Psoriasis is an inflammatory (possibly autoimmune) skin disease that is usually found on the elbow, knees, scalp, low back and buttock fold regions. Ten to 30 percent of psoriasis patients also have inflammatory joint issues (psoriatic arthritis). While the immune system is at fault, environmental and genetic factors also play a role. Psoriasis tends to wax and wane: flares often follow life stressors and/or illness/infection. As a highly visible condition, it can greatly impact quality of life. In some with severe disease, there may be increased risk for certain chronic illness, such as kidney and heart disease.
Often following an insult to immune system (life stress, bacterial/strep/viral infection, immunization, medications, trauma, alcohol, weight gain), psoriasis may suddenly onset at any age as one or many small areas of itchy, scaly redness. It may progress with or without associated nail findings, joint pain, and/or eye or eyelid redness (some have only joint pain without rash). The same insults that trigger psoriasis onset may also cause flares. Hot weather, sunlight, sea swimming and pregnancy can ameliorate some cases. Once psoriasis is established, sunburn and other skin trauma should be avoided, as damaged areas may subsequently become psoriatic.
Psoriasis occurs when the immune system’s white blood cells (WBCs, T cells) invade the skin in large numbers for unclear reasons. The excessive WBCs produce skin cell abnormalities/overgrowth and initiate the immune system over-activity that produces inflammation. Inflammation damages cells. Damaged cells produce/release chemicals signalers (immune mediators) that signal back to the immune system to “keep fighting,” so the immune system mistakenly believes the skin area (with the extra WBCs and abnormal skin cells) is continuously under attack, as if it had ongoing infection. One of these chemicals signalers (TNF-α) also plays a role many autoimmune diseases. Medications that “soak up” this chemical signaler are now used in psoriasis. Gene locations for psoriasis have been identified (HLA-Cw6 and others).
Usually, psoriasis can be identified visually, without biopsy. There are various forms of it depending upon location, and whether or not a flare is present or joints are involved. While most blood testing is normal, blood work may help distinguish it from other conditions; fungal studies checking for infection help when feet are involved. By evaluating X-rays and/or joint fluid, a rheumatologist can help distinguish (inflammatory) psoriatic arthritis from autoimmune (rheumatoid) or other types of arthritis. Specialists should manage eye involvement.
Conventional pharmaceutical medications include topical steroids, steroid injections, coal tar, Vitamin D analogs (calcitrol), topical retinoids (tazarotene), medications that decrease cell proliferation (anthralin, methotrexate), immune modulators (tacrolimus/Protopic topical, cyclosporine, alefacept, ustekinumab) which “gear down” the immune system, and specific TNF-α inhibitors (infliximab, etanercept, adalimumab) that are more often used in autoimmune disease. The last two classes decrease immunity and increase risk for infection, requiring that risks and benefits be weighed. UV (PUVA/B) or sunlight and stress reduction are also recommended. Therapy is tailored to each patient depending upon response and other illnesses/conditions.[1]
In Traditional Chinese Medicine (TCM), psoriasis is considered a sign of significant derangement of the body’s overall “balance” (homeostasis), and as in Western Medicine, there are various psoriasis types based on appearance and location. For example, the common form of pale, dry plaques with a thin layer of white scales may be due to “Blood Deficiency and Dryness” and/or “Liver and Kidney Yin Deficiencies”. More rapidly developing, small, bright-red lesions may be due to “Heat in the Blood Division” or “Damp Heat”. Dark purple plaques with very thick scales may be due to “Blood Stasis”. All psoriasis sufferers will likely to benefit from “calming Wind”, as “Wind” produces dryness, especially during flare-ups. Because of the multiple causes, different people require different treatments at different times to address psoriasis.
As a complex problem, multiple treatment modalities are usually used. Acupuncture starts to balance the system, while Chinese Herbal Medicine more profoundly addresses the underlying problem. Since psoriasis is considered a “deeper” problem in TCM, Chinese herbs require compliance usually for 6 to 24 months to achieve the longest lasting effects. TCM, Ayurveda and Western Medicine all link alcohol to psoriasis, and alcohol avoidance is a cornerstone of improvement without pharmaceuticals. Herbs and foods that “cool the ‘Blood’” help for the conditions caused by heat: turmeric, mint, cilantro etc are added to the diet. [2,3]
Learn more about Psoriasis
X
These brief overviews of conditions represent distillations of basic and current medical reviews from the following sources:
[1] Conventional Medical Sources“Harrison’s Principles of Internal Medicine: Volumes 1 and 2, 18th Edition”. Dan Longo Anthony Fauci, Dennis Kasper, Stephen Hauser, J. Jameson, Joseph Loscalzo. McGraw-Hill Professional; (July, 2011)
Medscape eMedicine Physician’s online resource. Various review articles:
Allergic and Environmental Asthma: an Overview of Asthma
William F Kelly III, MD Associate Professor of Medicine, Uniformed Services University of the Health Sciences; Staff physician, Division of Pulmonary/Critical Care Medicine, Department of Medicine, Walter Reed National Military Medical Center
Allergic Rhinitis
Javed Sheikh, MD Assistant Professor of Medicine, Harvard Medical School; Clinical Director, Division of Allergy and Inflammation, Clinical Director, Center for Eosinophilic Disorders, Beth Israel Deaconess Medical Center
Food Allergies
Scott H Sicherer, MD Professor of Pediatrics, Jaffe Food Allergy Institute, Mount Sinai School of Medicine of New York University
Atopic Dermatitis
Brian S Kim, MD Clinical Instructor, Department of Dermatology, Hospital of the University of Pennsylvania, Perelman School of Medicine, University of Pennsylvania
Seborrheic Dermatitis
Samuel T Selden, MD Assistant Professor Department of Dermatology Eastern Virginia Medical School; Consulting Staff, Chesapeake General Hospital; Private Practice
Psoriasis
Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio
Urticaria
M Scott Linscott, MD, FACEP Adjunct Professor of Surgery (Clinical), Division of Emergency Medicine, University of Utah School of Medicine
Cholinergic Urticaria
Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School
- “Acupuncture Energetics: A Clinical Approach for Physicians”. Joseph M. Helms. Medical Acupuncture Publishers; 1st Edition. (1995)
- “Foundations of Chinese Medicine: A Comprehensive Text for Acupuncturists and Herbalists”. Giovanni Maciocia. Churchill Livingstone; 2 Edition (July, 2005).
