Alpha-1 Antitrypsin Deficiency - is is an underlying cause of fibromyalgia?
The research concluded: "Our calculations predict that AAT deficiency would remain undetected in around nine percent of FMS patients, with about eight percent of them carrying moderate deficiency phenotypes [MS, SS, and MZ], and less than one percent with severe deficiency phenotypes [SZ and ZZ].
Conclusions: Therefore, AAT phenotype characterization should be recommended in FMS patients and the possible efficacy of AAT replacement therapy in severe deficiency FMS patients should warrant further studies.
Abstract
"Estimates of the Prevalence and Number of Fibromyalgia Syndrome
Patients and Their Alpha-1 Antitrypsin Phenotypic Distribution in Ten
Countries
Journal of Musculoskeletal Pain, Volume: 15, Issue: 4, Page Range:
9-23, 2007
Contributors:
Ignacio Blanco MD, Department of Internal Medicine, Hospital Valle
del Nalón, Langreo, 33920, Spain,
Frederick de Serres PhD, Laboratory of Molecular Toxicology,
Environmental Toxicology Program, National Institute of Environmental
Health Sciences, Research Triangle Park, NC, 27709-2233
Sabina Janciauskiene PhD, Department of Clinical Sciences, Malmö
University Hospital, Malmö, Sweden
Daniel Arbesú PhD, Department of Rehabilitation Medicine, Hospital
Valle del Nalón, Langreo, 33920, Spain
Enrique Fernández-Bustillo PhD, Biostatistics Unit, Hospital
Universitario Central de Asturias, Oviedo, 33006, Spain
Victoriano Cárcaba PhD, Department of Internal Medicine, Hospital
Valle del Nalón, Langreo, 33920, Spain
Izabela Nita PhD, Department of Clinical Sciences, Malmö University
Hospital, Malmö, 20502, Sweden
Aurora Astudillo PhD, Department of Pathology, Hospital Universitario
Central de Asturias, Oviedo, 33006, Spain
Objectives: During the last few years, clinical, epidemiological, and
pathological evidence has suggested that inherited alpha-1
antitrypsin [AAT] deficiency might play a role in the development of
the fibromyalgia syndrome [FMS], probably because of the loss of AAT
anti-inflammatory efficacy. The objective of this study was to
estimate the prevalence and number of FMS patients, and their AAT
phenotypic distribution worldwide.
Methods: A critical review selecting reliable studies on the subject.
Results: Studies on AAT gene frequencies and FMS prevalence were
retrieved for ten countries worldwide, namely Canada, the United
States of America [USA], Denmark, Finland, Germany, Italy, the
Netherlands, Spain, Sweden, and Pakistan. The severe deficiency Z
allele was found in all these countries, with very high frequencies
in Denmark and Sweden [23 and 27 per 1,000, respectively], high
frequencies in Italy and Spain [16 and 17], intermediate frequencies
in Germany, the Netherlands, Canada, and the USA [10 to 14], and a
low frequency in Pakistan [nine per 1,000]. The calculated prevalence
of AAT deficiency and the number of FMS patients with AAT deficiency
were 1/10 and 25,408 in Canada, 1/11 and 478,681 in the US, 1/9 and
3,124 in Denmark, 1/ 36 and 726 in Finland, 1/16 and 48,523 in
Germany, 1/13 and 84,876 in Italy, 1/15 and 9,639 in the Netherlands,
1/4 and 114,359 in Spain, 1/11 and 9,065 in Sweden, and 1/25 and
85,965 in Pakistan. Our calculations predict that AAT deficiency
would remain undetected in around nine percent of FMS patients, with
about eight percent of them carrying moderate deficiency phenotypes
[MS, SS, and MZ], and less than one percent with severe deficiency
phenotypes [SZ and ZZ].
Conclusions: Therefore, AAT phenotype characterization should be
recommended in FMS patients and the possible efficacy of AAT
replacement therapy in severe deficiency FMS patients should warrant
further studies"
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