About

Karen McCowen is a Clinical Professor of Medicine at UCSD, with her address listed as 9500 Gilman Drive, La Jolla, CA. Her research focuses on endocrinology, metabolism, and critical care, with significant contributions to understanding glycemic control in the intensive care setting, the effects of nutritional support, and the metabolic implications of various endocrine disorders. Her work includes investigating the roles of glucagon-like peptide-1 receptor agonists in sleep apnea and obesity, hyperthyroidism secondary to radiofrequency ablation, and the interplay between sleep apnea, metabolic disease, and therapy. She has also contributed to research on the effects of medications such as pioglitazone and SSRI antidepressants on metabolic and endocrine parameters, as well as the metabolic consequences of conditions like hyperglycemia, parathyroid disorders, and the impact of nutritional interventions in critically ill patients.

Research topics

• Internal medicine
• Medicine
• Endocrinology
• Radiology
• Virology
• Pathology
• Pharmacology
• Intensive care medicine
• Biology
• Bioinformatics
• Surgery
• Emergency medicine

Selected publications

• Treatment preferences for comorbid obesity and obstructive sleep apnea (PRO-CON OSA) survey: Patient and provider preferences for CPAP and/or tirzepatide

  Journal of Clinical Sleep Medicine · 2026-02-23

  articleOpen access
  PublisherOA PDFDOI

• Glucagon-like peptide-1 receptor agonists for the treatment of obstructive sleep apnea

  Current Opinion in Pulmonary Medicine · 2025-08-22 · 4 citations

  articleOpen access

  PURPOSE OF REVIEW: This review highlights the emerging data on the use of incretin therapies, including glucagon-like peptide-1 receptor agonists (GLP-1RA) and dual GLP-1RA and glucose-dependent insulinotropic peptide (GIP) receptor agonists, on the treatment of obstructive sleep apnea (OSA). Given known cardiometabolic and neurocognitive consequences of OSA, optimizing treatment is essential. In the setting of widespread research efforts and clinical implementation of dual agonists in managing OSA, obesity and other cardiometabolic diseases, this review is timely. RECENT FINDINGS: Several randomized controlled trials and meta-analyses have shown GLP-1 and GIP receptor agonists to reduce apnea-hypopnea index (AHI) and body weight in patients with OSA. This impact has been demonstrated with the use of pharmacotherapy alone and in combination with traditional positive airway pressure (PAP) therapy. GLP-1RA may positively affect OSA through reducing systemic inflammation and decreasing adiposity, including via hormone changes, delayed gastric emptying, and central mechanisms impacting appetite regulation and sleep-wakefulness. SUMMARY: Novel pharmacological advances in individuals with OSA and obesity have shown promise in cardiometabolic disease control. Longitudinal follow-up to monitor the efficacy and adverse effects of incretin therapies, and further comparison studies with PAP therapy, are warranted.

  PublisherOA PDFDOI

• The Potential Role of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists and Glucose-Dependent Insulinotropic Polypeptide (GIP) Receptor Agonists in Obstructive Sleep Apnea and Obesity

  Current Pulmonology Reports · 2025-07-25 · 3 citations

  reviewOpen access

  Purpose of Review: Strong associations exist between obstructive sleep apnea (OSA) and obesity. Prior studies have demonstrated that weight reduction in people with OSA and obesity improves severity of OSA. Until recently, there were no approved pharmacotherapies for OSA. We aim to review recent literature on GLP-1 receptor agonists and GIP agonists and their potential role in the management of OSA. Recent Findings: Novel pharmacotherapies developed to target obesity include glucagon-like peptide-1 (GLP-1) receptor agonists and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists. These therapies have proven to be helpful in many comorbid conditions, with published studies suggesting a benefit in OSA. Summary: GLP-1 receptor agonists and GIP agonists are emerging potential therapies for OSA and associated cardiometabolic risk.

