Bio

Dr. Nitasha Khullar is a board-certified, fellowship-trained rheumatologist at Stanford Health Care. She is also a clinical assistant professor in the Department of Medicine, Division of Immunology and Rheumatology at Stanford University School of Medicine.

Dr. Khullar specializes in caring for people with autoimmune and inflammatory diseases that affect the joints, muscles, and immune system. She treats conditions like lupus, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, vasculitis, gout and other complex rheumatic disorders. She provides personalized care for each patient, focusing on early diagnosis and working closely with other medical specialists to help manage these diseases. She values shared decision-making and a patient-centric approach to her care.


Dr. Khullar’s work has been presented at national and international conferences, including the American College of Rheumatology and the American Association of Immunology. She has authored peer-reviewed publications in journals such as Viruses, Molecular Neurobiology, Age (Dordrecht, Netherlands), and Current Treatment Options in Rheumatology.

She is a member of the American College of Rheumatology.

Clinical Focus

  • Rheumatology

Academic Appointments

Honors & Awards

  • Resident of the Year, State of Nevada Poster Contest Finalist, American College of Physicians
  • Resident of the Year, University of Nevada, Las Vegas Internal Medicine Residency Program
  • National Poster Contest Finalist, American College of Physicians

Boards, Advisory Committees, Professional Organizations

  • Fellow, American College of Rheumatology (ACR) (2022 - Present)

Professional Education

  • Board Certification: American Board of Internal Medicine, Rheumatology (2022)
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2019)
  • Fellowship: University of Alabama School of Medicine (2021) AL
  • Residency: University of Nevada Internal Medicine Residency (2019) NV
  • Medical Education: University of Missouri - Kansas City (2016)

Contact

  • Academic
    nkhullar@stanford.edu
    Department: Medicine - Med/Immunology & Rheumatology Position: Clinical Assistant Professor
  • Clinical (Primary)  Stanford Health Care - ValleyCare 5575 W Las Positas Blvd Ste 210 Pleasanton, CA 94588 (925) 263-5272 (fax)

Additional Clinical Info

All Publications

  • Prediction of Survival by IL-6 in a Randomized Placebo-Controlled Trial of Anakinra in COVID-19 Cytokine Storm. Viruses Jackson, L. E., Khullar, N., Beukelman, T., Chapleau, C., Kamath, A., Cron, R. Q., Chatham, W. W. 2023; 15 (10)

    Abstract

    (1) Background: Some severe COVID-19 patients develop hyperinflammatory cytokine storm syndrome (CSS). We assessed the efficacy of anakinra added to standard of care (SoC) in hospitalized COVID-19 CSS patients. (2) Methods: In this single-center, randomized, double-blind, placebo-controlled trial (NCT04362111), we recruited adult hospitalized patients with SARS-CoV-2 infection, evidence of pneumonia, new/increasing oxygen requirement, ferritin ≥ 700 ng/mL, and at least three of the following indicators: D-dimer ≥ 500 ng/mL, platelet count < 130,000/mm3, WBC < 3500/mm3 or lymphocyte count < 1000/mm3, AST or ALT > 2X the upper limit of normal (ULN), LDH > 2X ULN, C-reactive protein > 100 mg/L. Patients were randomized (1:1) to SoC plus anakinra (100 mg subcutaneously every 6 h for 10 days) or placebo. All received dexamethasone. The primary outcome was survival and hospital discharge without need for intubation/mechanical ventilation. The data were analyzed according to the modified intention-to-treat approach. (3) Results: Between August 2020 and January 2021, 32 patients were recruited, of which 15 were assigned to the anakinra group, and 17 to the placebo group. Two patients receiving the placebo withdrew within 48 h and were excluded. The mean age was 63 years (SD 10.3), 20 (67%) patients were men, and 20 (67%) were White. At Day 10, one (7%) patient receiving anakinra and two (13%) patients receiving the placebo had died (p = 1.0). At hospital discharge, four (27%) patients receiving anakinra and four (27%) patients receiving the placebo had died. The IL-6 level at enrollment was predictive of death (p < 0.01); anakinra use was associated with decreases in CXCL9 levels. (4) Conclusions: Anakinra added to dexamethasone did not significantly impact the survival of COVID-19 pneumonia patients with CSS. Additional studies are needed to assess patient selection and the efficacy, timing, and duration of anakinra treatment for COVID-19 CSS.

