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)

Malabsorption is the main functional abnormality in gluten-sensitive enteropathy or endemic sprue. The malabsorption is related to villous flattening, which is the main histological feature. The diagnosis is also based on a good response to gluten-free diet. On the other hand, collagenous sprue is not an independent disease but a variant of gluten-sensitive enteropathy, as documented in three personal cases. Its course is characterised by a malabsorption syndrome unresponsive to gluten withdrawal, with massive subepithelial collagen formation. The pathogenesis remains unknown, prognosis poor, compared to the endemic gluten-sensitive enteropathy.
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PMID:[Collagenous sprue (author's transl)]. 63 16

Scleroderma is an uncommon complex disease. The onset is slow and the progress is chronic. The main pathophysiological changes vary; they affect blood vessels, connective tissue, collagen fibres, cause fibrin deposition and inflammatory reactions. There may be early oedema and a wide spectrum of organic involvement. Clinically, all the fibril-containing and connective tissue organs can be attacked in various degrees. The most common organ manifestations are the Raynaud's phenomenon in the arms and hands, vascular fibrosis, stiff and hard facial skin, restriction of joint movement by pericapsular hardening, calcium deposition and capsular rigidity. In the gastrointestinal tract muscle atrophy, collagen and connective tissue damage are common, especially at the cardia. Malabsorption may occur. Progressive pulmonary fibrosis leads to cor pulmonale and respiratory insufficiency. The liver, kidneys and the endocrine glands are, however, seldom involved. Therapeutic trials have been performed using many different groups of drugs: vasodilatating agents, corticosteroids, drugs found experimentally to influence connective tissue, thyroxine and a variety of anti-rheumatic agents. In the last decade best short-term clinical results have been achieved with penicillamine, some vasodilators, chlorambucil and in recent years with cyclofenil a potent anti-oestrogen, which has marked connective tissue and collagen metabolism influencing properties. Good therapeutic effects without serious side effects have been achieved.
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PMID:Scleroderma (progressive systemic sclerosis, PSS); pathophysiological, clinical and pharmacological aspects of the syndrome. 75 10

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.
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PMID:Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone. 97 17

The neurological and muscular complications seen in coeliac disease in adults are usually attributed to deficiency secondary to malabsorption. Amongst them, however, there exists a very rare cateogory, described by Cooke et al. (1966) taking the form of a chronic myeloneuropathy which cannot be explained in terms of the malabsorption syndrome. Our two cases of gluten intolerance enteropathy, confirmed by biopsy before and after diet, fell into this group of polyneuropathies. The patients, both women, suffered from an essentially sensory ataxic polyneuropathy with accessory motor component with pyramidal and posterior column signs. CSF findings showed a meningeal inflammatory reaction in one of the two cases. These neurological signs, appearing paradoxically during a digestive disease cured by diet, evolve chronically but become stabilised with corticosteroid therapy. Any vitamin deficiency may be excluded in the aetiology of these problems. Neuropathological study of neuromuscular biopsies in very fine serial sections confirmed the mild peripheral nervous involvement but revealed identical inflammatory lesions in the nerve and muscle which were remarkable by virtue of their very highly segmentally selective micro-vasculitis appearance. In these two cases, general, clinical and biological arguments, as well as the type of histological lesion, make it possible to exclude monoclonal gammapathies, malignant haemopathies, amyloidosis and the major collagen diseases. This micro-vasculitis, having transient forms with P.A.N. is no less distinctive, and may be integrated into the provisional group of "allergic angeitis", related to physiopathology of circulating immune complexes and very fashionable in theories as to the mechanism of gluten-sensitive enteropathies. The exact nature of the link between the latter and these types of polyneuropathy remains unknown.
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PMID:[Nondeficiency chronic polyneuropathies in celiac disease in adults (2 cases with inflammatory neuromuscular vascularitis)]. 100 65

As part of a comprehensive study in adult patients with severe primary protein malnutrition, jejunal ultrastructural studies have been performed in nine adults in the malnourished state. Malnutrition was severe in all. D-Xylose malabsorption and abnormal fecal fat excretion were present in most. The main ultrastructural abnormalities encountered were: microvillar abnormalities such as shortening, diminished numbers, abnormal positioning, branching, and mesalike fusion of the microvilli; and abnormalities in the lamina propria characterized by deposits of osmiodense material and collagen fibers below the basement membrane of the epithelial cells and of the capillaries. None of the aforementioned findings were noted in our control cases. These ultrastructural alterations of severely malnourished adults are nonspecific, since they have already been described in other enteropathies frequently encountered in the tropics.
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PMID:Enteropathy in adult protein malnutrition: ultrastructural findings. 114 53

