About

Michael Schivo, M.D., M.A.S. is a professor of Clinical Internal Medicine at UC Davis Health and serves as the Chair of the Clinical Research Graduate Group. He is also the Director of the Internal Medicine Residency Research Track and Co-Director of the Comprehensive COPD Clinic. His clinical interests include airway diseases, with a focus on chronic obstructive pulmonary disease (COPD) and other obstructive lung diseases such as asthma. Dr. Schivo is board-certified in internal medicine, pulmonary diseases, and critical care medicine, and he is part of the Reversible Obstructive Airway Diseases (ROAD) Center, the UC Asthma Network (UCAN) Clinics, and the Lung Center at UC Davis. His research centers on the analysis of exhaled and emitted volatile organic compounds (VOC) for non-invasive diagnostics, disease monitoring, and therapeutic response evaluation. He collaborates with biologists, chemists, chemometricians, engineers, and clinicians to coordinate clinical trials utilizing VOC analysis in various disease states, spanning from in-vitro models to human studies.

Research topics

• Artificial Intelligence
• Computer Science
• Medicine
• Pathology
• Risk analysis (engineering)
• Virology
• Biology
• Veterinary medicine
• Internal medicine
• Gastroenterology

Selected publications

• Two‐Staged Bronchoscopic Lung Volume Reduction: A Single US Academic Center Retrospective Analysis Demonstrating Reduction in Pneumothorax

  Respirology Case Reports · 2025-09-01

  articleOpen access

  Staged Bronchoscopic lung volume reduction (BLVR) has been proposed to reduce the risk of pneumothorax in patients with emphysema, though evidence to date is limited. We present a retrospective series from a single US academic centre, evaluating pneumothorax and other complications following staged BLVR. Seventeen patients underwent staged BLVR at our centre. Two illustrative cases are presented: (1) a case of pneumothorax post-staged BLVR managed conservatively without chest tube insertion, and (2) a patient who initially developed pneumothorax after single-stage BLVR, subsequently completing staged BLVR without complications. Overall, the pneumothorax rate within 45 days was 11.8%, and none of the events required tube drainage or valve removal. This retrospective analysis suggests that staged BLVR may reduce the incidence of pneumothorax. Larger, randomised controlled trials are warranted to confirm these potential benefits.

  PublisherDOI

• The Effect of Respiratory Therapist Case Managers Integrated into COPD Clinical Care

  Respiratory Care · 2025-01-28 · 2 citations

  article

  Background: Personalized education and treatment selection can improve health behaviors and outcomes in patients with COPD. However, many patients with COPD have incomplete knowledge of their disease, which leads to undertreated symptoms. We hypothesized that an interdisciplinary care approach to COPD with respiratory therapists (RTs) integrated in our dedicated clinic will significantly affect care as measured by COPD Assessment Test (CAT) scores, exacerbation rates, and COPD-related hospitalizations. Methods: This study was a retrospective analysis of patients enrolled in the UC Davis Comprehensive COPD Clinic registry. Between January 2018–January 2020, 241 patients were seen. Patients screened ( n = 101) had been followed 12 months post initial COPD clinic visit. Two subjects were excluded from analysis due to discrepancies in CAT assessments, leaving 99 subjects in total. The clinic RT provided assessment, education, and treatment recommendations. We collected CAT scores, exacerbation rates, and those that required hospitalization in the 12 months prior to and after the initial COPD clinic visit. Analysis for CAT is reported as median and interquartile range (IQR), with differences determined by Wilcoxon test. Summary data are reported as percentages, 95% CI, and chi-square test. Results: The initial median CAT score was 22 (IQR 7–34), and 2-month follow-up CAT median was 19 (IQR 11–24, P < .001). There were 115 exacerbations in the 12-month period prior to the initial clinic visit and 63 exacerbations in the 12 months post clinic visit ( P = .006). In the 12-month period prior to the clinic visit, there were 44 hospital admissions for COPD exacerbations compared to 20 hospital admissions for COPD exacerbations in the 12 months after initial clinic visit ( P = .06). Conclusions: Our retrospective study demonstrated significant improvements in symptoms and exacerbation rates and a non-significant reduction in hospitalizations for COPD. This suggests that an RT-facilitated program may improve meaningful clinical outcomes.

