Journal: Pharmacogenomics. 2007 January;8(1):67-74.
Authors and affiliations: Buskila D, Sarzi-Puttini P, Ablin JN. Ben Gurion University, Department of Medicine H, Soroka Medical Center and Faculty of Health Sciences, Beer Sheva, Israel (Buskila); L. Sacco University Hospital, Rheumatology Unit, Milano, Italy (Sarzi-Puttini); Tel-Aviv University, Departments of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv, Israel (Ablin). [E-mail: email@example.com ]
Fibromyalgia Syndrome (FMS) is a common chronic widespread pain syndrome mainly affecting women. Although the etiology of FMS is not completely understood, varieties of neuroendocrine disturbances, as well as abnormalities of autonomic function, have been implicated in its pathogenesis. The exposure of a genetically predisposed individual to a host of environmental stressors is presumed to lead to the development of FMS.
Fibromyalgia overlaps with several related syndromes, collectively compromising the spectrum of the functional somatic disorder. FMS is characterized by a strong familial aggregation. Recent evidence suggests a role for polymorphisms of genes in the serotoninergic, dopaminergic and catecholaminergic [all neurotransmitter] systems in the etiopathogenesis of FMS. [A polymorphism is defined as “a genetic variant that appears in at least 1 percent of a population.”]
These polymorphisms are not specific for FMS and are similarly associated with additional comorbid conditions. The mode of inheritance in FMS is unknown, but it is most probably polygenic [attributable to two or more genes]. Recognition of these gene polymorphisms may help to better subgroup FMS patients and to guide a more rational pharmacological approach.
Future genetic studies conducted in larger cohorts of FMS patients and matched control groups may further illuminate the role of genetics in FMS.