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)

The patient is a 25-year-old Filipino who showed polymorphous eruptions over the whole body, right ulnar nerve paresis, polyneuropathy and hypalgesia in the area of eruptions. Because the biopsy specimen showed foam cells, histiocytes, epithelioid cells, many Mycobacterium leprae and no giant cells, the diagnosis of borderline-lepromatous (BL) type was made. The symptoms were improved by the administration of 300 mg/day ofloxacin. Because the monotherapy using ofloxacin has been reported to be effective in all 5 previously reported cases of BL type leprosy, it may be recommended for a larger number of leprosy cases.
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PMID:Active leprosy treated effectively with ofloxacin. 891 6

We report on a 69-year-old woman who presented with myalgia, hearing impairment, fever, night sweats, weight loss, muscular weakness, paresthesia, hypesthesia, and hypalgesia. Sural nerve biopsy showed demyelinative and axonal polyneuropathy due to necrotizing vasculitis with fibrinoid necrosis. A positive test for antineutrophil cytoplasmic antibodies (ANCA) with a perinuclear immunofluorescence pattern directed against myeloperoxidase was more suggestive of microscopic polyangiitis (MPA) than of polyarteritis nodosa (PAN), the possible differential diagnoses. In addition, positive tests for cytomegalovirus (CMV) antibodies (immunoglobulin (Ig)M and IgG) and the detection of CMV-DNA in sputum specimens by polymerase chain reaction (PCR) were indicative of active CMV infection. Treatment with ganciclovir and anti-CMV immunoglobulin in addition to prednisolone medication for 6 months resulted in rapid improvement of the clinical symptoms without relapse. CMV infection has been described to be related to ANCA-associated vasculitis in non-immunocompromized patients and may be either a causative agent or an opportunistic infection. Identification of a viral etiology in patients with atypical ANCA-associated vasculitides may lead to different, less aggressive treatment approaches, including antiviral therapy.
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PMID:Cytomegalovirus infection in systemic necrotizing vasculitis: causative agent or opportunistic infection? 1114 60

A 71-year-old man with cryoglobulinemia associated with severe symmetrical sensorimotor polyneuropathy was successfully treated with intravenous immunoglobulin (IVIG) and a corticosteroid. Within 2-3 months, he developed distal motor and sensory deficits and burning feet deteriorating after cold exposure. On examination, symmetric hypesthesia and hypalgesia were found along with bilateral loss of vibration and position sense, loss of ankle jerks, and paralysis of the pretibial muscles with step-page gait. The laboratory exam revealed elevated cryoglobulin levels and reduced complement C4. Nerve conduction studies were consistent with a severe axonal sensorimotor polyneuropathy. Sural nerve biopsy showed chronic neuropathy with an acute component. The patient underwent a combined treatment with prednisolone (initially 100 mg) and intravenous immunoglobulin. His condition markedly improved after almost a year of treatment. Unfortunately, the treatment with intravenous immunoglobulin had to be interrupted due to an allergic reaction after the sixth application.
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PMID:[Intravenous immunoglobulin and prednisolone treatment of cryoglobulinemic polyneuropathy]. 1143 4

Neurofibromatosis 2 (NF2) is an autosomal dominant disease characterised by development of tumours in the central and peripheral nervous system. Some NF2 patients develop acro-distal sensory motor polyneuropathy that can hardly be explained by the tumour burden alone. In the present study eight sural nerve biopsy specimens from seven NF2 patients suffering from polyneuropathy were investigated, data including clinical course of the disease, electrophysiological findings, teased fibre preparations, histopathological, morphometric, immunohistochemical, electron microscopic and molecular genetic findings. All patients suffered from distal symmetric reflex loss, symmetrical stocking-like hypalgesia and hypesthesia and loss of vibration sense later followed by a slowly progressive distal muscle atrophy and paresis. Sural nerve biopsy specimens revealed a pathological reduction of nerve fibre density correlating with age. In addition, diffuse proliferation of Schwann cells was observed in five of eight biopsies, and small endoneurial tumourlets of schwannomas and perineuriomas were found in two of eight and one of eight samples, respectively. Ki-67 labelling revealed a slight endoneurial proliferative activity in three cases. Schwann cell onion bulbs with or without central myelinated axon were seen in two cases. The findings suggest an axonopathy of multifactorial origin resulting not only from gross tumour growth but, in addition, from small endoneurial tumourlets, diffuse proliferation of Schwann cells and proliferation of perineurial cells.
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PMID:Polyneuropathy in neurofibromatosis 2: clinical findings, molecular genetics and neuropathological alterations in sural nerve biopsy specimens. 1211 61

