
Dean Winslow
Professor of Medicine (Hospital Medicine) at the Stanford University Medical Center and Senior Fellow, by courtesy, at the Freeman Spogli Institute for International Studies
Bio
Dr. Dean Winslow specializes in infectious diseases and hospital-based internal medicine. He has practiced medicine for more than 40 years. Dr. Winslow has a special interest in bedside teaching of medical students, residents and fellows.
Clinical Focus
- Infectious Disease
- Hospital Medicine and Infectious Diseases
Academic Appointments
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Professor - Med Center Line, Medicine
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Senior Fellow (By courtesy), Freeman Spogli Institute for International Studies
Administrative Appointments
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Professoriate Appointment and Promotions Committee, Stanford University School of Medicine (2018 - Present)
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Faculty, Bing Overseas Studies Program, University of Oxford, Stanford University (2017 - 2017)
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Academic Physician-In-Chief, Stanford/ValleyCare, Stanford University School of Medicine (2015 - 2017)
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Vice Chair, Department of Medicine, Stanford University School of Medicine (2015 - 2017)
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Stanford Department of Medicine Core Faculty, Stanford University (2014 - Present)
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Stanford Department of Medicine Professional Practice Evaluation Committee, Stanford University (2014 - Present)
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Resident Fellow, Robinson House, Stanford University (2013 - 2017)
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Clinician Educator Appointment and Promotions Committee, Stanford University (2004 - 2015)
Honors & Awards
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Alwin C. Rambar-James B.D. Mark Award for Excellence in Patient Care, Stanford University School of Medicine (2019)
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Society Citation, Infectious Diseases Society of America (2017)
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Legion of Merit, Air Medal (3), Combat Action Medal, Afghanistan Campaign (2), Iraq Campaign (4), United States Air Force (2015)
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David A. Rytand clinical teaching award, Department of Medicine, Stanford University (2014, 2015)
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Award for Humanitarian Service to the People of Iraq, Iraqi Armed Forces (2008)
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Humanitarian Service Award, American College of Physicians (2007)
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George W. Bush Award- outstanding Air National Guard officer, Air Force Association (2006)
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Malcom C.Grow Award - outstanding Air Force flight surgeon (ANG command), Society of USAF Flight Surgeons (1988)
Boards, Advisory Committees, Professional Organizations
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Chair, Ethics and Conflict of Interest Committee, Infectious Diseases Society of America (2018 - Present)
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Member, Sepsis Task Force, Infectious Diseases Society of America (2017 - Present)
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Associate Editor, Diagnostic Microbiology and Infectious Disease (2014 - Present)
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Chair, Standards and Practice Guidelines Committee, Infectious Diseases Society of America (2011 - 2017)
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Associate Editor, Infectious Disease Alert (2005 - Present)
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Editorial board, AIDS (London) (1993 - 2016)
Professional Education
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Distinguished graduate, United States Air Force School of Aerospace Medicine, Flight surgeon (1983)
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Graduate, United States Air Force, Air War College (2007)
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Medical Education: Thomas Jefferson University (1976) PA
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Fellowship: Oschner Foundation Hospital (1981) LA
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Residency: Christiana Health Care Medical Center of Delaware (1979) DE
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Board Certification: American Board of Internal Medicine, Infectious Disease (1982)
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Board Certification: American Board of Internal Medicine, Internal Medicine (1979)
Community and International Work
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Lead Physician, U.S. Antarctic Program, McMurdo Station, Antarctica
Partnering Organization(s)
National Science Foundation
Populations Served
Researchers
Location
International
Ongoing Project
No
Opportunities for Student Involvement
No
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Global AIDS Interfaith Alliance, Malawi
Topic
HIV and TB
Populations Served
HIV patients
Location
International
Ongoing Project
Yes
Opportunities for Student Involvement
Yes
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United States Air Force, Afghanistan, Iraq
Topic
Military Medicine
Partnering Organization(s)
ANG/USAF
Populations Served
military and civilian
Location
International
Ongoing Project
No
Opportunities for Student Involvement
No
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The Eagle Fund, International
Topic
Humanitarian aid
Partnering Organization(s)
Silicon Valley Community Foundation
Populations Served
currently focusing on Syrian and Iraqi refugees
Location
International
Ongoing Project
Yes
Opportunities for Student Involvement
No
2020-21 Courses
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Independent Studies (2)
- Directed Reading in Medicine
MED 299 (Spr) - Undergraduate Research
MED 199 (Sum)
- Directed Reading in Medicine
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Prior Year Courses
2019-20 Courses
2018-19 Courses
All Publications
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Reply to Al-Hasan and Justo.