  PublisherDOI

• Fixed, High-dose Bivalirudin – A Novel Solution to a Fatal Problem

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01 · 1 citations

  articleSenior author

  Abstract INTRODUCTION: Fixed, high-dose bivalirudin is frequently used in percutaneous coronary interventions (PCI) and heparin-induced thrombocytopenia and thrombosis (HITT) with cardiovascular consequences. This dosing is rarely used for other reasons. Here we present a case where fixed, high-dose bivalirudin was used in the successful treatment of progressive HITT associated with venous and arterial thromboses in a patient without PCI. CASE PRESENTATION: A 77-year-old male with a history of chronic obstructive pulmonary disease and presented with chest pain. Baseline platelets at the time were 218 K/uL. There was concern for non-ST elevated myocardial infarction and the patient received unfractionated heparin. He eventually received coronary artery bypass grafting within a few days of admission. 13 days from initial heparin exposure, the patient was noted to have no palpable radial pulse. Urgent CT imaging found a right brachial artery occlusion and a small right-sided pulmonary embolism with no evidence of RV strain. He was subsequently transferred to our facility for further management of limb ischemia.Within 5 hours of admission to our facility, his platelet count declined from 72 to 29 K/uL in the setting of both arterial and venous thromboses. HITT was suspected, and he was transitioned to bivalirudin at a dose of 0.12 mg/kg/hr with goal activated partial thromboplastin time (aPTT) of 55-70 seconds. Despite being on bivalirudin, he had progression of the pulmonary embolism with obstructive shock. He was emergently transferred to interventional radiology for thrombectomy (Figure 1). In the interim, the patient's heparin-platelet factor 4 antibody resulted strongly positive. Given suspicion for progressive thrombus formation despite treatment with bivalirudin, we proceeded with high dose bivalirudin. Bivalirudin 1.75 mg/kg/hr was given for 3 hours, followed by 0.2 mg/kg/hr (non-titratable) for 20 hours. Our patient stabilized overnight with no recurrence of emboli or evidence of bleeding. DISCUSSION: In this case, we introduced a novel application for fixed, high-dose bivalirudin in life-threatening and progressive HITT without PCI. Untreated HITT can have a mortality rate of 20%; however, even in presumed treated HITT, similar to our patient, there may be gaps between aPTT checks where the bivalirudin is subtherapeutic. Progression of HITT despite therapy should be considered for fixed, high-dose bivalirudin for a trial period. It remains to be seen whether specific phenotypes of HITT would benefit from high-dose bivalirudin.

  PublisherDOI

• Low TET1 Expression Levels in COPD Are Associated with Airway and Blood Neutrophilia

  medRxiv · 2025-04-16

  preprintOpen access

  Epigenetic dysregulation, particularly DNA methylation variations, is implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Ten-eleven translocation (TET) proteins (TET1, TET2, and TET3) regulate DNA methylation and gene transcription. Impaired TET1 expression was previously associated with airway inflammation and asthma. Here we investigated TET gene associations with COPD severity. We found that reduced TET1 expression in peripheral blood mononuclear cells was associated with higher sputum and blood neutrophil counts, decreased lung function and increased disease severity in patients. These findings support a potential protective role and warrant further mechanistic investigations into the actions of TET1 in COPD.

  PublisherOA PDFDOI

• Go With the Flow: Diagnosis of Pulmonary T-Cell Prolymphocytic Leukemia

  2024-04-30

  articleSenior author
  PublisherDOI

• Hypoxemic Respiratory Failure and Coccidioidomycosis-Associated Acute Respiratory Distress Syndrome

  Open Forum Infectious Diseases · 2024-02-01 · 4 citations

  articleOpen access

  Abstract Background Severe coccidioidomycosis presenting with respiratory failure is an uncommon manifestation of disease. Current knowledge of this condition is limited to case reports and small case series. Methods A retrospective multicenter review of patients with coccidioidomycosis-associated acute respiratory distress syndrome (CA-ARDS) was conducted. It assessed clinical and laboratory variables at the time of presentation, reviewed the treatment course, and compared this cohort with a national database of patients with noncoccidioidomycosis ARDS. Survivors and nonsurvivors of coccidioidomycosis were also compared to determine prognostic factors. Results In this study, CA-ARDS (n = 54) was most common in males, those of Hispanic ethnicity, and those with concurrent diabetes mellitus. As compared with the PETAL network database (Prevention and Early Treatment of Acute Lung Injury; n = 1006), patients with coccidioidomycosis were younger, had fewer comorbid conditions, and were less acidemic. The 90-day mortality was 15.4% for patients with coccidioidomycosis, as opposed to 42.6% (P < .0001) for patients with noncoccidioidomycosis ARDS. Patients with coccidioidomycosis who died, as compared with those who survived, were older, had higher APACHE II scores (Acute Physiology and Chronic Health Evaluation), and did not receive corticosteroid therapy. Conclusions CA-ARDS is an uncommon but morbid manifestation of infection. When compared with a national database, the overall mortality appears favorable vs other causes of ARDS. Patients with CA-ARDS had a low overall mortality but required prolonged antifungal therapy. The utility of corticosteroids in this condition remains unconfirmed.