Polyneuropathy associated with antibodies directed against myelin-associated glycoprotein (MAG) is a chronic symmetric sensorimotor demyelinating neuropathy caused by monoclonal IgM against MAG (anti-MAG neuropathy). Intravenous immunoglobulin therapy (IVIg) has been partially successful in patients with anti-MAG neuropathy. A placebo-controlled trial of rituximab in patients with anti-MAG neuropathy has been reported. We report rapid improvement in a patient with anti-MAG neuropathy using rituximab. A 58-year-old man presented with abnormal sensation, weakness of the limbs, and unsteadiness. He was previously diagnosed with chronic inflammatory demyelinating neuropathy and was treated with steroid pulse therapy and IVIg. However, these treatments were not effective. On examination at our hospital, he showed areflexia in all limbs, mild weakness in distal portions of upper and lower extremities, sensory ataxia, and hypesthesia/hypalgesia except for his face. He showed high serum IgM levels (323mg/dl). He did not show M protein on immunoelectrophoresis; however, anti-MAG and anti-sulfoglucuronyl paragloboside (SGPG) antibodies were detected by immunoblot and enzyme-linked immunosorbent assay, respectively. He was diagnosed with anti MAG neuropathy and was administered four cycles of intravenous rituximab at a dose of 375mg/m(2)/week. After the first cycle of rituximab administration, he showed improvement in two-point discrimination of middle fingers (10/13 before therapy to 7/7mm after administration). Two-point discrimination and vibration markedly improved after four cycles of rituximab administration. Romberg sign became negative after 7 months. Anti-SGPG antibody titers reduced from 0.554 before rituximab administration to 0.307 (OD) at 1,600 dilution, 4 months after administration. We concluded that rituximab was effective for the treatment of anti-MAG neuropathy. We suggested that rapid and long-term improvement in our patient might be caused not only by preventing the formation of new antibody-secreting cells and antibody-titer reduction but also affecting the balance of proinflammatory cytokines and regulatory cytokines production.
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PMID:[Rapid improvement by rituximab treatment in a case of demyelinating polyneuropathy with anti-myelin-associated glycoprotein antibody]. 2201 68

The pathophysiology of pain in neuropathy is complex and may be linked to sensory phenotypes. Quantitative sensory testing, a standardized method to evaluate sensory profiles in response to defined stimuli, assesses functional integrity of small and large nerve fiber afferents and central somatosensory pathways. It has revealed detailed insights into mechanisms of neuropathy, yet it remains unclear if pain directly affects sensory profiles. The main objective of this study was to investigate sensory profiles in patients with various neuropathic conditions, including polyneuropathy, mononeuropathy, and lesions to the central nervous system, in relation to self-reported presence or absence of pain and pain sensitivity using the Pain Sensitivity Questionnaire. A total of 443 patients (332 painful and 111 painless) and 112 healthy participants were investigated. Overall, loss of sensation was equally prevalent in patients with and without spontaneous pain. Pain thresholds were equally lowered in both patient groups, demonstrating that hyperalgesia and allodynia are just as present in patients not reporting any pain. Remarkably, this was similar for dynamic mechanical allodynia. Hypoalgesia was more pronounced in painful polyneuropathy, whereas hyperalgesia was more frequent in painful mononeuropathy (compared with painless conditions). Self-reported pain sensitivity was significantly higher in painful than in painless neuropathic conditions. Our results reveal the presence of hyperalgesia and allodynia in patients with central and peripheral lesions of the somatosensory system not reporting spontaneous pain. This shows that symptoms and signs of hypersensitivity may not necessarily coincide and that painful and painless neuropathic conditions may mechanistically blend into one another.
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PMID:No pain, still gain (of function): the relation between sensory profiles and the presence or absence of self-reported pain in a large multicenter cohort of patients with neuropathy. 3286 52