An Evaluation of Alternate Means to Diagnose Chronic Inflammatory Response Syndrome and Determine Prevalence

Main Article Content

Scott W McMahon

Abstract

Chronic inflammatory response syndrome (CIRS) is an illness of unreported prevalence first described in 1997 (Shoemaker 1997).  This study is the first reporting prevalence and evaluating alternate methods of CIRS diagnosis vs. the existing two case definitions (CD) in the literature.  Both CD require improvement with therapy to confirm the diagnosis (Shoemaker and House 2006, GAO 2008).  Compliance is difficult and improvement may take months.  Definitive diagnosis, via CD, requires time.  1061 consecutive patients of all ages assessed at a CIRS specialty clinic were retrospectively evaluated using CD.  371 met CIRS criteria.  Cluster analysis, a series of 10 lab tests and 3 screening tests were applied to these 371 patients in 4 age groups.  Clusters demonstrated high sensitivity.  The number of abnormal lab tests and failing 3 screening tests each demonstrated good sensitivity.  Applying Clusters with Screens or Labs demonstrated excellent diagnostic accuracy with combined age group error rates ranging from 1.24 x 10 x 10-3 to 1.10 x 10-6.  These approaches were applied to the 690 patients failing CD criteria.  302 additional patients achieved one or both Clusters and Screens or Labs raising the total to 673 confirmed CIRS cases.  Partnership with a pediatric practice revealed 246 of these confirmed cases were from that practice yielding a minimum pediatric prevalence of 7.01%.  Adult prevalence is likely even higher.  At a prevalence of ≥ 7.01%, CIRS is one of the greatest public health dilemmas in existence.

Article Details

How to Cite
MCMAHON, Scott W. An Evaluation of Alternate Means to Diagnose Chronic Inflammatory Response Syndrome and Determine Prevalence. Medical Research Archives, [S.l.], v. 5, n. 3, mar. 2017. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/1125>. Date accessed: 18 dec. 2024.
Keywords
CIRS, inflammation, diagnosis, prevalence, cluster analysis, cytokine overproduction, haplotype
Section
Research Articles

References

Bredesen DE. Inhalational Alzheimer's disease: an unrecognized—and treatable—epidemic. Aging (Albany NY). 2016 Feb; 8(2): 304–313. Published online 2016 Feb 10. Found at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4789584/.

Butte W, Heinzow B. Pollutants in house dust as indicators of indoor contamination. Reviews of Environmental Contamination and Toxicology. 2002; 175:1-46.

“GAO Report to the Chairman, Committee on Health, Education, Labor and Pensions, U.S. Senate, Indoor Mold” (September 2008). Found at: http://www.gao.gov/new.items/d08980.pdf. Retrieved 2010-02.

Gonzales-Rey E, Chorny A, Delgado M. Regulation of immune tolerance by anti-inflammatory neuropeptides. Nature Publishing Group 7:52-63, January 2007.

Gunn SR, Gunn GG, Mueller FW. Reversal of Refractory Ulcerative Colitis and Severe Chronic Fatigue Syndrome Symptoms Arising from Immune Disturbance in an HLADR/DQ Genetically Susceptible Individual with Multiple Biotoxin Exposures. Am J Case Rep. 2016; 17: 320–325. Published online 2016 May 11. Found at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913732/.

Heiman ML, Ahima RS, Craft LS, Schoner B, Stephens TW, Flier JS. Leptin inhibition of the hypothalamicpituitary-adrenal axis in response to stress. Endocrinology September 1997; 138 (9): 3859–63. PMID 9275075.

Hirvonen MR, Huttunen K, Roponen M. Bacterial strains from moldy buildings are potent inducers of inflammatory and cytotoxic effects. Indoor Air. 2005; 15(Suppl 9):65-70.

http://bioimformatics.nmdp.org/HLA/Haplotype_Frequencies/Haplotype_Frequencies.aspx. Retrieved February 2013.

http://www.socscistatistics.com/tests/chisquare/Default2.aspx

http://vassarstats.net/tab2x2.html

Kettleson E, Kumar S, Reponen T, Vesper S, Meheust D, Grinshpun SA, Adhikari A. Stenotrophomonas, Mycobacterium and Streptomyces in home dust and air: associations with moldiness and other home/family characteristics. Indoor Air. 2013 Oct; 23(5):387-96.

