Literature DB >> 13130485

Favorable preliminary experience with etanercept in two patients with the hyperimmunoglobulinemia D and periodic fever syndrome.

Kazuki Takada1, Ivona Aksentijevich, Vijayabhanu Mahadevan, Jane A Dean, Richard I Kelley, Daniel L Kastner.   

Abstract

OBJECTIVE: The hyperimmunoglobulinemia D and periodic fever syndrome (HIDS; MIM 260920) is caused by recessive mutations in the mevalonate kinase gene (MVK), which encodes an enzyme involved in cholesterol and nonsterol isoprenoid biosynthesis. HIDS is characterized by persistently elevated polyclonal IgD and recurrent febrile episodes. Although abnormalities in tumor necrosis factor alpha (TNF alpha) are not the primary cause of HIDS, plasma TNF alpha levels are elevated in HIDS patients during attacks and thus may be a therapeutic target. This study assessed the effects of etanercept, a soluble p75 TNF alpha receptor-Fc fusion protein, in 2 patients with HIDS.
METHODS: We performed biochemical and molecular genetic analyses on 2 girls with periodic episodes of fever, skin rash, abdominal pain, and arthralgia, of whom 1 had elevated levels of serum IgD. After the diagnosis of HIDS was made, treatment with etanercept was initiated in both patients. Clinical response was recorded in a standardized diary, and serum levels of cytokines and their decoy receptors were serially measured in 1 of the 2 patients.
RESULTS: Urinary mevalonate levels were elevated in both girls. Patient 1 was heterozygous for a known MVK missense mutation (V377I) and a novel mutation that led to skipping of exon 3. Patient 2 was found to have V377I and a new missense mutation, S329R. Neither patient had mutations in TNFRSF1A or MEFV, the genes for the TNF receptor-associated periodic syndrome and familial Mediterranean fever, respectively. Etanercept reduced the frequency and severity of symptoms in both patients, whereas the levels of serum IgD and urine mevalonate remained unchanged.
CONCLUSION: Our favorable experience with etanercept for the treatment of HIDS suggests that further investigation of this therapy is warranted.

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Year:  2003        PMID: 13130485     DOI: 10.1002/art.11218

Source DB:  PubMed          Journal:  Arthritis Rheum        ISSN: 0004-3591


  36 in total

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4.  Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2006.

Authors:  D E Furst; F C Breedveld; J R Kalden; J S Smolen; G R Burmester; P Emery; E C Keystone; M H Schiff; P L C M van Riel; M E Weinblatt; M H Weisman
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Review 5.  Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2007.

Authors:  D E Furst; F C Breedveld; J R Kalden; J S Smolen; G R Burmester; J Sieper; P Emery; E C Keystone; M H Schiff; P Mease; P L C M van Riel; R Fleischmann; M H Weisman; M E Weinblatt
Journal:  Ann Rheum Dis       Date:  2007-11       Impact factor: 19.103

Review 6.  Monogenic autoinflammatory diseases: disorders of amplified danger sensing and cytokine dysregulation.

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7.  A patient with hyper-IgD syndrome responding to anti-TNF treatment.

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8.  Treatment with anakinra in the hyperimmunoglobulinemia D/periodic fever syndrome.

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10.  Developments in the scientific and clinical understanding of autoinflammatory disorders.

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