Development of polyneuropathy during thalidomide therapy

Wulff, C H; Høyer, H; Asboe-Hansen, G; Brodthagen, H

doi:10.1111/j.1365-2133.1985.tb02323.x

Cited by 132 publications

(59 citation statements)

References 18 publications

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“…9 It has been suggested that neuropathy might possibly be related to cumulative dose or duration of treatment. 22 However, one of our two cases developed neuropathy after 9 months of thalidomide, which is a shorter treatment period than many of those reported by others.…”

Section: Discussioncontrasting

confidence: 39%

The role of thalidomide in the treatment of refractory chronic graft-versus-host disease following bone marrow transplantation in children

Rovelli

Arrigo

Nesi

et al. 1998

Bone Marrow Transplant

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Summary:Chronic graft-versus-host disease (cGVHD) is a frequent complication of allogeneic bone marrow transplantation (BMT). Thalidomide was found to have immunosuppressive properties and it has been used in a limited number of children with cGVHD. We report our experience with refractory and/or high-risk cGVHD in 14 children. Six children showed complete clinical response to thalidomide in a median time of 2 months. Four children had partial responses and four failed. Side-effects were usually mild (somnolence, constipation) and only two patients developed sensory peripheral neuropathy. An increased incidence of infectious complications attributable to thalidomide was not observed. Nine out of 10 responding patients are alive 49-111 months post-BMT. Thalidomide can be effective particularly in children with prevailing mucocutaneous cGVHD. All patients should be carefully monitored to detect peripheral neuropathy early.

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Section: Discussioncontrasting

confidence: 39%

The role of thalidomide in the treatment of refractory chronic graft-versus-host disease following bone marrow transplantation in children

Rovelli

Arrigo

Nesi

et al. 1998

Bone Marrow Transplant

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“…Sensory symptoms may persist, and sometimes get worsen, after withdrawal of the drug and the pathologic findings suggest axonal neuropathy 34 . Although the frequency and the severity of neuropathy are not always found to be related to total dosage 34 , Wulff et al, confirmed that the neuropathy began after a total of 40-50g of thalidomide in most patients 35 . Despite the increased use of thalidomide around the world, we worry about the possible side effects, mainly teratogenicity and neuropathy of this drug 36 , but we believe that more than prohibit their production, the governments need to do more restrict laws to permit their use.…”

Section: Results Results Results Resultsmentioning

confidence: 99%

Long-term thalidomide use in refractory cutaneous lesions of systemic lupus erythematosus

Sato¹,

Assis²,

Lourenzi³

et al. 1998

Rev. Assoc. Med. Bras.

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SUMMARY -Were selected 18 SLE patients (ACR criteria) with active cutaneous patients (ACR criteria) with active cutaneous patients (ACR criteria) with active cutaneous patients (ACR criteria) with active cutaneous patients (ACR criteria) with active cutaneous lesions not responsive to chloroquine, photolesions not responsive to chloroquine, photolesions not responsive to chloroquine, photolesions not responsive to chloroquine, photolesions not responsive to chloroquine, photoprotectors and low doses prednisone and who protectors and low doses prednisone and who protectors and low doses prednisone and who protectors and low doses prednisone and who protectors and low doses prednisone and who presented good response to thalidomide but represented good response to thalidomide but represented good response to thalidomide but represented good response to thalidomide but represented good response to thalidomide but relapsed after withdrawal of the drug. All female lapsed after withdrawal of the drug. All female lapsed after withdrawal of the drug. All female lapsed after withdrawal of the drug. All female lapsed after withdrawal of the drug. All female patients had no risk of pregnancy. Thalidomide patients had no risk of pregnancy. Thalidomide patients had no risk of pregnancy. Thalidomide patients had no risk of pregnancy. Thalidomide patients had no risk of pregnancy. Thalidomide was reintroduced and maintained at low dose was reintroduced and maintained at low dose was reintroduced and maintained at low dose was reintroduced and maintained at low dose was reintroduced and maintained at low dose (25-100mg/day) for a minimum of 6 months.

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“…This is believed to be related to the total dose administered [19,20]. A previous study showed that of seven patients with prurigo nodularis, given 40-115 g of thalidomide for 1-6 years, all developed peripheral neuropathy [21]. The reason for this was not clear until now: the higher dose of thalidomide (200 mg/kg/ day) that we used in rats, in comparison with doses used in humans (6-15 mg/kg/day) [22], may be responsible for induction of neuropathy or neurotoxicity in rats.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide Prolongs Experimental Autoimmune Neuritis in Lewis Rats

et al. 1998

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Thalidomide is reported to have immunomodulatory and anti‐inflammatory effects, which have led to its use in the treatment of a number of immune‐mediated disorders, including leprosy, discoid lupus and Behcet's disease, and to prevent immunological rejection phenomena following skin and bone marrow grafts. Experimental autoimmune neuritis (EAN) is a CD4+ T‐cell‐mediated demyelinating autoimmune disease, which represents an animal model for the study of the immunopathogenesis and immunotherapy of Guillain–Barré syndrome (GBS) in humans. We examined the effect of thalidomide in Lewis rats with EAN, which was induced by immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant (CFA). Thalidomide prolonged clinical EAN when given at a dose of 200 mg/kg/day by gavage. This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon‐γ (IFN‐γ) mRNA‐expressing cells among lymph node mononuclear cells from thalidomide‐treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN. The finding that thalidomide prolongs clinical EAN is in agreement with the clinical polyneuropathy reported in patients receiving treatment with thalidomide and limits its clinical usefulness.

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Development of polyneuropathy during thalidomide therapy

Cited by 132 publications

References 18 publications

The role of thalidomide in the treatment of refractory chronic graft-versus-host disease following bone marrow transplantation in children

The role of thalidomide in the treatment of refractory chronic graft-versus-host disease following bone marrow transplantation in children

Long-term thalidomide use in refractory cutaneous lesions of systemic lupus erythematosus

Thalidomide Prolongs Experimental Autoimmune Neuritis in Lewis Rats

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