Lucinda Bateman

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history
Jump to: navigation, search
LucindaBateman.jpeg

Lucinda Bateman (Cindy Bateman), MD, is an ME/CFS doctor and researcher. She founded and is Chief Medical Officer of the Bateman Horne Center of Excellence for ME/CFS and Fibromyalgia in Salt Lake City, Utah. [1]

Dr. Bateman was one of the authors of the 2011 case definition, International Consensus Criteria,[2] and was one of the experts on the "Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome" that was convened for the 2015 Institute of Medicine report.[3]

Suzanne Vernon, PhD, the Research Liaison at Bateman Horne Center of Excellence works closely with Dr. Bateman on ME/CFS and fibromyalgia research.[4]

Open Letter to The Lancet[edit]

Two open letters to the editor of The Lancet urged the editor to commission a fully independent review of the PACE trial, which the journal had published in 2011. In 2016, Dr. Bateman, along with 41 colleagues in the ME/CFS field, signed the second letter.

Notable studies[edit]

  • 2016, Treatment of postural orthostatic tachycardia syndrome and management of myalgic encephalomyelitis/chronic fatigue syndrome following suspected West Nile virus infection Abstract[5]
  • 2015, Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome. Abstract[6]
  • 2015, Chronic fatigue syndrome and co-morbid and consequent conditions: evidence from a multi-site clinical epidemiology study. Abstract[7]
  • 2015, Distinct plasma immune signatures in ME/CFS are present early in the course of illness FULL TEXT
    "Abstract: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone. There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease. We considered the possibility that inability to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness. Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables. Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex. We report here distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer duration of illness (n = 246). Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines as well as dissociation of intercytokine regulatory networks. We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity, suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS."[8]
  • 2012, A double-blind, placebo-controlled, randomized, clinical trial of the TLR-3 agonist rintatolimod in severe cases of chronic fatigue syndrome.
    Abstract: "A Phase III prospective, double-blind, randomized, placebo-controlled trial comparing twice weekly IV rintatolimod versus placebo was conducted in 234 subjects with long-standing, debilitating CFS/ME at 12 sites. The primary endpoint was the intra-patient change from baseline at Week 40 in exercise tolerance (ET). Secondary endpoints included concomitant drug usage, the Karnofsky Performance Score (KPS), Activities of Daily Living (ADL), and Vitality Score (SF 36). Subjects receiving rintatolimod for 40 weeks improved intra-patient placebo-adjusted ET 21.3% (p = 0.047) from baseline in an intention-to-treat analysis. Correction for subjects with reduced dosing compliance increased placebo-adjusted ET improvement to 28% (p = 0.022). The improvement observed represents approximately twice the minimum considered medically significant by regulatory agencies. The rintatolimod cohort vs. placebo also reduced dependence on drugs commonly used by patients in an attempt to alleviate the symptoms of CFS/ME (p = 0.048). Placebo subjects crossed-over to receive rintatolimod demonstrated an intra-patient improvement in ET performance at 24 weeks of 39% (p = 0.04). Rintatolimod at 400 mg twice weekly was generally well-tolerated.[9]
  • 2011, Evidence for a heritable predisposition to Chronic Fatigue Syndrome
    "BACKGROUND-Chronic Fatigue Syndrome (CFS) came to attention in the 1980s, but initial investigations did not find organic causes. Now decades later, the etiology of CFS has yet to be understood, and the role of genetic predisposition in CFS remains controversial. Recent reports of CFS association with the retrovirus xenotropic murine leukemic virus-related virus (XMRV) or other murine leukemia related retroviruses (MLV) might also suggest underlying genetic implications within the host immune system. METHODS-We present analyses of familial clustering of CFS in a computerized genealogical resource linking multiple generations of genealogy data with medical diagnosis data of a large Utah health care system. We compare pair-wise relatedness among cases to expected relatedness in the Utah population, and we estimate risk for CFS for first, second, and third degree relatives of CFS cases. RESULTS-We observed significant excess relatedness of CFS cases compared to that expected in this population. Significant excess relatedness was observed for both close (p <0.001) and distant relationships (p = 0.010). We also observed significant excess CFS relative risk among first (2.70, 95% CI: 1.56-4.66), second (2.34, 95% CI: 1.31-4.19), and third degree relatives (1.93, 95% CI: 1.21-3.07). CONCLUSIONS-These analyses provide strong support for a heritable contribution to predisposition to Chronic Fatigue Syndrome. A population of high-risk CFS pedigrees has been identified, the study of which may provide additional understanding.[10]

