PMID- 15694694
OWN - NLM
STAT- MEDLINE
DCOM- 20050927
LR  - 20050207
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 64
IP  - 4
DP  - 2005
TI  - alpha1-Antitrypsin and fibromyalgia: new data in favour of the inflammatory 
      hypothesis of fibromyalgia.
PG  - 759-69
AB  - alpha1-Antitrypsin (AAT) circulates in high serum concentrations, and impregnates 
      most body tissues. AAT has a broad anti-inflammatory spectrum, and modulates most 
      inflammatory reactions occurring in human body. Recently, a possible relationship 
      between AAT deficiency (AAT-D) and fibromyalgia (FM) has been raised, with the 
      finding that intravenous infusions of purified human AAT efficiently controlled 
      FM symptoms in two patients with severe hereditary AAT-D. On the other hand, 
      functional magnetic resonance imaging has detected a significant greater activity 
      in pain sensitive areas of the brain in patients with FM, in response to 
      cutaneous stimuli, providing further evidence for a physiological explanation for 
      FM pain. In recent studies abnormal profiles of inflammation markers in serum and 
      biopsies have been found in FM patients. Since most of these inflammation 
      mediators can be inhibited by AAT, these observations would suggest that at least 
      a subset of the FM syndrome could be related to an inflammatory process, possibly 
      due to an imbalance between inflammatory and anti-inflammatory substances, in the 
      soft body tissues. Future directions of research would be: (1) to develop 
      epidemiological studies to determine the gene frequency of AAT deficiency alleles 
      in FM patients; (2) implementation of a double-blind placebo-controlled clinical 
      trial to determine the specific role of AAT augmentation therapy in AAT-D 
      patients with FM; (3) identification of specific laboratory markers for 
      diagnostic and clinical evaluation purposes in FM; (4) application of the newest 
      medical imaging techniques for diagnosis; and (5) identification of genetic, 
      familial, and environmental risk factors suspected to participate in the FM 
      syndrome development.
FAU - Blanco, Lgnacio Eduardo
AU  - Blanco LE
AD  - Department of Internal Medicine, Hospital Valle del Nalon, 33920 Riano-Langreo, 
      Principado de Asturias, Spain. ignacio.blanco@sespa.princast.es
FAU - de Serres, Frederick Joseph
AU  - de Serres FJ
FAU - Fernandez-Bustillo, Enrique
AU  - Fernandez-Bustillo E
FAU - Kassam, Daniel Al
AU  - Kassam DA
FAU - Arbesu, Daniel
AU  - Arbesu D
FAU - Rodriguez, Carmen
AU  - Rodriguez C
FAU - Torre, Juan Carlos
AU  - Torre JC
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (alpha 1-Antitrypsin)
SB  - IM
MH  - Fibromyalgia/drug therapy/epidemiology/*physiopathology
MH  - Humans
MH  - alpha 1-Antitrypsin/*physiology/therapeutic use
EDAT- 2005/02/08 09:00
MHDA- 2005/09/28 09:00
CRDT- 2005/02/08 09:00
PHST- 2004/07/30 00:00 [received]
PHST- 2004/10/15 00:00 [accepted]
PHST- 2005/02/08 09:00 [pubmed]
PHST- 2005/09/28 09:00 [medline]
PHST- 2005/02/08 09:00 [entrez]
AID - S0306-9877(04)00566-3 [pii]
AID - 10.1016/j.mehy.2004.10.005 [doi]
PST - ppublish
SO  - Med Hypotheses. 2005;64(4):759-69. doi: 10.1016/j.mehy.2004.10.005.