About

Dr. David Bleich is the Chief of the Division of Endocrinology, Diabetes, & Metabolism and a Professor of Medicine at Rutgers New Jersey Medical School. He has more than 20 years of experience in the field of Diabetes and Endocrinology, with a practice focused on complex diabetes management and other aspects of general endocrinology. Dr. Bleich is a nationally recognized expert in both type 1 and type 2 diabetes and has played leadership roles in diabetes organizations including the American Diabetes Association, the Juvenile Diabetes Research Foundation International, and the Department of Defense Diabetes Grant Review. He has conducted grant-funded bench research in pancreatic beta-cell function and has spent over 10,000 hours caring for individuals with diabetes, as well as mentoring and teaching medical students, residents, and endocrine fellows. His current interests and focus are on improving the quality of diabetes care and developing a data-driven holistic approach to patient care. Dr. Bleich is also a strong education professional, serving as the Fellowship Director of Endocrinology, Diabetes, and Metabolism at Rutgers, with fellowship training from Harvard Medical School. He holds an MD from New York Medical College and a BA from Haverford College.

Research topics

• Endocrinology
• Internal medicine
• Medicine
• Bioinformatics
• Genetics
• Intensive care medicine
• Biology

Selected publications

• The Association of Impaired Vibration Sensation in the Lower Limb with Tests of Cognition in Older People: The Cardiovascular Health Study

  Dementia and Geriatric Cognitive Disorders · 2024-11-19 · 1 citations

  articleOpen access

  INTRODUCTION: The prevalence of peripheral neuropathy (PN) in the lower limb increases with age and with the presence of diabetes. Studies show an association of PN with advanced cognitive impairment. Here we examine the association of PN with measures of early cognitive deficits in a cohort of older adults without apparent cognitive impairment, with or without diabetes. METHODS: A total of 2,798 participants from the Cardiovascular Health Study were examined, mean age 80 years. All underwent tests of overall cognition (3MSE), executive function (DSST), and visual memory (BVRT). Impairment of vibration sensation in the toes, ankles, and tibial tuberosities was ascertained. Participants were graded according to the extent of impairment. Adjusted linear regression analyses of the extent of impaired vibration sensation with cognitive tests were performed. Results were further categorized by the presence or absence of diabetes. RESULTS: 70% of participants had intact vibration sensation in the toes; 8% had no vibration sensation in the tibial tuberosities or below. Compared to participants with intact vibration sensation in the toes, those with no vibration sensation in the tibial tuberosities had lower 3MSE scores. Tests of executive function were lower in a stepwise manner with greater impaired vibration sensation. Visual memory was less strongly associated with impaired vibration sensation. Findings did not differ significantly by diabetes status. CONCLUSION: In older adults, impaired vibration sensation in the lower limb is associated with impaired executive function and visual memory. These findings did not differ by diabetes status.

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• 6366 Elevated Baseline Triglycerides As an Independent Risk Factor For Coronary Artery Disease