Magaki S, Mueller C, Dickson C, Kirsch W. Increased production of inflammatory cytokines in mild cognitive impairment. Exp Gerontol 2007; 42(3): 233-240.

McMahon SW, Shoemaker RC, and Ryan, JC Reduction in Forebrain Parenchymal and Cortical Grey Matter Swelling across Treatment Groups in Patients with Inflammatory Illness Acquired Following Exposure to Water-Damaged Buildings. J Neurosci Clin Res 2016; 1:1. April 12, 2016.

Perry VH. The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease. Brain Behav Immun 2004; 18(5):407-413.

Pestka JJ, Yike I, Dearborn DG, Ward MD, Harkema JR. Stachybotrys chartarum, trichothecene mycotoxins, and damp building-related illness: new insights into a public health enigma. Toxicological Sciences. 2008 Jul; 104(1):4-26.

Qin L, Liu Y, Wang T, Wei SJ, Block ML, Wilson B, Liu B, Hong JS. NADPH oxidase mediates lipopolysaccharideinduced neurotoxicity and proinflammatory gene expression in activated microglia. J Biol Chem 2004; 279(2): 1415-1421.

Roeder A, Kirschning C, Rupec R, Schaller M, Weindl G, Korting H. Toll-like receptors as key mediators in innate antifungal immunity. Med Mycol 2004; 42: 485-98.

Ryan JC, Shoemaker RC. RNA-Seq on patients with chronic inflammatory response syndrome (CIRS) treated with vasoactive intestinal peptide (VIP) shows a shift in metabolic state and innate immune functions that coincide with healing. Medical Research Archives. Volume 4, Issue 7 (in press).

Shoemaker R. Diagnosis of Pfiesteria-human illness syndrome. Maryland Medical Journal 1997; 521-523.

Shoemaker R, Giclas P, Crowder C, House D. Complement split products C3a and C4a are early markers of acute Lyme disease in tick bite patients in the United States. International Archives of Allergy Immunol 2008; 146: 255-261.

Shoemaker R, House D. SBS and exposure to water damaged buildings: time series study, clinical trial and mechanisms. Neurotoxicol Teratol 2006; 28: 573-588.

Shoemaker RC, House D, Ryan JC. Structural brain abnormalities in patients with inflammatory illness acquired following exposure to water-damaged buildings: a volumetric MRI study using NeuroQuant®. Neurotoxicol Teratol. 2014 Sep-Oct;45:18-26. doi: 10.1016/j.ntt.2014.06.004. Epub 2014 Jun 17.

Shoemaker R, Hudnell K. Possible Estuary-Associated Syndrome: Symptoms, vision, and treatment. Environmental Health Perspectives 2001; 109: 539-545.

Shoemaker R, Hudnell K, House D, Domenico P. Association of nasal carriage of methicillin resistant and multiple antibiotic resistant coagulase negative staphylococci species with deficiency of alpha melanocyte stimulating hormone in Chronic Fatigue Syndrome: implication for expanded treatment options. American Society of Microbiology 2003. Found at: http://www.survivingmold.com/docs/Association_of_nasal_carriage.PDF.

Shoemaker R, Rash J, Simon E. Sick Building syndrome in water damaged buildings: generalization of the chronic biotoxin associated illness paradigm to indoor toxigenic fungi. Bioaerosols, fungi, bacteria, mycotoxins and human health. Dr med Eckardt Johanning MD editor 2006.

Shoemaker RC, Schmidt P. Surviving Mold: Life in the Era of Dangerous Buildings. Ed. Hudson MC. 2010.

Smoragiewicz W, Cossette B, Boutard A, Krzystyniak K. Trichothecene mycotoxins in the dust of ventilation systems in office buildings. International Archives of Occupational and Environmental Health. 1993; 5:113-7.

Suihko ML, Priha O, Alakomi HL, Thompson P, Malarstig B, Stott R, Richardson M. Detection and molecular characterization of filamentous actinobacteria and thermoactinomycetes present in water-damaged building materials. Indoor Air. 2009 Jun; 19(3):268-77.

Vojdani A, Lambert J. The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part I. e-published on eCAM 2009:1-8. Found at: https://www.ncbi.nlm.nih.gov/pubmed/19622600/.