  PublisherOA PDFDOI

• PD33-12 BISPHOSPHONATE TREATMENT IS ASSOCIATED WITH LOWER INCIDENCE OF UROLOGY ENCOUNTERS, KIDNEY STONE DIAGNOSES AND PROCEDURES

  The Journal of Urology · 2025-04-08

  article
  PublisherDOI

• 8270 A Rare Case Of PTHrP Induced Severe Hypercalcemia Secondary To Squamous Cell Carcinoma Of Tongue

  Journal of the Endocrine Society · 2024-10-01

  articleOpen accessSenior author

  Abstract Disclosure: N. Vennelaganti: None. S. Vennelaganti: None. K. McCowen: None. Background: PTHrP-mediated hypercalcemia is often associated with solid organ malignancies and indicates a poor prognosis. The occurrence of this condition due to SCC of the head and neck, particularly of the tongue, is uncommon. This case report aims to shed light on this rare clinical presentation. Clinical Case: A 70-year-old woman with a history of tobacco use disorder, alcoholic liver cirrhosis, and a chronic fungal prosthetic joint infection presented with altered mental status and acute kidney injury. Laboratory tests revealed a corrected calcium level of 15.4 mg/dL and suppressed PTH of 3 pg/mL, indicating non-PTH-dependent hypercalcemia. Differentials considered included malignancy, multiple myeloma, 1,25 OH Vit D mediated hypercalcemia via fungal granuloma formation, and immobilization. Diagnostic evaluation revealed normal levels of 25 hydroxy Vitamin D ie: 54 ng/mL, normal kappa to lambda ratio suggestive of negative myeloma screen, normal TSH of 2.81 uIU/mL, and a low 1,25 OH Vit D level ie: 11.4 pg/mL (Ref range: 19.9-79.3 pg/mL). An elevated PTHrP concentration of 9.7 pmol/L (ref range 0-3.4 pmol/L) was noted. CT angiography performed for stroke evaluation incidentally discovered a base of tongue mass, which was difficult to appreciate on exam due to obtundation. A biopsy confirmed SCC of the tongue, and she was determined to be Stage IVA. The patient's hypercalcemia was determined to be secondary to PTHrP production from the tongue SCC compounded by immobilization. She was treated with IV fluids and subcutaneous calcitonin, normalizing her calcium levels over 20 days. IV Bisphosphonates were held inpatient due to poor renal function. She was seen by oncology and determined to not be fit for surgical management or chemotherapy. Radiation therapy was advised for management and patient was discharged. While awaiting her outpatient radiation treatment, the patient had another episode of altered mental status and was found to have a serum calcium of 16.4 mg/dL. She was managed with IV fluids, calcitonin and IV Zoledronate which improved her serum calcium. She has since been receiving monthly IV Zometa with oncology for hypercalcemia of malignancy. She was recently readmitted with severe oropharyngeal and pharyngeal dysphagia and has received a PEG tube for feeding. She is still pending radiation therapy for SCC tongue. Conclusion: Initially, during the workup of this case, we believed her hypercalcemia was likely immobilization-induced, but thorough investigation and the elevated PTHrP levels steered us towards malignancy as a potential etiology. This case is an example of an occult malignancy which lead to severe hypercalcemia. It also contributes to the understanding of hypercalcemia in cancer patients and highlights the rare association of SCC of the tongue with PTHrP-mediated hypercalcemia . PTHrP secreting SCC of head and neck are typically associated with a poor prognosis. Presentation: 6/2/2024

  PublisherOA PDFDOI

• Medical Management of the Patient After Bariatric Surgery

  2024-05-28

  book-chapterSenior author

  Important complications of obesity include nonalcoholic fatty liver disease (NAFLD) and dyslipidemia. While the former is more clearly directly related to obesity and in particular central distribution of obesity, in both conditions insulin resistance is an important contributor to the pathogenesis. Medical therapy of NAFLD is poor, other than weight loss. Dyslipidemia does improve with weight loss, although there are many other contributing influences upon dyslipidemia, such that it is not uncommon in lean individuals. One might anticipate a better effect of bariatric surgery upon NAFLD compared to dyslipidemia, but in both cases these conditions need reevaluation at regular intervals after surgery.

