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)

To investigate the pathogenesis of osteoporosis in male hypogonadism we have investigated a heterogeneous group of 13 men with hypogonadism: 7 men (median age 60, range 31-79) with two or more vertebral crush fractures and 6 men (median age 61.5, range 28-76) without vertebral fractures. The group with crush fractures had trabecular and cortical osteoporosis as assessed by Singh grade, iliac crest trabecular bone volume, and metacarpal cortical area/total area. This was accompanied by an altered trabecular architecture with a reduction in number of trabeculae but no change in trabecular width, which contrasts with age-related bone loss in men where there is no reduction in trabecular number but thinning of trabeculae. The fracture group had significantly lower plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations than the nonfracture group, and this was associated with malabsorption of calcium. Irrespective of the presence or absence of osteoporosis, treatment with testosterone led to a significant increase in total and free plasma 1,25(OH)2D and an improvement in calcium absorption measured with radiocalcium and by balance techniques. In addition, urine biochemistry, metabolic balance studies, and bone biopsy suggest that skeletal retention of calcium and bone formation are increased by testosterone treatment. We conclude that male hypogonadism causes both cortical and trabecular osteoporosis and altered trabecular architecture. A major risk factor for the development of osteoporosis is reduction in plasma 1,25(OH)2D, leading to malabsorption of calcium and reduced bone formation.
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PMID:Osteoporosis in hypogonadal men: role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation. 376 4

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

The vast majority of patients with celiac disease respond to a gluten-free diet; yet, a small number of refractory patients do not respond and have persistent malabsorption and residual mucosal abnormalities of the small intestine. The histologic features of refractory/unclassified sprue have been published as case reports, often without long-term follow up, and no clear histologic picture has emerged. We present the results of a long-term study of the clinical and histologic features of 10 patients with refractory/unclassified sprue. The histologic features of small bowel biopsies in this group of patients were compared with those of 10 patients with responsive celiac disease and with 10 patients without malabsorption who had normal duodenal biopsies. Five of the 10 refractory patients ultimately developed collagenous sprue as a distinct histologic marker of refractory disease. Additional distinctive findings found in small bowel biopsies in the refractory group were subcryptal chronic inflammation (10 of 10) and marked mucosal thinning in three patients. Other nonspecific findings included acute inflammation and gastric metaplasia. One patient with collagenous sprue developed a B-cell lymphoma of the ileum, and in general collagenous sprue was associated with a poor prognosis. Two of five patients died whereas two others require total parenteral nutrition for survival. Pathologists evaluating small bowel biopsies in the setting of malabsorption should be aware of the subtle histologic changes described here that may portend a refractory course.
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PMID:The histologic spectrum and clinical outcome of refractory and unclassified sprue. 1125 32

There is no one cause of bone fragility; genetic and environmental factors play a part in development of smaller bones, fewer or thinner trabeculae, and thin cortices, all of which result in low peak bone density. Material and structural strength is maintained in early adulthood by remodelling; the focal replacement of old with new bone. However, as age advances less new bone is formed than resorbed in each site remodelled, producing bone loss and structural damage. In women, menopause-related oestrogen deficiency increases remodelling, and at each remodelled site more bone is resorbed and less is formed, accelerating bone loss and causing trabecular thinning and disconnection, cortical thinning and porosity. There is no equivalent midlife event in men, though reduced bone formation and subsequent trabecular and cortical thinning do result in bone loss. Hypogonadism contributes to bone loss in 20-30% of elderly men, and in both sexes hyperparathyroidism secondary to calcium malabsorption increases remodelling, worsening the cortical thinning and porosity and predisposing to hip fractures. Concurrent bone formation on the outer (periosteal) cortical bone surface during ageing partly compensates for bone loss and is greater in men than in women, so internal bone loss is better offset in men. More women than men sustain fractures because their smaller skeleton incurs greater architectural damage and adapts less effectively by periosteal bone formation. The structural basis of bone fragility is determined before birth, takes root during growth, and gains full expression during ageing in both sexes.
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PMID:Pathogenesis of bone fragility in women and men. 1204 92