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
2019; 68 (8): 1432
View details for PubMedID 30102343
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Acute Kidney Injury Due to Systemic Absorption of Antibiotics Impregnated in a Bone Cement Spacer: An Underrecognized Complication of a Common Intervention
INFECTIOUS DISEASES IN CLINICAL PRACTICE
2018; 26 (5): 291–93
View details for DOI 10.1097/IPC.0000000000000575
View details for Web of Science ID 000444393100022
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Seroconversion on preexposure prophylaxis
AIDS
2018; 32 (9): 1199–1200
View details for PubMedID 29746319
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Infectious Diseases Society of America (IDSA) POSITION STATEMENT: Why IDSA Did Not Endorse the Surviving Sepsis Campaign Guidelines
CLINICAL INFECTIOUS DISEASES
2018; 66 (10): 1631–35
Abstract
IDSA did not endorse the 2016 Surviving Sepsis Campaign Guidelines despite being represented in the working group that drafted the guidelines document. Leadership from the IDSA, the Surviving Sepsis Campaign Guidelines, and the Society of Critical Care Medicine had numerous amicable discussions primarily regarding the bolded, rated guidelines recommendations. Our societies had different perspectives, however, regarding the interpretation of the major studies that informed the guidelines' recommendations, thus leading us to different conclusions and different perspectives on the recommendations. IDSA consequently elected not to endorse the guidelines. IDSA nonetheless hopes to be able to continue collaborating with the Surviving Sepsis Campaign and the Society of Critical Care Medicine to resolve our differences and to develop further strategies together to prevent sepsis and septic shock as well as reduce death and disability from these conditions both nationally and globally.
View details for DOI 10.1093/cid/cix997
View details for Web of Science ID 000432184200027
View details for PubMedID 29182749
- "I spoke my mind on guns. Then my Senate confirmation was put on hold". Washington Post Op/Ed Washington Post. Washington Post. 2017
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Treatment as prevention: some additional thoughts
AIDS
2012; 26 (4): 519-520
View details for DOI 10.1097/QAD.0b013e32834fa17e
View details for Web of Science ID 000300411500015
View details for PubMedID 22156975
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HIV AND THE HOMELESS: THE EFFECTS OF HOUSING STATUS ON HIV DISEASE PROGRESSION AND HEALTHCARE ACCESS
SPRINGER. 2011: S52–S53
View details for Web of Science ID 000208812700091
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Efavirenz Plasma Concentrations and Cytochrome 2B6 Polymorphisms
ANNALS OF PHARMACOTHERAPY
2010; 44 (10): 1572-1578
Abstract
Interpatient variability in efavirenz concentrations may be due to CYP2B6 genetic polymorphisms. Efavirenz concentration and pharmacogenomic data are scarce in Latino patients.To evaluate the difference in trough and midpoint efavirenz plasma concentrations between HIV-positive Latino and white patients. In addition, this study evaluated the association between efavirenz concentrations and CYP2B6 polymorphisms in Latino and white HIV-positive subjects.This pilot study included 10 Latinos and 10 whites. Two efavirenz blood concentrations were determined: a trough and a midpoint. CYP2B6 genetic polymorphisms were analyzed at the 516 (G to T) and 785 (A to G) codons. The Mann-Whitney test was used to determine whether efavirenz concentrations varied with ethnicity. The Kruskal-Wallis test was used to determine whether efavirenz concentrations varied with CYP2B6 genetic polymorphisms. Efavirenz concentrations were expressed as medians (minimum, maximum).Midpoint concentrations were 1.58 μg/mL (1.36, 6.02) and 3.14 μg/mL (1.74, 7.72) for whites and Latinos, respectively (p < 0.05). Trough concentrations did not vary as a function of ethnicity. Ten percent of Latinos and whites tested positive for homozygous variants of CYP2B6-516 and CYP2B6-785. One white subject tested positive for the homozygous variant of CYP2B6-1459. Trough concentrations for 516TT, 516GT, and 516GG (wild type) were 5.13 μg/mL (4.13, 6.12), 2.13 μg/mL (1.33, 3.37), and 1.44 μg/mL (0.59, 2.92), respectively (p < 0.05). Trough concentrations for 785GG, 785AG, and 785AA (wild type) were 5.12 μg/mL (4.13, 6.12), 1.98 μg/mL (1.33, 3.37), and 1.27 μg/mL (0.59, 2.92), respectively (p < 0.05). None of the patients took concomitant medications that impacted CYP2B6 metabolism.Trough efavirenz concentrations were significantly higher in patients with the 785 (A to G) and 516 (G to T) variants. Midpoint efavirenz concentrations in Latinos were significantly higher than those of whites.