  Journal of the Endocrine Society · 2024-10-01

  articleOpen accessSenior author

  Abstract Disclosure: E. Askar: None. H. Moran: None. D. Bleich: None. Introduction: Diabetes is considered a coronary artery disease (CAD) risk equivalent. Studies have shown that the baseline level of triglycerides plays a role in cardiovascular risk independent of LDL levels lowered with statins. Numerous studies demonstrate that, in the general population, coronary artery calcium (CAC) scoring predicts and reclassifies cardiovascular disease (CVD) events, even in the absence of other risk factors. Here, we present a case of a 65 -year-old Caucasian male with elevated baseline triglycerides and a high CAC score, increasing his CVD risk despite the normalization of his triglycerides with statin therapy.Case presentation: A 65-year-old Caucasian male with a history of hypertension, hyperlipidemia, and diabetes presented to our endocrinology clinic for the management of hyperlipidemia and diabetes. His medications included empagliflozin 10 mg daily, repaglinide 1 mg three times a day, atorvastatin 20 mg daily, and amlodipine 10 mg daily. He had no complaints, and the physical examination was unremarkable. His recent HbA1c was 7.4%. Six months prior to presentation, he was found to have elevated triglycerides of 253 mg/dL (normal range: 10-149 mg/dL), low HDL of 34 mg/dL (normal range: >39 mg/dL), LDL of 84 mg/dL (normal range: 0-99 mg/dL), and total cholesterol of 167 mg/dL (normal range: 100-200 mg/dL). At that time, he was started on atorvastatin, and his recent triglycerides and HDL levels normalized. He was referred for CAC scoring, and the result was 2733 , which is above the 90th percentile for men between the ages of 65 and 69. As a result, he was further referred to a coronary angiogram. Conclusion: McGarry at the University of Texas Southwestern Medical Center was the first to describe the elevated triglyceride along with low HDL phenotype associated with insulin resistance. They explained this phenotype as a result of hepatic insulin resistance. Elevated insulin levels reduce the activity of lipoprotein lipase (LPL). As a result of that, the VLDL triglycerides rise, forming small dense LDL with a strong atherogenic potential.In the 2010 published ACCORD study, the effects of simvastatin alone versus simvastatin and fenofibrate were compared in 5500 Patients with type 2 diabetes. The experimental group did not exhibit any significant adverse cardiovascular events after eight years. However, the mean triglyceride was only 162 mg/dL. Consequently, no assumptions about the impact of the treatment on cardiovascular events in a more pertinent subset of people with greater baseline triglycerides could be made.While there has been controversy on the role of triglycerides in CVD, the idea of lowering triglycerides in diabetes patients with high triglycerides and low HDL to lower the risk of CVD is well supported. Presentation: 6/2/2024

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• SURVEY OF RECENT HALAKHIC LITERATURE: Of Ovum Donation, Surrogacy and Conversion

  Tradition - A Journal of Orthodox Jewish Thought · 2024-01-01

  article1st authorCorresponding
  PublisherDOI

• 6616 Copeptin Use To Reduce Hospital Stay In A Complicated DI Case

  Journal of the Endocrine Society · 2024-10-01

  articleOpen accessSenior author

  Abstract Disclosure: S.S. Kowsika: None. H. Moran: None. Introduction: While there is literature describing the use of copeptin for the diagnosis of polyuria-polydipsia syndrome, its utilization remains very limited in many hospitals. We present a case where the patient, initially misdiagnosed with central diabetes insipidus (DI), was appropriately diagnosed with partial nephrogenic DI through the use of copeptin. Case: A 48-year old female with a history of cardiac arrest, anoxic brain injury and diabetes insidious (DI) presented to the emergency department with hypernatremia (Na 154 mmol/L). The patient had been initiated on desmopresin (DDAVP) at an outside facility prior to her current admission. Despite receiving high doses of DDAVP, her sodium levels remained elevated, prompting further investigation. DDAVP administration was discontinued. A water deprivation test was subsequently performed, followed by IV administration of 2 mcg of DDAVP, which resulted in an increase in urine osmolality from 191 to 331 mosm/kg, which was less than the expected 50% increase observed in central DI. Additionally, a baseline copeptin level was obtained and noted to be 31 pmol/L, confirming the diagnosis of partial nephrogenic DI. The patient was started on Amiloride, leading to normalization of sodium levels. Discussion: Many patients with polyuria-polydipsia syndrome are frequently misdiagnosed and receive incorrect treatment, potentially worsening their clinical condition. Copeptin (Carboxy-Terminal-Pro-vasopressin) is the C-terminal peptide of pro-vasopressin, co-secreted with arginine vasopressin (AVP). It has been proposed as a direct test for diagnosing polyuria-polydipsia syndrome. Baseline Copeptin testing without stimulation can accurately diagnose nephrogenic DI if elevated (>21.4, pmol/L). To differentiate between central DI and chronic polyuria, prior thirsting with hypertonic saline or glucagon stimulation is necessary, with stimulated copeptin <4.9 pmol/L diagnosing central DI. Despite its diagnostic potential, Copeptin is underutilized in many settings. In this case, using Copeptin to accurately diagnose our patient led to appropriate treatment and the resolution of hypernatremia. Presentation: 6/1/2024

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• Familial tumoral calcinosis: a rare autosomal recessive disease

  BMJ Case Reports · 2024-10-01

  articleSenior author

  Familial tumoral calcinosis (FTC) is a rare autosomal recessive disorder where renal tubular phosphate excretion is decreased in the absence of renal failure. The underlying defect is due to inactivating mutations in the fibroblast growth factor 23 , α-Klotho or UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyl transferase-3 genes, resulting in hyperphosphatemia. Patients typically present with calcified soft tissue masses resulting from calcium phosphate deposits. Medical management with phosphate binders, a carbonic anhydrase inhibitor, in addition to limiting phosphorus intake, is the mainstay of treatment. This case serves to highlight the pathophysiology of a rare diagnosis of FTC and the efficacy of the limited therapeutic options available.