Clinic location[edit]

The Bateman Horne Center 24 S. 1100 E. Suite 205 Salt Lake City, Utah 84102 1-801-359-7400

Talks & interviews[edit]

Webinars[edit]

Science to patients / Wetenschap voor patienten

Solve ME/CFS Initiative

IAMECFS Conference[edit]

Blog posts[edit]

Awards[edit]

  • 2016, Rudy Perpich Senior Lectureship Award, presented to a distinguished CFS/FMS scientist, physician or healthcare worker awarded by IACFS/ME[11]

Online presence[edit]

Learn more[edit]

See also[edit]

References[edit]

  1. https://batemanhornecenter.org/
  2. Carruthers, BM; van de Sande, MI; De Meirleir, KL; Klimas, NG; Broderick, G; Mitchell, T; Staines, D; Powles, A C P; Speight, N; Vallings, R; Bateman, L; Baumgarten-Austrheim, B; Bell, DS; Carlo-Stella, N; Chia, J; Darragh, A; Jo, D; Lewis, D; Light, A; Marshall-Gradisnik, S; Mena, I; Mikovits, JA; Miwa, K; Murovska, M; Pall, ML; Stevens, S (2011), "Myalgic encephalomyelitis: International Consensus Criteria.", Journal of Internal Medicine, 270 (4): 327-38, PMID 21777306, doi:10.1111/j.1365-2796.2011.02428.x 
  3. http://www.ncbi.nlm.nih.gov/books/NBK284904/
  4. https://batemanhornecenter.org/suzanne-d-vernon-phd/
  5. Baldwin, Nicole L.; Murray, Kristy O.; Garcia, Melissa N.; Bateman, Lucinda (2016), "Treatment of postural orthostatic tachycardia syndrome and management of myalgic encephalomyelitis/chronic fatigue syndrome following suspected West Nile virus infection", Fatigue: Biomedicine, Health & Behavior, 4 (4): 226-236, doi:10.1080/21641846.2016.1247971 
  6. Klimas, N.G.; Ironson, G.; Carter, A.; Balbin, E.; Bateman, L.; Felsenstein, D.; Levine, S.; Peterson, D.; Chiu, K.; Allen, A.; Cunningham, K.; Gottschalk, C.G.; Fletcher, M; Hornig, M.; Canning, C.; Komaroff, A.L. (2015), "Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome", Fatigue: Biomedicine, Health & Behavior, 3 (2): 75-96, doi:10.1080/21641846.2015.1023652 
  7. Bateman, L.; Darakjy, S.; Klimas, N.; Peterson, D.; Levine, S.M.; Allen, A.; Carlson, S.A.; Balbin, E.G.; Gottschalk, G.; March, D. (2015), "Chronic fatigue syndrome and co-morbid and consequent conditions: evidence from a multi-site clinical epidemiology study", Fatigue: Biomedicine, Health & Behavior, 3 (1): 1-15, doi:10.1080/21641846.2014.978109 
  8. Hornig, M; Montoya, JG; Klimas, NG; Levine, SM; Felsenstein, D; Bateman, L; Peterson, DL; Gottschalk, CG; Schultz, AF; Che, X; Eddy, ML; Komaroff, AL; Lipkin, WI (2015), "Distinct plasma immune signatures in ME/CFS are present early in the course of illness", Science Advances, 1 (1), doi:10.1126/sciadv.1400121 
  9. Strayer, DR; Carter, WA; Stouch, BC; Stevens, SR; Bateman, L; Cimoch, PJ; Lapp, CW; Peterson, DL; Chronic Fatigue Syndrome AMP-516 Study Group; Mitchell, WM (2012), "A double-blind, placebo-controlled, randomized, clinical trial of the TLR-3 agonist rintatolimod in severe cases of chronic fatigue syndrome.", PLoS One, 7 (3): e31334, PMID 22431963, doi:10.1371/journal.pone.0031334 
  10. Albright, Frederick; Light, Kathleen; Light, Alan; Bateman, Lucinda; Cannon-Albright, Lisa A (2011), "Evidence for a heritable predisposition to Chronic Fatigue Syndrome", BMC Neurology, 11 (62), doi:10.1186/1471-2377-11-62 
  11. https://twitter.com/BatemanHorne/status/792750279758323712


The information provided at this site is not intended to diagnose or treat any illness.

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history