- “Diagnosis in Chinese Medicine: A Comprehensive Guide”. Giovanni Maciocia. Churchill Livingstone; 1st Edition (January, 2004).
4. “Chinese Scalp Acupuncture”. Jason Ji-shun Hao, Linda Ling-zhi Hao and Honora Lee Wolfe. Blue Poppy Press; 1st Edition. (November, 2011)
5. Ege MJ, Mayer M, Normand AC, Genuneit J, Cookson WO, Braun-Fahrländer C, et al. Exposure to environmental microorganisms and childhood asthma. N Engl J Med. Feb 24 2011;364(8):701-9. [Medline]
6. Tsai JD, Chang SN, Mou CH, Sung FC, Lue KH. Association between atopic diseases and attention-deficit/hyperactivity disorder in childhood: a population-based case-control study. Ann Epidemiol. Apr 2013;23(4):185-8. [Medline].
7. JPEN J Parenter Enteral Nutr. 2012 Jan;36(1 Suppl):68S-75S. doi: 10.1177/0148607111426276
8. Rubio-Tapia A, Kyle RA, Kaplan EL, et al. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology.2009;137:88-93.
9. Thompson T. Gluten contamination of commercial oat products in the United States. N Engl J Med. 2004;351:2021-2022.
10. Häuser W, Janke KH, Klump B, Gregor M, Hinz A. Anxiety and depression in adult patients with celiac disease on the gluten free diet. World J Gastroenterol. 2010;16:2780-2787.
11. Am. J. Epidemiol. (2013)178 (12):1721–1730doi:10.1093/aje/kwt234
12. Addolorato G, Di Guida D, De Rossi G, et al. Regional cerebral hypoperfusion in patients with celiac disease. Am J Med. 2004;116:312-317.
13. Sapone A, Lammers KM, Casolaro V, et al. Divergence of gut permeability and mucosal immune gene expression in two glutenassociated conditions: celiac disease and gluten sensitivity. BMC Med. 2011;9:23.
14. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011;106:508-514.
15. Yamini D, Pimentel M. Irritable bowel syndrome and small intestinal bacterial overgrowth. J Clin Gastroenterol. 2010;44:672-675.
16. Wahnschaffe U, Schulzke J-D, Zeitz M, Ullrich R. Predictors of clinical response to gluten-free diet in patients diagnosed with diarrhea-predominant irritable bowel syndrome. Clin Gastroenterol Hepatol. 2007;5:844-850.
17. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, et al. Clinical, radiological, neurophysiological and neuropatholgical characteristics of gluten ataxia. Lancet. 1998;352:1582-1585.
18. Hadjivassiliou M, Boscolo S, Davies-Jones A, et al. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002;58:1221-1226.
19. Dieterich W, Ehnis T, Bauer M, et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med. 1997;7:797-801.
20. Korponay-Szabo IR, Halttunen T, Szalai Z, et al. In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies. Gut. 2004;53:641-648.
21. Hadjivassiliou M, Maki M, Sanders DS, et al. Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Neurology. 2006;66:373-377.
22. Tengah CP, Lock RJ, Unsworth DJ, Wills A. Multiple sclerosis and occult gluten sensitivity. Neurology. 2004;62:2326-2327.
23. Hadjivassiliou M, Sander DS, Grünewald RA. Multiple sclerosis and occult gluten sensitivity. Neurology. 2005;64:933-934.
24· Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs. Pediatr Allergy Immunol. Feb 1998;9(1):13-9. [Medline].
25. Branum AM, Lukacs SL. Food allergy among children in the United States. Pediatrics. Dec 2009;124(6):1549-55. [Medline].
26. Fleischer DM, Burks AW, Vickery BP, Scurlock AM, Wood RA, Jones SM, et al. Sublingual immunotherapy for peanut allergy: a randomized, double-blind, placebo-controlled multicenter trial. J Allergy Clin Immunol. Jan 2013;131(1):119-27.e1-7. [Medline]. [Full Text].
27. Hand L. Probiotics may protect infants from allergy, but not asthma. Medscape Medical News [serial online]. August 19, 2013;Accessed August 25, 2013. Available at http://www.medscape.com/viewarticle/809604.
28. Elazab N, Mendy A, Gasana J, Vieira ER, Quizon A, Forno E. Probiotic Administration in Early Life, Atopy, and Asthma: A Meta-analysis of Clinical Trials. Pediatrics. Aug 19 2013;[Medline].
29. O’Connel RA. SPECT brain imaging in psychiatric disorders: current clinical status. In: Grünwald F, Kasper S, Biersack HJ, Möller HJ, eds. Brain SPECT Imaging in Psychiatry. Berlin: de Gruyter; 1995:35-57.
30. Grasby PM, Bench C. Neuroimaging in mood disorders. Curr Opin Psychiatry. 1997;10:73-78.