Patients with fragility fractures may have abnormalities in bone structural and material properties such as larger or smaller bone size, fewer and thinner trabeculae, thinned and porous cortices, and tissue mineral content that is either too high or too low. Bone models and remodels throughout life; however, with advancing age, less bone is replaced than was resorbed within each remodeling site. Estrogen deficiency at menopause increases remodeling intensity: a greater proportion of bone is remodeled on its endosteal (inner) surface, and within each of the many sites even more bone is lost as more bone is resorbed while less is replaced, accelerating architectural decay. In men, there is no midlife increase in remodeling. Bone loss within each remodeling site proceeds by reduced bone formation, producing trabecular and cortical thinning. Hypogonadism in 20-30% of elderly men contributes to bone loss. In both sexes, calcium malabsorption and secondary hyperparathyroidism increase remodeling: more bone is removed from an ever-diminishing bone mass. As bone is removed from the endosteal envelope, concurrent bone formation on the periosteal (outer) bone surface during aging partly offsets bone loss and increases bone's cross-sectional area. Periosteal apposition is less in women than in men; therefore, women have more net bone loss because they gain less on the periosteal surface, not because they resorb more on the endosteal surface. More women than men experience fractures because their smaller skeleton incurs greater architectural damage and adapts less by periosteal apposition.
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PMID:Invited Review: Pathogenesis of osteoporosis. 1455 75

Collagenous sprue is a rare clinicopathological condition of the small bowel. It is characterised by abnormal subepithelial collagen deposition and is typically associated with malabsorption, diarrhoea and weight loss. The clinical features of collagenous sprue often resemble those of coeliac disease and together with frequent histological findings like mucosal thinning and intraepithelial lymphocytosis the diagnosis may be hard to reach without awareness of this condition. While coeliac disease is treated using gluten restriction, collagenous sprue is, however, not improved by this intervention. In cases of diet-refractory 'coeliac disease' it is therefore essential to consider collagenous sprue to initiate treatment at an early stage to prevent the fibrotic progression. Here, we report a case of a 78-year-old man with collagenous sprue and present the clinical and histological manifestations as well as the successful treatment course that he underwent.
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PMID:Collagenous sprue: a coeliac disease look-alike with different treatment strategy. 2468 41

Congenital central hypoventilation syndrome (CCHS) patients show major autonomic alterations in addition to their better-known breathing deficiencies. The processes underlying CCHS, mutations in the PHOX2B gene, target autonomic neuronal development, with frame shift extent contributing to symptom severity. Many autonomic characteristics, such as impaired pupillary constriction and poor temperature regulation, reflect parasympathetic alterations, and can include disturbed alimentary processes, with malabsorption and intestinal motility dyscontrol. The sympathetic nervous system changes can exert life-threatening outcomes, with dysregulation of sympathetic outflow leading to high blood pressure, time-altered and dampened heart rate and breathing responses to challenges, cardiac arrhythmia, profuse sweating, and poor fluid regulation. The central mechanisms contributing to failed autonomic processes are readily apparent from structural and functional magnetic resonance imaging studies, which reveal substantial cortical thinning, tissue injury, and disrupted functional responses in hypothalamic, hippocampal, posterior thalamic, and basal ganglia sites and their descending projections, as well as insular, cingulate, and medial frontal cortices, which influence subcortical autonomic structures. Midbrain structures are also compromised, including the raphe system and its projections to cerebellar and medullary sites, the locus coeruleus, and medullary reflex integrating sites, including the dorsal and ventrolateral medullary nuclei. The damage to rostral autonomic sites overlaps metabolic, affective and cognitive regulatory regions, leading to hormonal disruption, anxiety, depression, behavioral control, and sudden death concerns. The injuries suggest that interventions for mitigating hypoxic exposure and nutrient loss may provide cellular protection, in the same fashion as interventions in other conditions with similar malabsorption, fluid turnover, or hypoxic exposure.
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PMID:Impaired neural structure and function contributing to autonomic symptoms in congenital central hypoventilation syndrome. 2657 72

