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From Our Readers: Comments & Suggestions – 9/10/14

 
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Alpha-1 antitrypsin and chronic fatigue syndrome: a case study from pathophysiology to clinical practice

  [ 5 votes ]   [ 1 Comment ]
By J. Alegre et al. • www.ProHealth.com • April 8, 2014


Editor’s Comment: Alpha -1 Antitrypsin protects tissues from enzymes of inflammatory cells. The FDA has approved the use of three alpha 1-antitrypsin products derived from human plasma: Prolastin, Zemaira, and Aralast. Alpha -1 Antitrypsin treatment is extremely expensive.

By J. Alegre et al.

Abstract

Background: Several lines of evidence support the involvement of inflammatory and immunologic abnormalities in chronic fatigue syndrome (CFS). Since recent studies have shown that alpha-1 antitrypsin (AAT) possesses anti-inflammatory properties, the potential therapeutic effect of AAT treatment on CFS has been investigated.

Case presentation: A 49-year-old woman diagnosed with CFS was treated with intravenous infusions of a human plasma-derived AAT concentrate (60 mg/kg body weight weekly for 8 consecutive weeks). The patient's monocyte elastase, a regulator of inflammatory processes, was 1170 U/mg.

At completion of treatment, improvement in maximal workload was observed (54.0-71.7% of predicted). Additionally, amelioration in working memory (scores: 83-94) and perceptual organization (scores: 75-83) were detected on the Wechsler Adult Intelligence Scale-III test. Monocyte elastase decreased to a normal range (<150 U/mg).

Improvement in functional capacity allowed the patient to work in part-time employment.

Conclusion: These findings suggest a possible role for AAT in the treatment of CFS.

Source: Alegre J, Camprubí S, García-Quintana A. Pain Manag. 2013 Mar;3(2):119-22. doi: 10.2217/pmt.12.84.



Please Discuss This Article:   Post a Comment 

A1AT study
Posted by: ashley96
Apr 24, 2014
A very interesting case report. Sadly this is a very expensive drug although a company in Italy were
apparently looking at a way of delivering the same via a nose spray a few years ago for A1At deficiency. They were bought up and nothing heard of it since. A few other studies are looking at
the wider impact of A1AT in other inflammatory disorders, as well as diabetes.Like everything else
cost will inevitably put a break on this promising area of research. Just a note, but it doesn't say if the patient had A1AT deficiency or not.
Greg
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