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uonderuoman.
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http://www.ncf-net.org/forum/JustAsk-S07.htm
Q: I have been diagnosed with CFS. My doctor wants to put me on IVIG. Is there any information in the medical literature that you may be aware of regarding its use for this disease? (Internet question)
A: For those who may not be familiar with the terminology, IVIG is intravenous immunoglobulin. IVIG is a blood product that contains the pooled IgG immunoglobulins which are antibodies extracted from the plasma of blood donors. Now, to answer your question, there is information in the medical literature. Let me expand on this as best as I can. CFIDS/ME patients have been found to have diminished amounts immunoglobulins
and in fact, subclass deficiencies (IgG1 and IgG3), have been seen [1 - 6]. As such, immunoglobulin replacement may be helpful to some patients [7 - 10]. I suggest you take these references to your physician and once they have reviewed this material with you, then perhaps you can make an informed decision regarding treatment. This may take on additional significance in light of the CD19 B-cell abnormalities that were found in patients. This research was recently published [11] and it was further highlighed by the NCF [12].
1. Immunologic abnormalities in chronic fatigue syndrome; Klimas NG, Salvato FR,
Morgan R, Fletcher MA; J Clin Microbiol. 1990 Jun;28(6):1403-10
2. Immunological abnormalities in the chronic fatigue syndrome; Lloyd AR, Wakefield D,
Boughton CR, Dwyer JM; Med J Aust. 1989 Aug 7;151(3):122-4
3. IgG1 subclass deficiency in patients with chronic fatigue syndrome; Read R, Spickett G,
Harvey J, Edwards AJ, Larson HE; Lancet. 1988 Jan 30;1(8579):241-2
4. Immunoglobulin subclass abnormalities in patients with chronic fatigue syndrome;
Wakefield D, Lloyd A, Brockman A; Pediatr Infect Dis J. 1990 Aug;9(8 Suppl):S50-3
5. IgG subclass deficiencies in chronic fatigue syndrome; Komaroff AL, Geiger AM,
Wormsely S; Lancet. 1988 Jun 4;1(8597):1288-9
6. IgG subclass deficiency and chronic fatigue syndrome; Linde A, Hammarstrom L,
Smith CI; Lancet. 1988 Apr 16;1(8590):885-6
7. A double-blind, placebo-controlled trial of intravenous immunoglobulin therapy
in patients with chronic fatigue syndrome; Lloyd A, Hickie I, Wakefield D, Boughton C,
Dwyer J; Am J Med. 1990 Nov;89(5):561-8
8. A controlled trial of intravenous immunoglobulin G in chronic fatigue syndrome;
Peterson PK, Shepard J, Macres M, Schenck C, Crosson J, Rechtman D, Lurie N;
Am J Med. 1990 Nov;89(5):554-60
9. Double-blind randomized controlled trial to assess the efficacy of intravenous
gammaglobulin for the management of chronic fatigue syndrome in adolescents;
Rowe KS; J Psychiatr Res. 1997 Jan-Feb;31(1):133-47
10. Intravenous immunoglobulin treatment for the chronic fatigue syndrome; Straus SE;
Am J Med. 1990 Nov;89(5):551-3
11. Clinical activity of folinic acid in patients with chronic fatigue syndrome; Lundell K,
Qazi S, Eddy L, Uckun FM; Arzneimittelforschung. 2006;56(6):399-404
12. It Is What It Is: Searching for Truth; The NCF's report on important keynote medical
discrepancies regarding a severe B-cell immunodeficiency in CFIDS/ME patients; 2006
Q: I heard rumors over the internet that the NCF had interests in folinic acid as a possible treatment option. Can you share any information with the patient community? (Internet question)
A: This is true. Several patients associated with the NCF went on folinic acid at a 5 mg dosage, three times per day for several months. Each patient was under physician care. Before the volunteer patients began any treatment, their physicians did complete lymphocyte profiles. These included absolute and percentage cell counts for CD3 (total lymphocytes), CD4 (helper T-cells), CD8 (cytotoxic/suppressor T-cells) and CD19 (B-cells). Then these patients went on therapy as outlined above for several months. At completion, these lymphocyte profiles were run again on each patient. We were certainly interested in the biological mechanism of folinic acid and what