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Seven genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis

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http://www.ncbi.nlm.nih.gov/sites/entrez?

Db=pubmed & Cmd=ShowDetailView & TermToSearch=18057078 & ordinalpos=5 & itool=

EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum :

Seven genomic subtypes of Chronic Fatigue Syndrome / Myalgic

Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and

clinical phenotypes.Kerr J, Burke B, Petty R, Gough J, Fear D,

M, Axford J, Dalgleish A, Nutt D.

St 's University of London, United Kingdom.

Chronic Fatigue Syndrome / myalgic encephalomyelitis (CFS/ME) is a

multisystem disease, the pathogenesis of which remains undetermined.

We have recently reported a study of gene expression which identified

differential expression of 88 human genes in patients with CFS/ME.

Clustering of QPCR data from CFS/ME patients revealed 7 distinct

subtypes with distinct differences in SF-36 scores, clinical

phenotypes and severity. In this study, for each CFS/ME subtype, we

determined those genes whose expression differed significantly from

that of normal blood donors, and then determined gene interactions,

disease associations and molecular and cellular functions of those

gene sets. Genomic analysis was then related to clinical data for

each CFS/ME subtype. Genomic analysis revealed some common

(neurological, cancer, immunological, inflammatory, haematological)

and some distinct (metabolic, endocrine, dermatological,

cardiovascular, connective tissue) disease associations among the

subtypes. Subtypes 1, 2 and 7 were the most severe, and subtype 3 was

the mildest. Clinical features of each subtype were as follows:

subtype 1 (cognitive, musculoskeletal, sleep, anxiety / depression);

subtype 2 (musculoskeletal, pain, anxiety / depression); subtype 3

(mild); subtype 4 (cognitive); subtype 5 (musculoskeletal,

gastrointestinal); subtype 6 (postexertional); subtype 7 (pain,

infectious, musculoskeletal, sleep, neurological, gastrointestinal,

neurocognitive, anxiety / depression). It is particularly interesting

that in these genomically derived subtypes, there were distinct

clinical syndromes and that those which were most severe were also

those with anxiety / depression, as would be expected in a disease

with a biological basis.

PMID: 18057078 [PubMed - as supplied by publisher]

1: J Clin Pathol. 2007 Dec 5 [Epub ahead of print]

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