Thalidomide in the Treatment of Actinic Prurigo

Londoño, F

doi:10.1111/j.1365-4362.1973.tb00066.x

Cited by 122 publications

(54 citation statements)

References 3 publications

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“…Thalidomide has also been shown to enhance the production of interleukins 4 and 5, and inhibit interferon-c production in peripheral blood mononuclear cell cultures (11). Thalidomide also reduces monocyte phagocytosis by PMNs, which perhaps accounts for its action in inflammatory processes with mononuclear cell accumulation in conditions such as DLE, LP, subacute cutaneous lupus erythematosus, actinic prurigo and erythema multiforme (12)(13)(14)(15). We also found it beneficial in various inflammatory dermatoses other than ENL.…”

Section: Discussionmentioning

confidence: 98%

Thalidomide: An experience in therapeutic outcome and adverse reactions

Sharma

Mahajan

et al. 2007

Journal of Dermatological Treatment

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Thalidomide appears promising in a number of inflammatory dermatological conditions and will probably find new usages in future. The treating physicians need to be wary of the thrombo-embolic complications due to thalidomide especially when glucocorticoids or other chemotherapeutic agents such as doxorubicin, gemcitabine, 5-fluorouracil or dexamethasone-cyclophosphamide pulse therapy are being used concomitantly, and in patients of metastatic renal carcinoma, myelodysplastic syndrome or multiple myeloma receiving thalidomide/chemotherapy. Antiphospholipid or anticardiolipin antibodies appear to be other possible risk factors for this complication.

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Section: Discussionmentioning

confidence: 98%

Thalidomide: An experience in therapeutic outcome and adverse reactions

Sharma

Mahajan

et al. 2007

Journal of Dermatological Treatment

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“…has been reported to be beneficial in patients with diverse immunologic or inflammatory disorders. 26,27 Endogenously synthesized NO has a short biological half-life (5 seconds or less), and is oxidized rapidly to More recently, it has been documented to be effective in treating and preventing graft-versus-host disease NO 0 2 and NO 0 3 stable compounds that are excreted in urine. 17 Several studies have shown that urinary excreafter bone marrow transplantation.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide Inhibits Tumor Necrosis Factor α, Decreases Nitric Oxide Synthesis, and Ameliorates the Hyperdynamic Circulatory Syndrome in Portal–Hypertensive Rats

et al. 1996

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A hyperdynamic circulatory state frequently is ob-Portal hypertension accompanied by anatomic or served in portal hypertension with liver failure or exten-functional portal-systemic shunting very often is assosive portal-systemic shunting. Tumor necrosis factor a ciated with a hyperdynamic circulatory state. The so-(TNF) causes marked hypotension in mammals by in-called hyperdynamic circulatory syndrome (HCS) is ducing nitric oxide synthesis and has been shown to play characterized by generalized vasodilatation with a dea role in the development of the hemodynamic changes crease in mean arterial pressure and systemic vascular observed in portal hypertension. Thalidomide selec-resistance and an increase in cardiac output and retively inhibits TNF production by enhancing messenger gional blood flows. Although the cause of this syndrome RNA degradation. We investigated the systemic and poris still a matter of controversy, it seems that vasodilatatal hemodynamic effects of thalidomide in a prehepatic model of portal hypertension and evaluated whether tion, induced by increased activity of endothelial-indesuppressing TNF synthesis decreases NO production. pendent and endothelial-dependent vasodilators, initiPortal hypertension was induced by partial ligation of ates the hyperdynamic state. 1 the portal vein (PVL). Animals received thalidomide (T)Various substances have been proposed as mediators (50 mg/kg/d) / water or water alone (W), orally, daily for of the HCS. Recently, a role for endogenous nitric oxide 2 days before and 13 days after PVL operation, at which in the regulation of blood flow and vascular tone of the time hemodynamic studies were performed and TNF systemic and splanchnic circulations in portal hypertenplasma levels were obtained. Sham-operated animals sion has been suggested by several in vivo and in vitro were studied identically. In an additional group of PVL animals, 24-hour urinary excretion of NO 0 2 and NO 0 3 was studies, implying that excessive synthesis of NO could measured during treatment. PVL animals receiving T be responsible for these circulatory abnormalities. 2,3 presented with a significantly higher mean arterial presTumor necrosis factor a (TNF), a 17-kd, mononusure and systemic vascular resistance and significantly clear-derived cytotoxic protein, causes marked hypolower portal pressure, TNF plasma levels, and 24-hour tension in mammals. 4 inhibiting TNF synthesis and decreasing NO synthesis,

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“…Thalidomide (α [N-phthalimido]-glutaramide) was synthesized in 1956 and sold as a sedative until 1961, when it was withdrawn from the market due to high teratogenicity and after having caused more than 10,000 cases of malformed babies 1 . After withdrawal, thalidomide was used in many countries for the treatment of several inflammatory dermatoses such as lepra reaction 2,3 , actinic prurigo 4 , aphtae and aphtosis 5,6 , pyoderma gangrenosum 7 , Weber-Christian disease 8 prurigo nodularis 9 Langerhans cell histiocytosis 10 and discoid lupus erythematosus 11 . More recently, due to the immunomodulatory effect, thalidomide has been used to treat graft-versushost disease 12 and patients with human immunodefficience virus 13 .…”

Section: And and M M M M Methods Ethods Ethods Ethods Ethodsmentioning

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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Thalidomide in the Treatment of Actinic Prurigo

Cited by 122 publications

References 3 publications

Thalidomide: An experience in therapeutic outcome and adverse reactions

Thalidomide: An experience in therapeutic outcome and adverse reactions

Thalidomide Inhibits Tumor Necrosis Factor α, Decreases Nitric Oxide Synthesis, and Ameliorates the Hyperdynamic Circulatory Syndrome in Portal–Hypertensive Rats

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

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