    View details for DOI 10.3390/v15102036

    View details for PubMedID 37896812

    View details for PubMedCentralID PMC10612044

  • The Effectiveness of Fracture Liaison Services in Improving Fragility Fracture Outcomes CURRENT TREATMENT OPTIONS IN RHEUMATOLOGY Khullar, N., Danila, M. I. 2022; 8 (2): 19-35

    View details for DOI 10.1007/s40674-021-00190-1

    View details for Web of Science ID 000777228200001

  • Social Determinants of Mortality in US Lupus Patients: Comment on the Article by Yelin et al. Arthritis care & research Khullar, N., Caseja, A. J., Yoo, J. W., Ukken, J., Froehlich, M., Yamashita, T., Liu, X. 2019; 71 (5): 697-698

    View details for DOI 10.1002/acr.23565

    View details for PubMedID 29609225

  • Loss of Spatial Memory, Learning, and Motor Function During Normal Aging Is Accompanied by Changes in Brain Presenilin 1 and 2 Expression Levels. Molecular neurobiology Kaja, S., Sumien, N., Shah, V. V., Puthawala, I., Maynard, A. N., Khullar, N., Payne, A. J., Forster, M. J., Koulen, P. 2015; 52 (1): 545-54

    Abstract

    Mutations in presenilin (PS) proteins cause familial Alzheimer's disease. We herein tested the hypothesis that the expression levels of PS proteins are differentially affected during healthy aging, in the absence of pathological mutations. We used a preclinical model for aging to identify associations between PS expression and quantitative behavioral parameters for spatial memory and learning and motor function. We identified significant changes of PS protein expression in both cerebellum and forebrain that correlated with the performance in behavioral paradigms for motor function and memory and learning. Overall, PS1 levels were decreased, while PS2 levels were increased in aged mice compared with young controls. Our study presents novel evidence for the differential expression of PS proteins in a nongenetic model for aging, resulting in an overall increase of the PS2 to PS1 ratio. Our findings provide a novel mechanistic basis for molecular and functional changes during normal aging.

    View details for DOI 10.1007/s12035-014-8877-4

    View details for PubMedID 25204494

    View details for PubMedCentralID PMC4362879

  • Homer-1a immediate early gene expression correlates with better cognitive performance in aging. Age (Dordrecht, Netherlands) Kaja, S., Sumien, N., Borden, P. K., Khullar, N., Iqbal, M., Collins, J. L., Forster, M. J., Koulen, P. 2013; 35 (5): 1799-808

    Abstract

    The molecular mechanisms underlying cognitive decline during healthy aging remain largely unknown. Utilizing aged wild-type C57BL/6 mice as a model for normal aging, we tested the hypothesis that cognitive performance, memory, and learning as assessed in established behavioral testing paradigms are correlated with the differential expression of isoforms of the Homer family of synaptic scaffolding proteins. Here we describe a loss of cognitive and motor function that occurs when Homer-1a/Vesl-1S protein levels drop during aging. Our data describe a novel mechanism of age-related synaptic changes contributing to loss of biological function, spatial learning, and memory formation as well as motor coordination, with the dominant negative uncoupler of synaptic protein clustering, Homer-1a/Vesl-1S, as a potential target for the prophylaxis and treatment of age-related cognitive decline.

    View details for DOI 10.1007/s11357-012-9479-6

    View details for PubMedID 23054826

    View details for PubMedCentralID PMC3776093