  PublisherDOI

• 8290 Hypervitaminosis A Induced Severe Hypercalcemia In A Patient With Cirrhosis

  Journal of the Endocrine Society · 2024-10-01 · 1 citations

  articleOpen accessSenior author

  Abstract Disclosure: N. Vennelaganti: None. S. Vennelaganti: None. R.L. Fitzgerald: None. K.C. McCowen: None. Introduction The liver stores vitamin A in hepatic stellate cells and regulates its absorption through bile production and distribution via retinol-binding protein 4 and transthyretin synthesis. Cirrhosis compromises these functions, resulting in vitamin A deficiency, which is inversely linked to the severity of nonalcoholic steatohepatitis. Addressing this deficiency in chronic liver diseases, particularly cirrhosis, is challenging due to the risk of vitamin A toxicity. This case describes a cirrhotic patient who developed hypervitaminosis A, leading to severe hypercalcemia. Clinical Case A 54-year-old male with alcoholic cirrhosis was diagnosed with hypovitaminosis A. He was prescribed 10,000 IU of vitamin A due to a low serum retinol level of less than 0.06 mg/L (reference range: 0.3-1.2 mg/L ). Two months later, he presented to the hospital with an erythematous patchy, scaling facial rash. His serum calcium corrected for albumin was high at 15.6 mg/dL. The rash and hypercalcemia, alongside vitamin A supplementation, raised suspicion of vitamin A toxicity. The patient, however, exhibited no hypercalcemia symptoms. He also had an acute kidney injury. His lab results revealed a PTH level of 10 pg/mL (normal range 15-65 pg/ml) and a normal myeloma screen, as well as normal vitamin D and TSH levels. An elevated PTHrP level of 5.2 pmol/l (normal range 0-2.3) was noted, which was attributed to the kidney injury(Cr 2.55 mg/l, eGFR 23 ml/min). Malignancy was excluded after a pan scan. Hypervitaminosis A is a clinical diagnosis, as serum vitamin A levels correlate poorly with toxicity. His serum retinol was normal at 0.83 mg/l, but his retinyl palmitate was high at 0.38 mg/L(reference range 0-0.10 mg/l), which supported our diagnosis. He received continuous IV 0.9% saline and subcutaneous calcitonin at 4 units/kg twice, and had a reduction in corrected calcium to 11 mg/dL over a week. The vitamin A-induced contact dermatitis improved with topical steroids. He was discharged; two months later, he remained asymptomatic with a corrected calcium of 11.1 mg/dL. He was not interested in further management as he was asymptomatic and serum calcium levels were improving. Labs were, however, notable for worsening renal function of unclear etiology. We will be trending his labs for improvement in serum calcium as the Vitamin A clears from his system. Clinical Lesson Vitamin A supplementation in cirrhotic patients is necessary in those with deficiency but carries a risk of toxicity. There are no definitive hepatology guidelines on the replacement of Vitamin A in patients with cirrhosis. This case emphasizes the importance of awareness of hypervitaminosis A-induced hypercalcemia in this population. Clinicians must carefully monitor and manage Vitamin A levels to avoid toxicity. Further research is essential for the management of this condition in cirrhotic patients. Presentation: 6/2/2024