Passage through the small intestine was significantly accelerated after intramuscular injection of ceruletide (synthetic caerulein, F.I. 6934), 0.50 to 0.75 mug/kg body-weight. Average passage took 62 +/- 41 min (106 patients, with various suspected or demonstrated small-intestinal involvement, excluding malabsorption syndrome, sprue or collagen diseases) after caerulein, while in a control group of 83 patients with radiologically normal small intestine it was 126 +/- 62 min (P less than 0.001). In 75% of patients there was no evidence of induced change in radiological pattern of the small intestine. Increased local contractions were observed in a quarter of patients, but did not impair the diagnostic interpretation.
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PMID:[Acceleration of passage through the small intestine by caerulein (author's transl)]. 120 25

We report coexistent collagenous colitis and collagenous sprue in a 62-year-old woman with diarrhea. Investigations suggested malabsorption, and small intestinal biopsies demonstrated a flattened mucosa with subepithelial collagen deposition. Colonic biopsies also showed a thickened subepithelial collagen band as well as a striking lamina propria inflammatory cell infiltrate. Symptomatic remission was induced with a gluten/lactose-free diet, oral prednisone, and sulfasalazine and has been maintained with gluten restriction alone. Repeat biopsies after 2 months demonstrated restoration of normal small intestinal and colonic collagen bands; only a chronic inflammatory cell infiltrate (consistent with microscopic/lymphocytic colitis) persisted in colonic biopsies. We propose that, in this instance, collagenous enterocolitis represented a diffuse manifestation of gluten sensitivity.
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PMID:Collagenous enterocolitis: a manifestation of gluten-sensitive enteropathy. 150 Jun 61

Collagenous colitis is a distinct cause of chronic watery diarrhea characterized by abnormal deposition of collagen in the subepithelial region of the colonic mucosa. Typically, laboratory tests of blood, urine, and stool are normal. A few patients have laboratory evidence of small bowel dysfunction and malabsorption, but excessive enteric protein loss is not a commonly recognized manifestation of collagenous colitis. We report a 62-yr-old woman who had collagenous colitis associated with a marked protein-losing enteropathy in the absence of obvious small intestinal disease or colonic ulceration. Biopsies of endoscopically normal-appearing colonic mucosa should be performed in patients with protein-losing enteropathy in whom no cause is apparent after initial evaluation.
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PMID:Protein-losing enteropathy with collagenous colitis. 159 Mar 20

We present a case of collagenous colitis with evidence of terminal ileal involvement. The patient suffered from chronic watery diarrhea of three months' duration, and colonoscopy revealed a normal endoscopic appearance. Histologic examination of biopsies revealed a broad subepithelial band of collagen, with similar histologic findings in the terminal ileum. Additionally, the patient exhibited abnormalities of d-xylose and vitamin B12 absorption, although there were no clinical signs of malabsorption. Biopsy of the proximal small intestine was normal. The significance of these findings for the definition of the clinicopathologic entity of collagenous colitis and its pathogenesis are discussed.
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PMID:Collagenous colitis with involvement of terminal ileum. 186 10

Diseases presenting with dyspepsia fall into two general categories: organic and functional. Overall, most patients with dyspepsia have no underlying identifiable disease process. The diagnostic yield of organic causes is less in younger patients, and, conversely, serious organic lesions are common in elderly dyspeptic patients. The commonest organic causes of dyspepsia are peptic ulcer disease, gastroesophageal reflux, biliary tract disease, and gastric cancer. Symptoms and physical signs may help to differentiate these organic causes from functional dyspepsia but endoscopic or radiographic/ultrasound studies are usually necessary to ensure the appropriate diagnosis. Less common organic causes of dyspepsia not to be overlooked include drugs, pancreatitis, malabsorption syndromes, metabolic disorders, ischemic heart disease, and collagen vascular disorders.
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PMID:Dyspepsia: organic causes and differential characteristics from functional dyspepsia. 189 24


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