The purpose of the work is improvement in treatment of patients with acute small bowel obstruction by justification for gastrointestinal decompression and different methods of small intestine intubation for effective evacuation of itscontents. We conducted morphological and morphometric study of the small intestine in 53 white rats. It was established that acute small bowel obstruction causes expansion of all parts of small bowel microvasculature with significant lesions of venous structures. We revealed thinning of intestinal muscular layer 2.15 timesand increase of submucosallayer 1.65 times. Changesin nuclear/cytoplasmic ratioof these structures showed tension and instability in structural homeostasis at cellular level. These changes lead to malabsorption and require evacuation of intestinal pathological contents. We analyzed 30 medical records of patients who died from acute small bowel obstruction. Decompression was performed only in 60.71% ofall cases and in 50.0% of re-laparotomy cases. The cause of death in 80.0% was syndrome of multiple organ failure due to progressiveintoxication caused by functional obstruction of the small intestine. 196 patients were operated. In 50% of cases nasointestinal intubation was used for small bowel decompression, in 11.22% - intraoperative one-stage evacuation of intestinal contents and in 3.57% - "open" methods of intestinal drainage. We drew attention to problems and errorsin performingsmall bowel intubation. We offered some variants of intubation using different probes according to the operating situation and aim of intubation. Design of probe for intubation and method of enterostomy was suggested. We also offered an algorithm for selectionof small intestinal decompression method in patients with acute small bowel obstruction depending on the operating situation. We emphasizethat intestinal decompression in patients with acute small bowel obstruction improves the results of surgery.
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PMID:[ABOUT THE ROLE OF DIGESTIVE TRACT DECOMPRESSION IN PATIENTS WITH ACUTE BOWEL OBSTRUCTION. MISTAKES, COMPLICATIONS AND THEIR PREVENTION]. 2872 65

Ochratoxin A (OTA) is a mycotoxin produced by various species of Aspergillus and Penicillium. Ochratoxin A was classified as a group 2B carcinogen and is one of the major intestinal pathogenic mycotoxins. One of the most frequent modes of intoxication is consumption of contaminated food with mycotoxins. Feed represents the major cost and has a direct impact on the economical viability of broiler's production system, since it must contain the necessary elements that allow the animal to express the maximum genetic potential while providing its nutritional requirements. Thus, the animal has to digest the feed and absorb its nutrients, which is in direct correlation with the gastrointestinal tract, especially the small intestine and the development of the mucosal surface area. Once ingested, OTA is absorbed by passive diffusion, mainly the jejunum. Ochratoxin A's presence affects lipid membranes and could lead to the degradation of their normal structure and functionality. All of these effects contribute to the development of malabsorption. It was very interesting to study the effect of OTA on the layer of phospholipids of the bowel. The experimental group received OTA (0.05 to mg/kg BW) through an intra-peritoneal injection, every other day for 21 days. We noted that feed conversion ratio and average daily gain were reduced. Histological studies showed important alterations at the level of the mucosal membrane of the intestine (villosities, crypts) following intra-peritoneal administration of the mycotoxin. Thinning and enlargement at the base of the villosities, hyperplasia and crypts in irregular forms, blunting and denudation were observed through the examination of intestinal morphology. Biochemical studies, such as total lipid and phospholipid compositions, allowed us to have more detailed results. All identified mucosal phospholipids were modified, particularly the phosphatidylcholine (PC) and the phosphatidylethanolamine (PE) in the jejunum mucosa. In fact, there was a decrease by 55.81% for PC, 56.66% for PE, while a significant increase by 32.91% was noted for phosphatidylserine in the jejunum. It was very interesting to study the effect of OTA on the phospholipids layer of the bowel, as the mucous membrane of the small intestine represents the main site of absorption and transformation of nutriments. To avoid such disturbances and prevent the effects of the OTA, precautions must be taken to inhibit mold growth at the level of the feed manufactory units. Phosphatidylcholine and PE administrations may represent an option that could allow reestablishment of phospholipid equilibrium in the intestine.
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PMID:Effects of ochratoxin A on membrane phospholipids of the intestine of broiler chickens, practical consequences. 3166 32