As devastating as Androgenetic Alopecia can be, the Autoimmune hair loss conditions, such as Alopecia Areata and Alopecia Universalis are cosmetically more catastrophic and much more difficult, if not impossible to manage. There are currently no reliable treatments for Alopecia Areata and Alopecia Universalis, and those afflicted can in most cases only hope for an unpredictably occurring spontaneous remission. It is said that the cure for most disease is in many cases right under our noses. Since there are no real treatments for Alopecia Areata as of yet, we felt compelled to feature this abstract in the hopes it be of use to someone. Because male pattern baldness, or Androgenetic Alopecia has an established and pronounced autoimmune component, there *may* be some crossover benefit for male pattern baldness as well.
Int Immunopharmacol. 2004 Mar;4(3):349-53.
Cetirizine and allopurinol as novel weapons against cellular autoimmune disorders.
Namazi MR
Dermatology Department, Shiraz University of Medical Sciences, P.O. Box 71955-687 Shiraz, Iran
Type 1, or cellular, immune response is characterized by overproduction of TNF-alpha, IFN-gamma, IL-1, IL-2 and IL-8 and is the underlying immune mechanism of psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis (EAU). Type 2 immune response is seen in antibody-mediated autoimmune diseases. Based on the pharmacokinetic effects of cetirizine and allopurinol, this paper introduces these two safe and inexpensive drugs as novel potential agents against cell-mediated autoimmune disorders. Cetirizine, supposed to inhibit DNA binding activity of NF-kappa B, inhibits the expression of adhesion molecules on immunocytes and endothelial cells and the production of IL-8 and LTB4, two potent chemoattractants, by immune cells. It induces the release of PGE2, a suppressor of antigen presentation and MHC class II expression, from monocyte/macrophages and reduces the number of tryptase positive mast cells in inflammation sites. Tryptase is a chemoattractant, generates kinins from kininogen, activates mast cells, triggers maturation of dendritic cells and stimulates the release of IL-8 from endothelial cells and the production of Th1 lymphokines by mononuclear immunocytes. Allopurinol is a free radical scavenger, suppresses the production of TNF-alpha and downregulates the expression of ICAM-1 and P2X(7) receptors on monocyte/macrophages. ICAM-1 serves as a ligand for LFA-1 (on T lymphocytes), allowing proper antigen presentation. P2X(7) receptors are thought to be involved in IL-1beta release, mitogenic stimulation of T lymphocytes and the probable cytoplasmic communication between macrophages and lymphocytes at inflammation sites. Allopurinol was markedly more effective than prednisolone in treating experimental autoimmune uveitis and in combination with cyclosporine suppressed the inflammatory reaction of this condition more effectively than either agent alone. As allopurinol is a competitive inhibitor of xanthine oxidase and decreases serum levels of uric acid, which is protective against multiple sclerosis, it should preferably be coadministered with uric acid precursors in the treatment of this condition. Cetirizine and allopurinol may prove of benefit in the treatment of various cellular autoimmune disorders.
