research Center for 8 days for sunlight deprivation and ultraviolet light substitution and for determinations of serum 25-hyroxyvitamin D(25(OH)) D2 and -D3, osteocalcin, and type I collagen telopeptide (ICTP), the last two being markers of bone formation and resorption, respectively. Samples were taken on admission, at discharge, and 1 month later. Results demonstrated low serum levels of osteocalcin and normal circulating levels of ICTP. Admission serum 25(OH)D2 levels were uniformly low or undetectable and remained so. Admission levels of circulating 25(OH)D3 were normal or low and did not rise during ultraviolet light therapy or subsequent resumption of oral vitamin D therapy and remained low 1 month later. These results indicate that in the face of low-normal to low total 25(OH)D levels, the low osteocalcin and normal ICTP levels suggest that decreased bone formation and not increased bone resorption is the main determinant of bone loss in a subset of children with chronic cholestatic liver disease.
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PMID:Hepatic osteodystrophy in chronic cholestasis: evidence for a multifactorial etiology. 1200 Apr 70

Metabolic bone disease (MBD) is abnormal bone metabolism and includes the common disorders of osteoporosis and osteomalacia, which can develop in patients receiving long-term parenteral nutrition (PN). Patients who require long-term PN have significant gastrointestinal failure and malabsorption, which is generally caused by severe inflammatory bowel disease, intestinal ischemia, or malignancy. The exact cause of MBD in long-term PN patients is unknown, but its origin is thought to be multifactorial, with factors including underlying disease, effect of medications used to treat this disease (eg, corticosteroids), and various components of the PN solution. Caring for patients on long-term PN requires routine assessment and monitoring for MBD. Appropriate adjustments of the PN solution can help reduce the risk for developing PN-associated MBD and in some instances improve bone mineral density. Recent developments in pharmacologic treatment for osteoporosis show promise for patients with MBD receiving PN.
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PMID:Metabolic bone disease and parenteral nutrition. 1524 4

Impaired bone metabolism following urinary diversion through intestinal segments has always been a controversial subject of unclear clinical relevance. Whereas the perpetuated pathophysiological considerations seem conclusive in theory, the role of acidosis and malabsorption is less clear in animal experimentation and, even more so, in the clinical reality of modern continent diversion. In hardly any of the available contemporary case series was overt derangement of the acid-base balance, rickets or osteomalacia encountered. No consistent changes in osteotropic serum parameters could be found with normal calcium and phosphate in all patients. The assumption that colonic reservoirs have a higher risk of developing metabolic bone disease could not be confirmed by clinical data. As early correction of base excess is easy and probably a common policy in patients with intestinal urinary reservoirs, it will be virtually impossible to further study the natural history of bone metabolism after urinary diversion. While there is no need for a bone specific follow-up in asymptomatic adults with a normal acid-base balance, particular attention should be paid to children and to all patients with impaired renal function.
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PMID:Bladder, bowel and bones--skeletal changes after intestinal urinary diversion. 1531 38


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