  PublisherDOI

• #1706237 Thyroid Nodule, Cyst, or Abscess?

  Endocrine Practice · 2024-05-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• 6891 Exclusive Normetanephrine Secreting Pheochromocytoma In A Young Male

  Journal of the Endocrine Society · 2024-10-01

  articleOpen accessSenior author

  Abstract Disclosure: E. Askar: None. H. Moran: None. IntroductionPheochromocytomas and paragangliomas arise from chromaffin cells and produce excessive catecholamines. Hypertension is their primary clinical symptom. they differ in their catecholamine secretory phenotype; paragangliomas typically secrete norepinephrine, while pheochromocytomas typically secrete epinephrine. Here, we present a case 21-year-old male with pheochromocytoma with elevated norepinephrine but normal epinephrine levels.Case presentationA 21 -year-old male with no past medical history presented with episodes of palpitations, sweating, and elevated blood pressure. He also reported abdominal pain. On admission, his blood pressure was 143/92 mmHg, pulse was 71/min, respiration was 16/min, and oxygen saturation was 100% in room air. The rest of physical exam was not significant. His electrolyte panel was normal. Computed tomography (CT) abdomen and pelvis with contrast was performed and showed a right adrenal mass measuring 4.9 x 4.0 x 6.5 cm which is predominantly hypoattenuating (approximately 30 Hounsfield units) with thick nodular rim of enhancement. Hormonal workup showed normal serum testosterone, DHEA-S, AM cortisol, ACTH, aldosterone, plasma metanephrine, and urine metanephrine, but profoundly high plasma normetanephrine 3641.6 (0.0-210.1) pg/mL. His 24-hour urinary normetanephrine was elevated at 14874 (80-440) ug/24hr, confirming a pheochromocytoma. The high norepinephrine level in the setting of normal epinephrine raised suspicion for Von Hippel Lindau (VHL). He was started on alpha and beta blockage and had laparoscopic removal of the right adrenal gland. The pathology report confirmed the diagnosis of pheochromocytoma confined to right adrenal. The patient was then referred for genetic testing. Conclusion: Pheochromocytoma can be a part of familial disorders, although being sporadic in nature most of the time. As demonstrated in our case, the hallmark of pheochromocytoma associated with VHL is nearly exclusive normetanephrine secretion and a high ratio of normetanephrine to metanephrine. Confirmation and testing of genes aid in proper monitoring and follow-up. The preferred course of treatment is radical resection. Presentation: 6/2/2024

  PublisherDOI

• Phenotyping lipid profiles in type 2 diabetes: Risk association and outcomes from the Cardiovascular Health Study

  American Journal of Preventive Cardiology · 2024-08-26 · 2 citations

  articleOpen access1st authorCorresponding

  To determine whether discrete lipid profiles (refer to as lipid phenotyping) can be used to stratify cardiovascular risk in individuals with type 2 diabetes. Cardiovascular Health Study participants with diabetes and fasting lipid profiles at baseline ( n = 866) were categorized separately by level of LDL cholesterol and HDL-C/Triglyceride (Tg) profiles (low Tg/high HDL-C; high Tg/low HDL-C; high Tg only or low HDL-C only). We performed Cox multivariate regression analysis to assess the risk of CVD mortality, incident myocardial infarction (MI), heart failure (HF), stroke, and composite MACE (MI, HF, stroke, and CVD mortality) associated with each lipid category. We also calculated risk estimates for MACE using lipid measures as continuous variables. In the fully adjusted model, the high triglyceride plus low HDL-C cholesterol phenotype demonstrated risk that was at least as high as the highest LDL-C sub-group phenotype for CVD mortality (Hazard ratio {HR} 1.58 vs 1.48), MI (HR 1.53 vs 1.58), HF (HR 1.47 vs 1.20), stroke (HR 2.02 vs 1.43), and MACE (HR 1.58 vs 1.38). When modeled continuously, the HR per SD for MACE was 1.12 ( p = 0.03) for LDL-C and 1.19–1.20 ( p < 0.001) for triglycerides or remnant cholesterol. Participants with the high triglyceride/low HDL-C phenotype had equivalent or higher CVD risk than those with the high LDL-C phenotype. Further studies are necessary to determine whether lipid phenotyping accounts for the substantial CVD risk not explained by LDL cholesterol among individuals with type 2 diabetes.