  PublisherDOI

• FRI233 Adrenal Insufficiency Due To An Unusual Culprit

  Journal of the Endocrine Society · 2023-10-01

  articleOpen accessSenior author

  Abstract Disclosure: S. Decamps: None. K.T. Yeung: None. K. McCowen: None. Background: Chronic exogenous use of glucocorticoids is the most common cause of reversible secondary adrenal insufficiency (AI). There is a significant risk of cortisol deficiency if the medication is abruptly discontinued. Chronic glucocorticoid therapy may cause hypothalamic-pituitary-adrenal (HPA) axis suppression, resulting in low ACTH, atrophy of the adrenal zona fasciculata and decreased cortisol production. Immunotherapy rarely causes reversible central AI, usually permanent. We present a case of an immunotherapy-receiving patient who presented with biochemical evidence of adrenal insufficiency after using an oral solution (swish and spit) of dexamethasone as prophylaxis for mucositis. Patient Summary: A 52-year-old woman with stage IIb triple negative breast cancer receiving neoadjuvant Datopotamab, Dertuxtecan and Durvalumab was evaluated for adrenal insufficiency. Prior to starting therapy, serum cortisol level measured 7.9 mcg/dL at 11 AM (normal 6.0-18.4 mcg/dL at 6-10 A.M). She had received a single dose of dexamethasone 10 mg IV with her first cycle, but not thereafter. As part of the immunotherapy protocol, serial cortisol levels were obtained, and 2 weeks after the baseline, noon serum cortisol was 1.0 ug/dL. Patient was asymptomatic. At no point were glucocorticoids replaced, but 1-week later serum cortisol level was 0.6ug/dL at 11:00 AM along with an ACTH of 5 pg/mL. Immunotherapy-induced AI was strongly suspected. Her only glucocorticoid exposure had been a dexamethasone oral mouth rinse (swish 10mL for 1 minute and spit out, four times daily). Cortisol level at 7AM a week later measured 3.5 mcg/dL with ACTH 18.7 pg/mL and a dexamethasone level 108.2 ng/dL (normal < 50 ng/dL for patients not on dexamethasone). Technique of swish and spit was reviewed with the patient, and she was not ingesting the medication. An observational approach was pursued at this time given hemodynamic stability, treatment was continued and several weeks later repeat labs showed cortisol levels of 3.3 (7AM), with a dexamethasone level of 84.3 ng/dL. Her course of therapy has been completed, so she has been off the dexamethasone solution, continues to be asymptomatic and repeat labs now show a 9AM Cortisol level of 9.5 mcg/dL and, given lack of other sources, it is most likely that these low cortisol levels along with elevated dexamethasone levels are related to the use of dexamethasone swish and spit rather than immunotherapy induced permanent HPA axis suppression. Conclusion: There is no literature on dexamethasone swish and spit being absorbed systemically possibly leading to potentially reversible HPA suppression. Our case will raise awareness of help guide clinicians expand their differential when working up these patients. Presentation: Friday, June 16, 2023

  PublisherDOI

• Hyperthyroidism Due to Graves Disease After Radiofrequency Ablation

  JCEM Case Reports · 2023-05-01 · 8 citations

  articleOpen access

  Management options for benign, autonomously functioning, and malignant thyroid nodules were limited to surgery or targeting by radioactive iodine before the availability of radiofrequency ablation (RFA). Despite being a relatively new technique, RFA may be favored for patients of high surgical risk, and for those who wish to avoid hypothyroidism. Although insurance coverage for the procedure can be a significant barrier, several groups of investigators have shown improved quality of life for RFA compared to surgery, due to the less invasive nature and favorable risk profile. Hyperthyroidism due to transient thyroiditis is a known risk of RFA, secondary to direct trauma and subsequent thyroid hormone release. Here we present a case of an adult with large, symptomatic, multinodular goiter, with no prior history of thyroid autoimmunity, who underwent RFA with successful volume reduction of two nodules, but who developed acute hyperthyroidism due to Graves disease eight weeks after RFA. Larger studies evaluating the risks of RFA should evaluate for incident hyperthyroidism, specifically for Graves disease/thyroid autoimmunity, as this could represent an additional risk of the procedure.

  PublisherDOI

• Voice Outcomes From Direct Vocal Fold Testosterone Injections, a Case Report

  The Laryngoscope · 2023-01-03 · 5 citations

  articleOpen accessSenior author

  Here we provide the first demonstration of targeted vocal fold testosterone injection to achieve voice masculinization in 2 transgender male patients. Successful voice outcome was achieved in 2-3 weeks, without side effects, and continues to be durable. Laryngoscope, 133:1211-1213, 2023.

  PublisherOA PDFDOI

Frequent coauthors

• Bruce R. Bistrian

  Harvard University

  53 shared

• Atul Malhotra

  University of California, San Diego

  48 shared

• Robert J. Smith

  Children's Hospital of Philadelphia

  22 shared

• Lalita Khaodhiar

  18 shared

• Guy Schuscheim

  Massachusetts General Hospital

  16 shared

• Giora Pillar

  Carmel Medical Center

  16 shared

• Farooq Bandali

  Saint Peter's University Hospital

  16 shared

• Zachariah Thomas

  Christian Medical College & Hospital

  16 shared

Education

• Ph.D., Molecular and Computational Biology

  University of California, San Diego

  1997

• M.S., Molecular and Computational Biology

  University of California, San Diego

  1993

• B.S., Biology

  University of California, San Diego

  1991