potential effects that it may have on these patients in light of the paper published by Dr. Uckun. We learned that the Chairman/CEO of EpiGenesis Pharmaceuticals had discovered that folinic acid is used to treat adenosine depletion. The other thing we came to realize is that we observed immune modulation that appeared to be represented, at least in our patients, by a reduction in some of the CD4 T-cell counts. Please keep in mind that this was an observation and not some double-blinded trial with age and sex matched controls. This information is very intriguing considering that some CFIDS/ME patients go on to develop Idiopathic CD4 Lymphocytopenia (ICL) which has been seen in HIV-negative AIDS patients as reported in the medical literature [1 - 4]. ICL itself has been associated with a deficiency of adenosine deaminase [1]. Technically speaking, adenosine deaminase deficiency causes an increase of dATP, which inhibits S-adenosyl-homocysteine hydrolase, causing an increase in S-adenosylhomocysteine. Both dATP and S-adenosylhomocysteine have toxic affects on lymphocytes, causing them to be functionally defective. The defective function is caused by a depletion of all of the dNTP pools. This causes a breakdown in DNA synthesis and repair of breaks occurring in the DNA. This makes for a very serious disease and that is why the presence of ICL in CFIDS/ME patients causes a severe immunodeficiency where patients become prone to repeated infections. In CFIDS/ME, this is an acquired condition due to the disease progression itself. I should point out that one treatment option for adenosine deaminase deficiency involves the replacement of the enzyme adenosine deaminase itself. The drug used for this is called Adagen by Enzon Pharmaceuticals and it has been used for the treatment of severe combined immunodeficiency disease, known also as SCID, due to adenosine deaminase deficiency.
1. Adenosine deaminase (ADA) deficiency as the unexpected cause of CD4+ T-lympho-
cytopenia in two HIV-negative adult female siblings; Fairbanks LD, Simmonds HA,
Webster AD, Shovlin CL, Hughes JM; Adv Exp Med Biol. 1994;370:471-4
2. Idiopathic CD4+ T-lymphocytopenia--immunodeficiency without evidence of HIV
infection; Ho DD, Cao Y, Zhu T, Farthing C, Wang N, Gu G, Schooley RT, Daar ES;
N Engl J Med. 1993 Feb 11;328(6):380-5
3. Unexplained opportunistic infections and CD4+ T-lymphocytopenia without HIV
infection. An investigation of cases in the United States. The Centers for Disease Control
Idiopathic CD4+ T-lymphocytopenia Task Force; Smith DK, Neal JJ, Holmberg SD;
N Engl J Med. 1993 Feb 11;328(6):373-9
4. Acquired T cell specific deficiency other than acquired immunodeficiency syndrome (AIDS);
Saiki O, Ogawa H, Ikeda T, Masuno T, Tanaka T, Deguchi Y, Endou T, Kishimoto S;
Intern Med. 1992 Jan;31(1):11-6
Q: At the recent IACFS Conference held in Fort Lauderdale, were there any research reports that stood out to the NCF researchers? (Internet question)
A: There was a research presentation from Dr. Rokutan, who is from Japan, on the "Application of a DNA chip for Fatigue Assessment." Though the study involved a small number of patient samples (11), several of the genes that were noted to be modulated included several that play an important role in the microenvironment of the bone marrow. One of the genes that was found to be altered in this study was Stat-5. A quick check of the medical literature from Pubmed reveals that Stat5 plays a critical role in the replication capability of stem cells.
This is a very significant finding due to the fact that all cells in the human body are derived from stem cells and if there is a problem that is occurring at this level of the cell in the bone marrow itself, then this provides a significant clue as to what is occurring. These concepts will be discussed in a future Forum. As noted above in this column, patients and physicians who choose to discount the findings and to downplay the importance of Dr. Uckun's research will do so at their own peril.
The National CFIDS Foundation
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