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)

2 patients, who were treated with clioquinol after radical resection of carcinoma of the rectum and colostomy, developed symmetrical sensorimotor polyneuropathy, mild posterior tract ataxia, bilateral pyramidal tract lesions and optic neuropathy, a clinical picture compatible with subacute myelo-optic-neuropathy (S.M.O.N.). One patient had neurological symptoms after having received 750 g of clioquinol, 3 years after treatment started, and impairment of vision was noted after having received 1200 g. The other patient had neurological symptoms 6 weeks after clioquinol was first given, having received 65 g, the average daily dose being 1.5 g, and vision was impaired after 765 g had been administered. On examination 12 and 14 months after clioquinol had been discontinued, the first patient's vision was slightly improved, but he was otherwise unchanged, while the vision of the other patient was unchanged, but she had otherwise deteriorated slightly neurologically. Electrophysiological examinations confirmed the clinical observations. A multifactor etiology of the syndrome: neurotoxicity of clioquinol, paraneoplastic neuropathy and malabsorption, is discussed.
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PMID:[Subacute myelo-optic-neuropathy (S.M.O.N.) following treatment with clioquinol (author's transl)]. 5 Oct 51

One case each of pernicious anemia and folic acid deficiency with chronic malabsorption with disease of the cord and histologically demonstrated concomitant disease of the peripheral nerve system in the sense of a polyneuropathy are described. The histological findings of nerve obtained by biopsy show, in both cases, the loss of individual nerve fibers as an expression of a chronic axonal degeneration. The pathogenetic basis to be considered in these cases is presented.
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PMID:[Polyneuropathy in vitamin B 12 and folic acid deficiency. Clinical and histopathological study with electron-microscopy analysis of the sural nerve]. 17 62

We studied five patients (two men and three women, age between 58 and 76 years) with clinical and electrophysiological signs of polyneuropathy. Routine neurological, hematological, and gastroenterological studies as well as procedures to test fat malabsorption were performed. Folate determinations were done using both radioactive and Lactobacillus casei methods. Two patients displayed the signs of subacute combined degeneration of the spinal cord with polyneuropathy, while three had only signs of neuropathy. All had low serum folate concentration, long-standing gastrointestinal disease, and deficient folate intake. The D-xylose absorption test gave values in all patients, while none displayed the classical malabsorption syndrome. The patients had substantial improvement or recovered (according to clinical and electrophysiological measurements) after periods ranging from 9 to 39 months of folate therapy. Such acquired folate-responsive polyneuropathy has two principal characteristics: mixed sensorimotor with mainly sensory deficits, and involvement of one or both of the lower extremities much more extensively than the upper extremities.
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PMID:Polyneuropathy and folate deficiency. 21 Jul 47

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

Xylose absorption was measured, within ten days of being admitted to hospital, in 54 alcoholics with neurological abnormalities. Small-intestine malabsorption was demonstrated in 19. Classified according to the customary clinical diagnoses, 16 of 49 with alcohol polyneuropathy had abnormal values, with no correlation to nerve conduction velocity. There was also no difference among 14 in predelirium and eight in delirium. However, all four patients with Wernicke's encephalopathy had a malabsorption syndrome. These results are similar, also quantitatively, to those reported in the literature in alcoholics without neurological signs. Alcohol may be involved in the pathogenesis of alcoholic polyneuropathy both as a toxic factor and also via nutritional deficiency.
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PMID:[Alcohol and malabsorption in the pathogenesis of peripheral and central nerve damage (author's transl)]. 113 26

The pathology of primary familia amyloidosis with polyneuropathy is described on the basis of post-mortem examination of six cases from Northern Sweden. Clinically the disease is characterized by progressive sensory and motor disturbances with loss of sensation, muscular wasting and flaccid paralysis. Impotence, urinary bladder dysfunction, motility disturbances of the gastro-intestinal tract and postural hypotension indicate affection of the autonomic nervous system as well. Malabsorption, cardiac insufficiency and vitreous opacites also occur. As regards the distribution of amyloid, the following findings seemed to be characteristic. Usually there were no gross lesions indicating the amyloid disease. Histopathologically, amyloid deposits were observed in great extent in the peripheral nervous system and in various parts of the peripheral autonomic nervous system as well. It occurred extensively in the walls of blood vessels of various calibres, in the perivascular collagenous connective tissue and adjacent to the smooth musculature. Amyloid deposition was also found more or less abundantly in various other organs and tissues. No deposits, however, or only insignificant amounts, were found in the central nervous system, either in the parenchyma of the liver, in the islets of Langerhans, or in the bone marrow. Clinical manifestations seemed to be related to the local deposition of the amyloid substance. Our clinical and pathological findings in this particular type of familial amyloidosis conformed mostly to those previously described.
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PMID:Postmortem findings in primary familial amyloidosis with polyneuropathy. 115 99