View details for DOI 10.1345/aph.1P141
View details for Web of Science ID 000282675100006
View details for PubMedID 20841522
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Gross Hematuria in a Young Iraqi Man - Diagnosis: infection due to Schistosoma haematobium
CLINICAL INFECTIOUS DISEASES
2010; 50 (8): 1144-?
View details for DOI 10.1086/651270
View details for Web of Science ID 000275645900017
View details for PubMedID 20233043
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Replication Capacity of HIV-1 in the Presence of Resistance-Associated Substitutions in Protease
CLINICAL INFECTIOUS DISEASES
2009; 49 (1): 165–66
View details for DOI 10.1086/599619
View details for Web of Science ID 000266766500024
View details for PubMedID 19500032
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Efavirenz-induced hypersensitivity reaction manifesting in rash and hepatitis in a Latino male
ANNALS OF PHARMACOTHERAPY
2008; 42 (3): 425-429
Abstract
To report a case of hypersensitivity manifesting in a rash, fever, and life-threatening hepatitis in a patient initiated on efavirenz therapy.A 30-year-old Latino male newly diagnosed with HIV was started on efavirenz-based highly active antiretroviral therapy (HAART) using tenofovir 300 mg, emtricitabine 200 mg, and efavirenz 600 mg once daily. Eleven days after beginning therapy, he developed a hypersensitivity reaction manifesting in rash and fever preceding severe drug-induced hepatitis. Liver enzyme peak values were aspartate transaminase 3410 U/L and alanine transaminase 2132 U/L. Hepatitis resolved with discontinuation of the HAART. The patient was rechallenged with tenofovir and emtricitabine one year later; no adverse reactions occurred.The Naranjo probability scale demonstrated a probable relationship between this adverse reaction and efavirenz. A MEDLINE search (2004 to September 2007) revealed 2 cases of rash preceding hepatitis with the initiation of efavirenz. Both cases were in women; there were no prior reported cases of efavirenz hypersensitivity in men. Although the mechanism of this reaction is unknown, a few factors may have contributed to this reaction. The half-life and the auto-induction of efavirenz may explain the continued rise in liver enzymes and severe hepatitis that continued to occur once the drug was discontinued. Another cause that may have contributed is the metabolism of the medication. CYP2B6 is responsible for almost 90% of the clearance of efavirenz. Data from a recent pharmacokinetic study showed that efavirenz concentrations were higher in both black and Latino patients when compared with those of white patients. In addition, it is highly probable that this patient's liver function was impaired when transaminase levels peaked, resulting in decreased clearance of efavirenz.Although such a hypersensitivity reaction is rare, efavirenz is the most probable cause of the erythematous maculopapular rash and acute hepatitis in this patient. Monitoring of liver function in patients who present with a rash following initiation of efavirenz-based HAART is recommended. In addition, clinicians should exercise caution in patients presenting with rash, fever, and increased liver enzymes (> 3 times the upper limit of normal or patient baseline). It is strongly recommended that efavirenz therapy be withheld in such cases and reevaluated once liver enzyme levels stabilize.
View details for DOI 10.1345/aph.1K574
View details for Web of Science ID 000254000200017
View details for PubMedID 18252833
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Treating the enemy.
Annals of internal medicine
2007; 147 (4): 278-279
View details for PubMedID 17709761
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Wind, rain, flooding, and fear: Coordinating military public health in the aftermath of Hurricane Katrina
CLINICAL INFECTIOUS DISEASES
2005; 41 (12): 1759-1763
Abstract
On 29 August 2005, a category 4 hurricane struck the Gulf Coast of Mississippi and southeast Louisiana, resulting in widespread destruction caused by winds in excess of 190 km/h (120 miles/h), heavy rain, and flooding. Communication, electricity, and fresh water supplies were disrupted throughout the region, rendering much of the area uninhabitable. Despite tremendous obstacles, the US military spearheaded the eventually successful rescue, recovery, and relief operations. This article describes the challenges of protecting the health and safety of these personnel in the immediate aftermath of Hurricane Katrina.
