About

Dr. Deirdre Cocks Eschler is a Clinical Associate Professor in Medicine at Stony Brook University. Her medical education was completed at the School of Medicine at Stony Brook University Medical Center in 2008. She completed her residency in Internal Medicine at Mount Sinai School of Medicine in 2012 and her fellowship in Endocrinology, Diabetes, and Metabolism at Mount Sinai School of Medicine in 2014. Dr. Eschler holds board certifications in Endocrinology, Diabetes, and Metabolism from the American Board of Internal Medicine, obtained in 2014, and in Endocrine Certification in Neck Ultrasound from 2017. Her clinical expertise includes endocrinology with a focus on adrenal tumors, autoimmune thyroid diseases, and related metabolic conditions. She has contributed to publications on the management of adrenal tumors in pregnancy, iodine supplementation in pregnancy, the etiology of autoimmune thyroid diseases, and the efficacy of topical antihistamines. Dr. Eschler is fluent in English and Spanish and practices at locations including Lake Grove, NY, and Commack, NY, providing specialized endocrine care.

Research topics

• Endocrinology
• Internal medicine
• Medicine
• Pediatrics
• Psychiatry

Selected publications

• LBSUN288 Improved Glycemic Control Following Oophorectomy In A Post-menopausal Woman With Ovarian Hyperthecosis

  Journal of the Endocrine Society · 2022 · 1 citations

  • Medicine
  • Internal medicine
  • Endocrinology

  Abstract Introduction While androgens are associated with decreased risk for type 2 diabetes in males, the opposite is seen in females. Despite this, a "chicken or the egg" argument exists regarding hyperandrogenism and insulin resistance in women. Ovarian hyperthecosis, a condition that mostly affects post-menopausal women, causes androgen excess due to hyperplasia of the theca interna of the ovaries. Akin to polycystic ovarian syndrome, it is associated with obesity and insulin resistance. We describe a case of ovarian hyperthecosis in a woman with type 2 diabetes with improved glycemic control following oophorectomy. Case A 63-year-old post-menopausal female with a history of autoimmune hepatitis, primary biliary cirrhosis, and chronic pancreatitis presented for recently diagnosed type 2 diabetes, discovered on routine point-of-care Hemoglobin A1c (HbA1c) testing in December 2020 (HbA1c 7.1%, weight: 86 kg). In January, she started repaglinide which was titrated to 2 mg with meals, also that month started prednisone for autoimmune hepatitis. Despite tapering doses of prednisone, her hyperglycemia paradoxically worsened and persisted following completion in June. In May, HbA1c was 7.8%. In August, she endorsed hirsutism, present for 2 years but worsening over the past few months. Labs showed elevated total testosterone (508 ng/dL), free testosterone (32.7 pg/mL), and androstenedione (305 ng/dL), with normal sex hormone binding globulin. DHEA-S was low (28.9 ug/dL, range: 29.4-220.5), midnight salivary cortisol was elevated (0.12 mcg/dL; range: <0. 09), and morning serum ACTH and cortisol were within normal range, with appropriate suppression to dexamethasone. Estradiol was above post-menopausal range (68.1 pg/mL; range: <6. 0-54.7). FSH and LH were within the post-menopausal range, with an approximate 1: 1 ratio. A pelvic ultrasound revealed two intramural myomas and a simple cyst of the right ovary, but otherwise unremarkable. She underwent bilateral salpingo-oophorectomy in October 2021. Post-surgical total testosterone was 27 ng/dL. Surgical pathology revealed unremarkable fallopian tubes and bilateral stromal hyperplasia and hyperthecosis of the ovaries. At one month follow-up, HbA1c was 6.5%, weight decreased from 89 kg pre-surgery to 86, and she endorsed improved hirsutism but frequent hypoglycemia on repaglinide 2 mg with meals. Repaglinide was decreased to 0.5 mg with meals. Three months later, HbA1c was 6.3% with unchanged weight. Conclusion Improved glycemic control, corresponding with timing of oophorectomy but not discontinuation of steroids, suggests insulin resistance in this case may be due to hyperandrogenism. Though some studies and case reports suggest hyperandrogenism causes insulin resistance, others suggest the contrary. The relationship between androgens and insulin sensitivity is likely complex, and further research is necessary. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

  PublisherOA PDFDOI

• Intravenous Insulin Resistance in a Critically Ill Patient Secondary to Decreased Peripheral Perfusion