  PublisherOA PDFDOI

• Elevated Sputum Group 2 Innate Lymphoid Cells Indicates Clinical Severity of Chronic Obstructive Pulmonary Disease and Involves IL-17A Plasticity

  2023-05-01

  article
  PublisherDOI

• Drug Withdrawn Pneumonitis? A Case of an Acute Pneumonitis Associated With Ruxolitinib Withdrawal

  2023-05-01 · 1 citations

  articleSenior author
  PublisherDOI

• COPD with elevated sputum group 2 innate lymphoid cells is characterized by severe disease

  medRxiv · 2023-11-22 · 3 citations

  preprintOpen access

  ABSTRACT Rationale Pulmonary innate immune cells play a central role in the initiation and perpetuation of chronic obstructive pulmonary disease (COPD), however the precise mechanisms that orchestrate the development and severity of COPD are poorly understood. Objectives We hypothesized that the recently described family of innate lymphoid cells (ILCs) play an important role in COPD. Methods Subjects with COPD and healthy controls were clinically evaluated, and their sputum samples were assessed by flow cytometry. A mouse model of spontaneous COPD [genetically deficient in surfactant protein-D (SP-D -/- )] and ozone (O 3 ) exposure were used to examine the mechanism by which lack of functional SP-D may skew ILC2s to produce IL-17A in combination with IL-5 and IL-13, leading to a mixed inflammatory profile and more severe disease. Measurements and Main Results COPD was characterized by poor spirometry, sputum inflammation, and the emergence of sputum GATA3 + ILCs (ILC2s), but not T-bet + ILCs (ILC1s) nor RORγt + ILCs (ILC3s). COPD subjects with elevated sputum ILC2s (the ILC2 high group) had worse spirometry and sputum neutrophilia and eosinophilia than healthy and ILC2 low subjects. This was associated with the presence of dual-positive IL-5 + IL-17A + and IL-13 + IL-17A + ILCs and nonfunctional SP-D in the sputum in ILC2 high subjects. SP-D -/- mice showed spontaneous airway neutrophilia. Lack of SP-D in the mouse lung licensed ILC2s to produce IL-17A, which was dose-dependently inhibited by recombinant SP-D. SP-D -/- mice showed enhanced susceptibility to O 3 -induced airway neutrophilia, which was associated with the emergence of inflammatory IL-13 + IL-17A + ILCs. Conclusions We report that the presence of sputum ILC2s predicts the severity of COPD, and unravel a novel pathway of IL-17A plasticity in lung ILC2s, prevented by the immunomodulatory protein SP-D.

  PublisherOA PDFDOI

• Respiratory Therapist Case Managers Integrated Into COPD Clinic Care Improve Symptomology and Exacerbation Rates

  Respiratory Care · 2022-10-01

  article
  PublisherDOI

Frequent coauthors

• Cristina E. Davis

  University of California, Davis

  60 shared

• Nicholas J. Kenyon

  VA Northern California Health Care System

  52 shared

• Mitchell M. McCartney

  VA Northern California Health Care System

  27 shared

• Brooks Kuhn

  University of California, Davis

  24 shared

• A. Linderholm

  21 shared

• Timothy E. Albertson

  University of California Davis Medical Center

  20 shared

• Narin Sriratanaviriyakul

  Queen's Medical Center

  20 shared

• Brian M. Morrissey

  20 shared

Labs

• Internal Medicine Pulmonary, Critical Care, and Sleep MedicinePI

Education

• MAS - Clinical Research, Graduate Studies

  UC Davis

  2011

• MD, School of Medicine

  Drexel University

  2003

• BA - Biological Sciences and English, Biological Sciences and English

  UC Davis

  1998

Awards & honors

• UC Davis Internal Medicine Chair's Recognition Award for Ser…
• Joan Ottinger Memorial Research Award, UC Davis School of Me…
• Fellow's Research Award, UC Davis Internal Medicine (2012)
• People's Choice Award, UC Davis Internal Medicine (2010)
• Golden Key Honor Society, UC Davis (2010)