Prominent adverse effects of thalidomide in primary Sjögren's syndrome

Pillemer, Stanley R.; Leakan, Rose Anne; Sankar, Vidya; Manny, Joan; Baum, Bruce J.; Smith, Janine A.; Chaudhry, Usha; Fox, Philip C.; Radfar, Lida; Ligier, Sophie; Brennan, Michael T.

doi:10.1002/art.20416

Cited by 21 publications

(12 citation statements)

References 10 publications

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“…Whereas one pilot study suggested that an inhibitor of TNFa (infliximab) might be beneficial [83], subsequent multicenter trials did not confirm these results. Double-blind studies have not shown significant benefit with the soluble TNF receptor (etanercept), which has been effective in RA [84,85], nor with thalidomide, another inhibitor of TNFa [86,87]. Unexpectedly, TNFa plasma levels in pSS patients actually increased after etanercept therapy, which provides further insight regarding etanercept inefficacy (Katsifis et al, in preparation) and lends credence to alternative modes of immunopathology underlying this disease.…”

Section: Tnfamentioning

confidence: 85%

T Lymphocytes in Sjögren’s Syndrome: Contributors to and Regulators of Pathophysiology

Katsifis

Moutsopoulos

Wahl

2007

Clinic Rev Allerg Immunol

101

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Sjögren's syndrome is a chronic autoimmune disorder characterized by lymphocytic infiltration and malfunction of the exocrine glands, resulting in dry mouth and eyes. This multigenic and multifunctional disease can present as primary Sjögren's syndrome or secondary to an underlying connective tissue disease. Immune activation subsequent to activation or apoptosis of glandular epithelial cells in genetically predisposed individuals may expose autoantigens, which engage self-perpetuating T cell dependent autoimmune sequelae. The cellular and molecular context of this immune response may drive proinflammatory (Th1 and Th17) and restrain inhibitory (Treg) pathways. Inability to suppress the immune response results in persistent tissue damage and compromised function of salivary and lacrimal glands. Defining the contributions of participating T cells may unravel strategies for therapeutic intervention.

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Section: Tnfamentioning

confidence: 85%

T Lymphocytes in Sjögren’s Syndrome: Contributors to and Regulators of Pathophysiology

Katsifis

Moutsopoulos

Wahl

2007

Clinic Rev Allerg Immunol

101

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“…6 According to the original study design, patients were to receive 300 mg/day or placebo orally, and the group randomisation was to be accomplished by a standard method using a random number table a priori. In the event of adverse effects dosing was to be reduced to 200 mg/day, 100 mg/day, 50 mg/day.…”

Section: Methodsmentioning

confidence: 99%

“…Because adverse effects were reported, three patients treated with thalidomide had to discontinue the study at 3 weeks and the protocol was modified, thereafter. The adverse effects identified included peripheral neuropathy, sedation, postural hypotension, rashes, vasculitis, and peripheral oedema, 6 and were probably attributable to the high starting dose of the drug (300 mg). Treatment of the remaining patients was started at 50 mg/day and increased by 50 mg each day, to achieve a maximal treatment dose of 300 mg. One patient reached a dose of 150 mg/day, when thalidomide had to be decreased to 50 mg/day and then discontinued at 3 weeks owing to severe adverse effects.…”

Section: Clinical Outcomementioning

confidence: 99%

Immunological consequences of thalidomide treatment in Sjogren's syndrome

Moutsopoulos

2006

Annals of the Rheumatic Diseases

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“…Following encouraging results in uncontrolled studies, well-designed RCTs of several anti-TNF agents, including infliximab, etanercept, and thalidomide have shown no significant efficacy in SS [53,54,55]. Interestingly, in the latter trial in primary SS patients, biological measures of cell activation were decreased with thalidomide use, although clinical outcome measures were not improved and the trial was discontinued prematurely due to an unacceptably high number of AEs [56].…”

Section: Biological Therapymentioning

confidence: 90%

Established and Novel Approaches for the Management of Hyposalivation and Xerostomia

Wolff¹,

Fox²,

Porter³

et al. 2012

CPD

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Hyposalivation, often symptomatically manifested as xerostomia (dry mouth sensation) may indicate the presence of altered salivary gland function and places patients at a higher risk for oral complications. Diverse symptoms and consequences have been associated with hyposalivation, such as difficulties with speaking, swallowing and tasting and a significant increase in dental caries and other oral infections. Although hyposalivation may be caused by a variety of conditions (head and neck radiotherapy, Sjogren's syndrome, medications, etc.), its hallmark symptom, xerostomia, is common to all such disorders, and varies only in intensity. Therefore, treatment is generally non-specific, and similar therapeutic approaches are used in all cases. In the present paper, available palliative oral care in the form of saliva substitutes, such as mouthwashes or gels, is detailed. Also salivary flow stimulants, such as certain pharmaceutical or gustatory preparations, acupuncture and electrostimulation are reviewed. Finally, other approaches, currently under investigation, such as biological and gene therapies, are discussed. The degree of evidence of the best known methods and their intended use are analyzed.

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Prominent adverse effects of thalidomide in primary Sjögren's syndrome

Cited by 21 publications

References 10 publications

T Lymphocytes in Sjögren’s Syndrome: Contributors to and Regulators of Pathophysiology

T Lymphocytes in Sjögren’s Syndrome: Contributors to and Regulators of Pathophysiology

Immunological consequences of thalidomide treatment in Sjogren's syndrome

Established and Novel Approaches for the Management of Hyposalivation and Xerostomia

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