  Journal of the Endocrine Society · 2021-05-01

  articleOpen accessSenior author

  Abstract Introduction: Intravenous (IV) insulin infusion is the preferred treatment modality for hyperglycemia in the intensive care unit (ICU) due to its short duration of action and easy titratability. However, administration of IV insulin has challenges. These include frequent monitoring, site infiltration, and high insulin dose requirements with other ICU medications such as epinephrine. There are, however, limited reports demonstrating an elevated insulin requirement due to poor peripheral perfusion. Below illustrates such a case, necessitating a change from peripheral to central IV insulin administration. Case Presentation: A 50 year old male with well controlled type 2 diabetes and previous aortic valve replacement presented to our facility for prosthetic valve endocarditis complicated by aortic root abscess. He was admitted to the ICU, treated with IV antibiotics, abscess washout and aortic valve replacement. Preoperatively, he was started on IV regular insulin via continuous infusion through a central line. During the pre and intraoperative periods, his hourly IV insulin requirement ranged from 2.4 to 5 units/ hour (hr). His blood glucose (BG) ranged from 107-251mg/dL (n 70-99mg/dL). The patient became hypotensive intraoperatively requiring vasopressor support. Dobutamine and norepinephrine infusions were started via central access and were continued postoperatively at steady rates. Vasopressin was added through central access as the patient failed to meet hemodynamic targets. Postoperatively, the propofol infusion was discontinued and the IV regular insulin infusion was moved to the peripheral line where the propofol had previously been administered. BG increased steadily to a maximum of 402 mg/dL despite an increase in the peripheral IV insulin rate to 152.4 units/hr. The site of the IV insulin drip was changed to another solitary peripheral access without success in decreasing the IV insulin infusion rate. The elevated requirements were deemed secondary to the patient’s lack of peripheral perfusion and should decrease with transition to a central line. A preemptive decrease in insulin drip rate to 10% of the peripheral dose was used to avoid hypoglycemia. The insulin drip was changed to a central access with a rate of 15units/ hr. BG values declined to a range of 140 -180 mg/dL. The patient remained on the multiple vasopressors for hemodynamic support, however, the insulin drip was able to be decreased and ultimately, discontinued. Conclusion: This case illustrates a unique challenge in the treatment of hyperglycemia with multifactorial shock and our approach to management. Elevated IV insulin requirements persisted despite stability in vasopressor dose, change to a solitary peripheral IV site, and lack of interfering medications in the treatment regimen. This is the first case to demonstrate a relationship between high IV insulin requirements and poor peripheral perfusion.

  PublisherOA PDFDOI

• Acute Sensorineural Hearing Loss - an Unusual Presentation of Uncontrolled DM

  Journal of the Endocrine Society · 2021-05-01

  articleOpen accessSenior author

  Abstract Background: Diabetes mellitus (DM) is a systemic metabolic disorder that possesses macro- and microangiopathic consequences. Studies have demonstrated that a relationship exists between sensorineural hearing loss (SNHL) and DM, particularly in patients of older age, longer disease duration, and uncontrolled DM. The pathophysiology of DM related hearing loss is poorly understood, however proposed mechanisms include ischemia, fibrosis, demyelination, and atrophy of the eighth cranial nerve. We however, present a case of acute, transient sensorineural hearing loss in the setting of diabetic ketoacidosis that resolved with blood glucose control. Clinical Case: A 34-year-old male with type 2 diabetes mellitus (A1c 6.5% -diagnosed 6 months prior), hypertension, hyperlipidemia, and morbid obesity presented with shortness of breath and acute hearing loss without tinnitus, after being treated for pneumonia and otitis media with a course of levofloxacin for 7 days. On presentation, patient was tachypneic and tachycardic. Physical examination was significant for mild erythema of the right tympanic membrane without bulging, fluid level, mastoid tenderness, or discharge. Laboratory values were significant for hyperglycemia with blood glucose of 628 mg/dL(n 70–99 mg/dL), A1c 15.9% (n 4.8–5.6%), bicarbonate 8 mmol/L (21–31 mmol/L), anion gap 37 mmol/L (9–16 mmol/L), beta-hydroxybutyrate 11.7 mmol/L (0.02–0.27 mmol/L). Venous gas was suggestive of metabolic acidosis, urinalysis was positive for moderate ketones and glucose >500 mg/dL. The patient was diagnosed with diabetic ketoacidosis and was started on an insulin drip. An audiogram revealed profound bilateral sensorineural hearing loss. A Computerized tomography (CT) scan of the bilateral temporal bones was negative for abnormalities, and a magnetic resonance imaging (MRI) of the brain was negative for morphologic abnormalities of 7th and 8th cranial nerves. Infectious and rheumatologic etiologies were excluded with normal syphilis FTA-ABs, Lyme PCR, Rheumatoid factor, ANCA, and ANA. The patient received one dose of empiric prednisone. His hearing improved after 2 days with normalization of blood glucose to a range of 100–200 mg/dL. A repeat audiogram and auditory brainstem response showed significant improvement with normal bilateral hearing. Discussion: SNHL in DM typically presents in a gradual progression with bilateral involvement, affecting higher frequencies. In patients with DM, studies show that chronicity (greater than 10 years) is strongly associated with SNHL. Other variables include older age and HbA1c greater than 8%. This is the first case to demonstrate acute bilateral SNHL, associated with uncontrolled type 2 diabetes mellitus, which resolved after blood glucose control. In the appropriate context, clinicians should consider significant hyperglycemia as a possible etiology of acute hearing loss.

