Motor neuropathy with multiple conduction blocks associated with TNF-alpha antagonist

Carrilho, Paulo Eduardo Mestrinelli; Araújo, Allan César Faria; Alves, Orival; Kotze, Paulo Gustavo

doi:10.1590/s0004-282x2010000300022

Cited by 12 publications

(7 citation statements)

References 9 publications

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“…Additionally, recent evidence suggests that the drugs which inhibit TNF-alpha synthesis and IL 6 are found to recover neuropathic pain condition in animals (Wang et al, 2012) as well as human beings (Carrilho et al, 2010). Therefore, we had targeted the effects of MC on TBARS, GSH, MPO, TNFalpha and IL 6 levels.…”

Section: Protective Effect Of Standardized MC In Vincristine Induced mentioning

confidence: 99%

Standardized fruit extract of Momordica charantia L protect against vincristine induced neuropathic pain in rats by modulating GABAergic action, antimitotoxic, NOS inhibition, anti-inflammatory and antioxidative activity

Jain

Pareek

Ratan

et al. 2015

South African Journal of Botany

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In the present experimental work, we investigate the protective potential of standardized Momordica charantia L fruit extract [gallic acid (GA) 6%; N8% bitters {momordicosides K (3%) and L (2%); and momordicines I (2%) and II (3%)}] (MC) comparable to its marker compound gallic acid in chemo-toxic neuropathy induced by vincristine [75 μg/kg intra-peritoneal (i.p.) for 10 consecutive days] in rats. An array of behavioral examinations was carried out on days 1st, 12th and 21st, followed by various biochemical and histopathological studies at the end. Vincristine significantly induced cold and dynamic mechanical allodynia, mechanical and heat hyperalgesia; functional deficit in walking and a rise in the levels of TNF-α, IL 6, mitochondrial complexes, myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), and nitrite along with decrease in glutathione (GSH). Administration of MC [400 and 800 mg/kg, per oral (p.o.)], GA (30 mg/kg, p.o.) and gabapentin (100 mg/kg, p.o.) attenuated the vincristine induced behavioral and biochemical changes. MC demonstrated superior antinociceptive activity in comparison to GA. Histopathological evaluation also divulged defending the effects of MC. Pretreatment of saclofen (1 mg/kg, i.p.), picrotoxin (1 mg/kg, i.p.) upturned the antinociceptive action of MC, but ingestion of GABA (100 mg/kg, i.p.) potentiated the action of MC. Additionally, pretreatment with L-arginine [nitric oxide (NO) donor; 100 mg/kg, i.p.] inverted the antinociceptive action of MC; whereas, aminoguanidine (iNOS inhibitor) and 7-nitroindazole (nNOS inhibitor) potentiated it. Besides this a PPARγ antagonist BADGE did not amend the effect of MC. Corroboratively, the attenuating effect of MC in vincristine induced neuropathy is attributed to its modulating action on GABAergic system along with antimitotoxic, NOS inhibition, anti-inflammatory and anti oxidative activities.

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Section: Protective Effect Of Standardized MC In Vincristine Induced mentioning

confidence: 99%

Standardized fruit extract of Momordica charantia L protect against vincristine induced neuropathic pain in rats by modulating GABAergic action, antimitotoxic, NOS inhibition, anti-inflammatory and antioxidative activity

Jain

Pareek

Ratan

et al. 2015

South African Journal of Botany

View full text Add to dashboard Cite

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“…In CIDP cases, elevated serum anti-ganglioside antibodies have been described suggesting a humoral attack against myelin [77][78][79]. Moreover, there are case reports of MMN following infliximab treatment; in these cases, patients developed asymmetric progressive weakness, and conduction blocks of various motor nerves on NS [80][81][82]. Finally, SFN, axonal sensory neuropathy, mononeuritis multiplex or sensorimotor polyneuropathy was also reported in patients treated with infliximab [75,[83][84][85].…”

Section: Tumor Necrosis Factor Inhibitor Therapymentioning

confidence: 99%

Peripheral neuropathy: An underreported neurologic manifestation of inflammatory bowel disease

García-Cabo

Morís

2015

European Journal of Internal Medicine

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“…Consequently, there were 27% (13/48) patients treated with corticosteroids, 58% (28/48) treated with IVIG, and 6% (3/48) of patients treated with plasma exchange. As defined by the respective studies, the majority of patients demonstrated clinical response, with either partial improvement [20,27,32,34,37,40], or complete resolution of symptoms [21,23,26,31,33,36,38,39,41,42]. Although most patients developed neuropathies within weeks to two years after onset of TNF-inhibitor therapy, patients were described as developing neuropathies 3–7 years after onset of TNF-inhibitor therapy [18–22].…”

Section: Literature Reviewmentioning

confidence: 99%

Non-length-dependent and length-dependent small-fiber neuropathies associated with tumor necrosis factor (TNF)-inhibitor therapy in patients with rheumatoid arthritis: Expanding the spectrum of neurological disease associated with TNF-inhibitors

Birnbaum

Bingham

2014

Seminars in Arthritis and Rheumatism

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Objective Small-fiber neuropathy causes severe burning pain, requires diagnostic approaches such as skin biopsy, and encompasses two subtypes based on distribution of neuropathic pain. Such biopsy-proven subtypes of small-fiber neuropathies have not been previously described as complications of tumor necrosis factor (TNF)-inhibitor therapy. Methods We therefore characterized clinical and skin biopsy findings in three rheumatoid arthritis (RA) patients who developed small-fiber neuropathies associated with TNF-inhibitors. We also conducted a systematic review of the literature to characterize subtypes of neuropathies previously reported in association with TNF-inhibitor therapy. Results Two patients presented with a “non-length-dependent” small-fiber neuropathy, experiencing unorthodox patterns of burning pain affecting the face, torso, and proximal extremities. Abnormal skin biopsy findings were limited to the proximal thigh, which is a marker of proximal-most dorsal root ganglia degeneration. In contrast, one patient presented with a “length-dependent” small-fiber neuropathy, experiencing burning pain only in the feet. Abnormal skin biopsy findings were limited to the distal feet, which is a marker of distal-most axonal degeneration. One patient developed a small-fiber neuropathy in the context of TNF-inhibitor-induced lupus. In all patients, neuropathies occurred during TNF-inhibitor-induced remission of RA disease activity and improved on withdrawal of TNF-inhibitors. Conclusions We describe a spectrum of small-fiber neuropathies not previously reported in association with TNF-inhibitor therapy, with clinical and skin biopsy findings suggestive of dorsal root ganglia as well as axonal degeneration. The development of small-fiber neuropathies during inactive joint disease and improvement of neuropathic pain upon withdrawal of TNF-inhibitor suggest a causative role of TNF-inhibitors.

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Motor neuropathy with multiple conduction blocks associated with TNF-alpha antagonist

Cited by 12 publications

References 9 publications

Standardized fruit extract of Momordica charantia L protect against vincristine induced neuropathic pain in rats by modulating GABAergic action, antimitotoxic, NOS inhibition, anti-inflammatory and antioxidative activity

Standardized fruit extract of Momordica charantia L protect against vincristine induced neuropathic pain in rats by modulating GABAergic action, antimitotoxic, NOS inhibition, anti-inflammatory and antioxidative activity

Peripheral neuropathy: An underreported neurologic manifestation of inflammatory bowel disease

Non-length-dependent and length-dependent small-fiber neuropathies associated with tumor necrosis factor (TNF)-inhibitor therapy in patients with rheumatoid arthritis: Expanding the spectrum of neurological disease associated with TNF-inhibitors

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