View details for Web of Science ID 000233698300012
View details for PubMedID 16288401
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HIV-1 protease and reverse transcriptase mutation patterns responsible for discordances between genotypic drug resistance interpretation algorithms
JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
2003; 33 (1): 8-14
Abstract
Several rules-based algorithms have been developed to interpret results of HIV-1 genotypic resistance tests. To assess the concordance of these algorithms and to identify sequences causing interalgorithm discordances, we applied four publicly available algorithms to the sequences of isolates from 2,045 individuals in northern California. Drug resistance interpretations were classified as S for susceptible, I for intermediate, and R for resistant. Of 30,675 interpretations (2,045 sequences x 15 drugs), 4.4% were completely discordant, with at least one algorithm assigning an S and another an R; 29.2% were partially discordant, with at least one algorithm assigning an S and another an I, or at least one algorithm assigning an I and another an R; and 66.4% displayed complete concordance, with all four algorithms assigning the same interpretation. Discordances between nucleoside reverse transcriptase inhibitor interpretations usually resulted from several simple, frequently occurring mutational patterns. Discordances between protease inhibitor interpretations resulted from a larger number of more complex mutation patterns. Discordances between nonnucleoside reverse transcriptase inhibitor interpretations were uncommon and resulted from a small number of individual drug resistance mutations. Determining the clinical significance of these mutation patterns responsible for interalgorithm discordances will improve interalgorithm concordance and the accuracy of genotypic resistance interpretation.
View details for Web of Science ID 000182805400002
View details for PubMedID 12792349
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Accuracy of the TRUGENE HIV-1 genotyping kit
JOURNAL OF CLINICAL MICROBIOLOGY
2003; 41 (4): 1586-1593
Abstract
Drug resistance and poor virological responses are associated with well-characterized mutations in the viral reading frames that encode the proteins that are targeted by currently available antiretroviral drugs. An integrated system was developed that includes target gene amplification, DNA sequencing chemistry (TRUGENE HIV-1 Genotyping Kit), and hardware and interpretative software (the OpenGene DNA Sequencing System) for detection of mutations in the human immunodeficiency virus type 1 (HIV-1) protease and reverse transcriptase sequences. The integrated system incorporates reverse transcription-PCR from extracted HIV-1 RNA, a coupled amplification and sequencing step (CLIP), polyacrylamide gel electrophoresis, semiautomated analysis of data, and generation of an interpretative report. To assess the accuracy and robustness of the assay system, 270 coded plasma specimens derived from nine patients were sent to six laboratories for blinded analysis. All specimens contained HIV-1 subtype B viruses. Results of 270 independent assays were compared to "gold standard" consensus sequences of the virus populations determined by sequence analysis of 16 to 20 clones of viral DNA amplicons derived from two independent PCRs using primers not used in the kit. The accuracy of the integrated system for nucleotide base identification was 98.7%, and the accuracy for codon identification at 54 sites associated with drug resistance was 97.6%. In a separate analysis of plasma spiked with infectious molecular clones, the assay reproducibly detected all 72 different drug resistance mutations that were evaluated. There were no significant differences in accuracy between laboratories, between technologists, between kit lots, or between days. This integrated assay system for the detection of HIV-1 drug resistance mutations has a high degree of accuracy and reproducibility in several laboratories.
View details for DOI 10.1128/JCM.41.4.1586-1593.2003
View details for Web of Science ID 000182179900037
View details for PubMedID 12682149
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Clinical resistance patterns and responses to two sequential protease inhibitor regimens in saquinavir and reverse transcriptase inhibitor-experienced persons
5th Conference on Retroviruses and Opportunistic Infections
UNIV CHICAGO PRESS. 1999: 1356–64
Abstract
The efficacy of sequential protease inhibitor therapy was studied in 16 human immunodeficiency virus (HIV) 1-infected persons in whom saquinavir with multiple nucleoside reverse transcriptase (RT) inhibitors (NRTI) had failed. Nelfinavir plus two NRTIs (new or continued) resulted in minimal (0.59 log RNA copies/mL) and transient (8 weeks) suppression of plasma HIV RNA levels. Rapid failure was surprisingly associated with baseline presence of protease gene mutation L90M (P=.04) in the absence of D30N and with RT mutations D67N (P<.01), K70R/S (P=.02), and K219Q/W/R/E (P<.01). Ten patients were subsequently switched to indinavir plus nevirapine and 2 NRTIs, resulting in a median 1.62 log reduction in plasma HIV RNA, with 3 patients maintaining 400 copies/mL for 24 weeks. These results suggest that nelfinavir may have limited utility after saquinavir failure, particularly without potent concomitant therapy. Combining an NRTI with a new protease inhibitor for rescue may improve response.
View details for Web of Science ID 000080561100007
View details for PubMedID 10228055