  PublisherDOI

• Euglycemic Diabetic Ketoacidosis Caused by SGLT2 Inhibitors and a Ketogenic Diet: A Case Series and Review of Literature

  AACE Clinical Case Reports · 2020 · 44 citations

  Senior authorCorresponding
  • Medicine
  • Internal medicine
  • Endocrinology

  OBJECTIVE: Sodium-glucose cotransporter-2 (SGLT2) inhibitors are a relatively novel class of oral medications for the treatment of type 2 diabetes mellitus (T2DM). Their use has increased recently due to their beneficial renal and cardiovascular outcomes, but they come with the rare risk of diabetic ketoacidosis (DKA) at normal or slightly elevated glucose values, termed euglycemic DKA (euDKA). Recently, carbohydrate-deprived, ketogenic diets have gained popularity due to benefits of weight loss and improved control of T2DM. We describe 2 patients with T2DM who developed euDKA caused by SGLT2 inhibitor use while on a ketogenic diet and provide a review of the literature. METHODS: We describe the hospital course, laboratory data, and treatment of 2 patients and provide a literature review. RESULTS: Both of our patients were found to have normal or mildly elevated serum glucose levels, with an elevated anion gap and ketosis, representative of euDKA. The first patient developed euDKA after only 1 dose of empagliflozin, while the second patient developed euDKA after only 1 week of being on a ketogenic diet while on an SGLT2 inhibitor. CONCLUSION: While there have been a few reports of euDKA with SGLT2 inhibitors and ketogenic diets, many physicians prescribing these medications may not be aware of this association. Therefore, they must inform their patients to avoid a ketogenic diet if on an SGLT2 inhibitor. If a patient presents with symptoms of DKA and is eating a carbohydrate-free diet while taking an SGLT2 inhibitor, there should be a low threshold to screen for DKA.

  PublisherOA PDFDOI

• Debunking Internet Myths: What Is the Best Approach?

  2019-01-01

  book-chapter1st author
  PublisherDOI

• Circulating Levels of Bone and Inflammatory Markers in Gestational Diabetes Mellitus

  BioResearch open access · 2018-08-01 · 20 citations

  articleOpen access1st authorCorresponding

  Gestational diabetes mellitus (GDM) can cause short- and long-term complications to the mother and fetus. While the precise mechanisms in preserving glucose balance in a healthy pregnancy are unknown, various growth factors and hormones have been implicated or associated with GDM risk in humans or rodents, including prolactin, tumor necrosis factor alpha (TNFα), osteoprotegerin (OPG), hepatocyte growth factor (HGF), and receptor activator of nuclear factor-kappa B ligand (RANKL). We aimed to evaluate the relationship of these and other protein markers in women with GDM. In this cross-sectional study, blood samples were collected from pregnant women with GDM and with normal glucose tolerance (NGT) at the 24- to 32-week obstetrical visit, during the 1-h oral glucose challenge test or 3-h oral glucose tolerance test. Blood plasma was analyzed for RANKL, OPG, prolactin, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), HGF, plasminogen activator inhibitor type 1 (PAI-1), and TNFα. Forty-six women with NGT and 47 women with GDM were included (mean ± standard deviation maternal age 31.6 ± 5.7, mean ± standard deviation gestational age 28.1 ± 2.2 weeks). Groups were similar in terms of age, body mass index, gestational age, and race/ethnicity. Serum levels of OPG, prolactin, TRAIL, HGF, PAI-1, and TNFα were similar in both groups. RANKL was lower in GDM subjects (p = 0.019). Contrary to previous reports in the literature, we found a lower serum RANKL level in women with GDM. Further investigation is needed to determine whether there are suitable serum markers for diagnosing GDM or determining prognosis or severity.

  PublisherOA PDFDOI

• Prolactinoma through the female life cycle

  Endocrine · 2017-11-24 · 40 citations

  review1st author
  PublisherDOI

• Management of Adrenal Tumors in Pregnancy

  Endocrinology and Metabolism Clinics of North America · 2015-05-30 · 57 citations

  review1st authorCorresponding
  PublisherDOI

• Thyroid Autoantibodies

  Elsevier eBooks · 2014-01-01 · 16 citations

  book-chapter
  PublisherDOI

• List of Contributors

  Elsevier eBooks · 2014-01-01

  book-chapter
  PublisherDOI

Frequent coauthors

• Serena Mistry

  Stony Brook Medicine

  4 shared

• Jagadeesh Bayry

  Indian Institute of Technology Palakkad

  3 shared

• Yaron Tomer

  Albert Einstein College of Medicine

  3 shared

• Rachel Pessah‐Pollack

  3 shared

• Jonathan Leffert

  2 shared

• Dharscika Arudkumaran

  Stony Brook Medicine

  2 shared

• Barbara Czarnocka

  Postgraduate School of Molecular Medicine

  2 shared

• Yaron Tomer

  Mount Sinai Medical Center

  2 shared

Education

• M.D., Medicine

  Stony Brook University School of Medicine

  1995

• B.S., Biochemistry

  University of California, San Diego

  1991