Disturbances of the central and peripheral nervous system in Crohn's disease can be directly or indirectly caused by the disease itself or by the treatment. The first mentioned disturbances are very seldom. Cerebral arterial and venous thromboses can be attributed to hypercoagulation. Malabsorption of vitamin B 12 or folic acid can lead to a subacute combined degeneration of the spinal cord, sometimes in combination with a polyneuropathy and an encephalopathy. Spinal abscesses very seldom occur. An opticusneuropathy can be caused either by vasculitis or by a lack of vitamin A and/or vitamin B. Polyneuropathies in Crohn's disease which are not induced by drugs are manifested as mononeuritis multiplex or as symmetrical sensory neuropathy. An autoimmune process is being discussed as the probable cause of there diseases. In some cases large doses and prolonged administration of metronidazole can lead to cerebral dysfunctions with state of confusion, alterations of consciousness, cerebral convulsions and cerebellar syndrome. Most of these symptoms disappear rapidly after this drug is not longer administered. In long-term administration of metronidazole 10-50% of the patients develop a sensory polyneuropathy with a total dosis of at least 22.5 g, but mostly above 60 g. After the use of metronidazole is stopped, it takes a substantial period of time until there is a full recovery from the symptoms.
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PMID:[Neurologic concomitant diseases in Crohn disease]. 128 45

Gastrointestinal dysfunction due to autonomous neuropathy is a complication described in various diseases such as diabetes mellitus, multiple sclerosis, and familial amyloidosis with polyneuropathy. We present the results of a prospective investigation of bile acid malabsorption in 17 patients with familial amyloidosis by means of 75Se-labelled homocholic-tauro acid (SeHCAT). The diagnosis was in all cases verified by the DNA test for mutation of transthyretin in position 30. Small-intestinal biopsy specimens were examined for deposits of amyloid, and the presence of gastric retention was evaluated by gastroscopy. In addition, the patients were investigated for bacterial overgrowth by means of the bile acid breath test (BABT). A high frequency of abnormal BABT results (44%) was encountered. However, 65% also had abnormal low SeHCAT values, indicating bile acid malabsorption. Only two patients had abnormal BABT and normal SeHCAT results, indicating bacterial contamination of the small intestine. Bile acid losses increased with the duration of gastrointestinal symptoms. Significantly lower SeHCAT values were encountered in patients with gastric retention, whereas the occurrence of amyloid deposits in small-intestinal biopsy specimens was without effect on SeHCAT retention. Bile acid malabsorption is frequently encountered in familial amyloidosis with polyneuropathy and seems to be more closely associated with gastrointestinal motility dysfunction than with amyloid deposits in the intestinal mucosa.
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PMID:Bile acid malabsorption caused by gastrointestinal motility dysfunction? An investigation of gastrointestinal disturbances in familial amyloidosis with polyneuropathy. 150 82

A case of hypobetalipoproteinemia is described; a 16-year-old girl had been suffering for nearly 2 years from diffuse abdominal pain. The only clinical features were liver steatosis, slightly increased amino transferases and an incipient polyneuropathy. No sign of malabsorption or gastrointestinal disease was found. She had extremely low levels of cholesterol and triacylglycerol in her serum, slightly decreased serum phospholipids and normal HDL-cholesterol levels. Apolipoprotein B-100 was approx. 8% of normal, whereas B-48 was present at essentially normal levels. Electron microscopy of lipoprotein particles showed normal morphology of LDL. Examination of close relatives showed no abnormalities. Southern blots revealed no major deletions or rearrangements at the genomic level. Although rare, a- and hypobetalipoproteinemia should be considered as possible etiologies in patients with unexplained steatosis in the liver.
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PMID:Liver steatosis in hypobetalipoproteinemia. A case report. 191 73

This case report concerns a patient with a vitamin B12 deficiency and a normal Schilling test, who had macrocytosis of many years' duration and finally polyneuropathy. All known causes of a vitamin B12 deficiency were excluded. When the Schilling test was performed with egg consumption, excretion of vitamin B12 was clearly diminished. It appears highly likely that this vitamin B12 deficiency developed as a result of malabsorption of protein-bound vitamin B12.
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PMID:[Macrocytosis, polyneuropathy and posterior column disorders caused by malabsorption of protein-bound vitamin B12]. 215 68


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