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Acute intermittent porphyria.

I noted with interest the article on hyperbaric oxygen therapy for patients with acute intermittent porphyria (AIP) (Townsend Letter, April 2008). I had AIP for about 30 years before it was properly diagnosed in 1973. From age eight, I had pains in my right side. At age 14, I had the first AIP crisis, which put me "out of commission" for a couple of weeks at least. Over the years, I developed symptoms of enzyme deficiencies, kidney stress, periodic crises, near-fainting spells on the street, and hepatomegaly. I had severely decreased ability to recognize faces, remember names, and memorize even phone numbers. I had chronic hypoglycemia, pernicious anemia, and sun sensitivity. I lost the ability to digest dairy products, some grains, and beef. (Relatives on one side of the extended family had various problems also, including liver cancer, hemochromatosis, enzyme deficiencies, and early-onset dementia; one man had spent a couple of years in his youth in a tuberculosis [TB] sanitarium.)

In 1974, Randolph K. Brown, MD, then of Howard University Hospital in Washington, DC, finally diagnosed my AIP and pulled me back from death's door with medications that removed excess porphyrins from my system. He also showed me the physical signs (which I discovered later were similar to those occurring in niacinamide deficiency) and counseled me to avoid aspirin and to be wary of pharmaceuticals in general because liver damage had left me very susceptible to adverse side effects.

Some time after I moved to the Arizona desert in the late '70s, I noted that the overall weakness that had plagued me for years was being replaced by increased physical strength and endurance and that sun exposure in moderation was now tolerable. However, I was not entirely well. I had an addiction to candy bars and sodas, and the more sweets I consumed, the worse I seemed to feel. So I finally was able to give up the addiction when I became aware that if I didn't quit, the sugar could wreck what was left of my health. By this time, I had become what is termed a "lay-trained researcher"--a mostly self-taught searcher for information on various medical subjects, and I began to suspect that somehow a sugar-dependent pathogen might be causing at least some of my health problems because about two weeks after "pigging out" on sugar, I had to spend a couple of days in bed, unable to function.

In the early '80s, I served as a volunteer research consultant to an AIDS-patient group and noted that some of the herbs I used for AIP seemed to help the AIDS patients also. Then in the early '90s, I came down with what appeared to be a full-blown case of TB, but a TB test at a local hospital was negative. Figuring that it might be an atypical mycobacterial infection, I quarantined myself and spent a month at home, much of it bedridden and extremely weak. During that month, I researched the medical literature (particularly older medical books in my home library) for what nonpharmaceutical measures might be of help for such a condition--using myself for a guinea pig. By the end of a month, I was well enough to return to work without worrying about giving whatever I had to others. I wrote up the results of my research, and Townsend Letter was kind enough to publish it in three parts (November 1997, December 1997, and January 1998). Since that time, while I still have dietary restrictions due to liver damage, I have been essentially free of all symptoms I experienced during my long illness.

Over the years, I had noted that some types of porphyria had been linked to liver infections--such as hepatitis C in cases of porphyria cutanea tarda. (1) Based on my experience, I believe that my case of AIP was due to a family-transmitted atypical mycobacterial infection and feel it might be useful for others with the condition to be tested for the presence of atypical mycobacterial infection.

1. See, for example, Maticic M. Lichen plan us in hepatitis C virus infection: an early marker that may save lives. Acta Dermatoveneraol, Alp Panonica Adriat. 2007 Mar;16(1):3-6.

Abstract: Hepatitis C virus (CV) represents a major public health problem as a causative agent in developing chronic hepatitis, cirrhosis, and hepatocellular carcinoma. In recent years, it has become known that HCV induces a broad spectrum of extrahepatic manifestations, including some cutaneous ones such as mixed cryoglobulinemia, porphyria cutanea tarda, leukocytoclastic vasculitis, lichen planus (LP), sicca syndrome, and others. Although the association of HCV infection with cryoglobulinemia has been well established, several controversies exist regarding the relationship between HCV infection and LP. This review focuses on the dilemma in evaluating the potential role of LP in diagnosing HCV infection as one of the first overt markers of potentially fatal chronic liver disease.

Maria Abdin

P.O. Box 21521

Seattle, Washington 98111

Please visit www.townsendletter.com to read Maria Abdin's previous letters on her personal journey through and research on acute intermittent porphyria (Townsend Letter. November 1997; December 1997; January 1998).
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Title Annotation:Letters
Author:Abdin, Maria
Publication:Townsend Letter
Article Type:Letter to the editor
Date:Feb 1, 2009
Words:847
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