Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 50-year-old woman, working as a dental assistant for more than ten years, chronic mercury poisoning developed insidiously, apparently from careless handling of mercury-amalgam. The main signs consisted of mental and neurological changes such as erethism, tremor and mercurial psellism. Peripheral arterial circulatory disorders occurred in the course of the disease, as well as abdominal colic and a polyneuropathy, which provided the first clues to panarteritis nodosa subsequently confirmed histologically.
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PMID:[An unusual case of panarteritis nodosa associated with chronic mercury poisoning (author's transl)]. 1 86

A 65-year-old woman with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes) developed severe upper right quadrant colic with jaundice, massive haematemesis and melaena following an apparently uncomplicated percutaneous liver biopsy performed for suspected liver involvement. Symptom onset occurred about 18 hours after the procedure. Haemobilia was diagnosed on endoscopic retrograde cholangiopancreatography. An arteriovenous fistula in the third hepatic segment was demonstrated by transfemoral arteriography and successfully embolized using Gelfoam pledgets mixed with Ivalon fragments. A review of percutaneous liver biopsy related haemobilia is presented.
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PMID:Massive haemobilia after percutaneous liver biopsy in a patient with POEMS syndrome successfully treated by arterial embolization. 882 76

Autonomic dysfunction constitutes a prominent clinical feature of equine grass sickness (EGS). Significant injury to the nervous control of the alimentary system is life threatening, partly because of dysphagia but also because of the failure of the unique regulatory mechanisms in equine digestion involving water and electrolyte balance. The neuropathology also indicates the presence of a somatic polyneuropathy. The morphological features of EGS are similar to those of excitotoxic neuronal degeneration, which resembles neuronal apoptosis. It is difficult to ascertain from published accounts the degree of damage to central neurones: the distribution is well documented and selective but the proportion of damage is poorly quantified. If lesions involve a significant number of regulatory neurones they should produce functional deficits. Any clinical assessment of horses, especially those with chronic EGS, should include a thorough neurological examination. Although this will not necessarily improve the outcome of the case, it may enable the rational selection of animals with a reasonable prognosis for recovery which is partly determined by the extent of CNS lesions. The evidence supports the following pathogenesis. There is an initial lesion in the enteric nervous system of susceptible horses. In the acute form of EGS, massive enteric neuronal damage occurs first functionally, then structurally leading to generalized alimentary smooth muscle atony, enhanced secretions and altered fluid fluxes. Severe distension of the stomach and small intestines rapidly develops, which augments the intestinal ileus by intersegmental inhibitory reflexes and causes colic and dehydration. In subacute cases, failure of intestinal bicarbonate buffer together with alimentary stasis rapidly reduces caecal-colonic fermentation. Thus the osmolality of large intestinal digesta reduces and water travels out of the bowel along osmotic gradients. Water returns to the circulation, but is eventually lost in the gastric and small intestinal secretions. The observation that pathological lesions may not be seen in the prevertebral ganglia within the first few days of acute cases supports the view that a functional deficit precedes structural lesions which may be secondary to a retrograde degeneration. It is therefore possible to resolve the observations that less damage may be seen in prevertebral ganglia and elsewhere in peracute and acute cases with the more common finding that greater neuronal damage is present in acute than in chronic cases. These different observations are probably time dependent. Chronic EGS occurs when there is less initial enteric nerve damage which may lead to less secondary prevertebral ganglionic pathology, and more time for functional and structural compensatory mechanisms to develop. Denervation hypersensitivity develops at target sites both in the gut and in peripheral somatic nerves which may account, in part, for the clinical signs of patchy sweating and muscle tremors. Raised circulating adrenaline levels may also account for generalized sweating, may contribute to gastrointestinal atony and may affect pacemakers at the pelvic flexure. Many of the features of EGS make worthwhile the re-investigation of Clostridium botulinum Group III toxins, which are known to prevent vesicular exocytosis, stimulate neurosecretion, produce neuronal chromatolysis and inhibit neutrophil migration. Also, evidence from other species suggests that increased nitrergic neuronal activity can account for many of the clinical signs of EGS, namely dysphagia, generalized ileus, gastric dilatation, sweating, peripheral vasodilatation, tachycardia, salivary hypersecretion, muscle wastage and cachexia.
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PMID:The neurology and enterology of equine grass sickness: a review of basic mechanisms. 1032 May 95

The authors, on performing a critical analysis of reported data on clinical manifestations of lead intoxication, suggest that the initial manifestations thereof presenting as changes in no other indices but laboratory ones, be regarded as a preclinical stage. Aside from generally recognized concepts of "mild" and "prominent" stages in lead intoxication the authors consider it logical and expediant to introduce a moderately severe stage manifested by vegetosensory polyneuropathy, astheno-vegetative syndrome, dyskinesia of the biliary and intestinal tracts, spastic colitis. It is in this very stage of lead intoxication that the patient, to the author's thinking, is to be assigned to some other job where he/she will not be exposed to lead or other adverse occupational factors. This will, we believe, permit preventing development of a clinically significant stage of lead intoxication manifested by encephalopathy, motor form of polyneuropathy, lead colic, anemia and hepatitis.
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PMID:[Clinical stages of lead intoxication]. 1258 28