  PublisherDOI

• Editorial: 21st century advances in type 1 diabetes research and immunotherapy

  Frontiers in Immunology · 2023-05-12

  editorialOpen access1st authorCorresponding

  The immunology of human type 1 diabetes (T1D) is complex and lacks detailed understanding. Rodent models of disease recapitulate certain molecular and genetic aspects of human disease but have not yielded high quality molecular targets to prevent or reverse progressive pancreatic beta-cell destruction. The predominant paradigm for the past 30 years of hypothesis-driven research is that a handful of carefully identified auto-antigens (both beta-cell specific and non-specific) might be able to induce tolerance in individuals at high risk for developing T1D (typically first-degree relatives of T1D subjects who have multiple T1D autoantibodies). Tolerance induction has been used successfully for decades in allergy immunotherapy, but so far has not been translated over to T1D. Such studies include major immunotherapy trials with insulin, insulin peptides, and glutamic acid decarboxylase 65 (GAD; a major T1D autoantigen). New research suggests that immune-mediated T1D might not follow a single molecular roadmap but develops through a variety of derangements culminating in beta-cell destruction. Moreover, novel neoantigens have been discovered with enhanced T-cell reactivity that might prove to be better for inducing tolerance. While antigen-specific immunotherapy for T1D has yet to demonstrate clinical success, autoantibodies continue to be useful tools for identifying at risk individuals and T1D subtypes.In this special issue of Frontiers, Peng and colleagues define three subtypes of diabetes in their large multi-institutional Chinese cohort: latent autoimmune diabetes in youth (LADY; age between ≥15 to <30 years, no ketoacidosis and insulin independence for 6 months, disease duration < 1 year, and autoantibody positive with either GAD, IA-2A, or ZnT8A), latent autoimmune diabetes in adults (LADA; age >30 years, no ketoacidosis and insulin independence for 6 months, disease duration <1 year, and autoantibody positive with either GAD, IA-2A, or ZnT8A) and type 2 diabetes (>30 years, disease duration <1 year, and autoantibody negative). Using epitope specific GAD assays that identified Cterminal, Middle region, and N-terminal autoantibodies, they determined that young T1D (<15 years), LADY, and old T1D (≥15 and <30 years) subjects had higher reactivity to multiple GAD epitopes than LADA patients. Moreover, T1D and LADY subjects had more high-risk susceptibility alleles for disease than LADA subjects. The authors suggest that different immune activity exists between T1D and LADA subjects https://doi.org/10.3389/fimmu.2022.836952.LADA has been defined primarily in Caucasian populations, but less so in Asian populations. With a population of ~ 1.4 billion people, China has a growing number of individuals with diabetes. Qiu and coauthors performed a systematic review of epidemiology, clinical characteristics, genetics, and immunology of LADA in this growing Chinese population. Importantly, they note that high risk allele HLA DR9/DR9 in Chinese LADA contrasts the well-established DR3/DR4 in Caucasian populations. In addition, GAD antibody positivity was only ~75% in Chinese LADA subjects compared to 90-95% in Caucasian disease. Additional features of LADA in China are well described including clinical manifestations and treatment options https://doi.org/10.3389/fimmu.2022.977413. Pathogenic effector T-cells (both CD4 + and CD8 + ) infiltrate the pancreatic islets in T1D. Identification of autoantigens that stimulate pathologic T cells has become a highly valued research endeavor. Li and colleagues used NOD mice as a T1D model to demonstrate the utility of a novel monoclonal antibody that targets the highly diabetogenic islet amyloid polypeptide (IAPP) K20. The K20 peptide is formed from IAPP that undergoes post-translational modification through a disulfide bridge between two cysteine residues and thereby becomes an autoantigen for the diabetic T cell clone BDC 5.2.9. LD96.24 is a monoclonal antibody that recognizes the IA g7 -K20 disulfide loop thereby blocking its interaction with the BDC T cell receptor. When prediabetic and newly diabetic NOD mice were treated with this monoclonal antibody disease prevention was sustained for the treatment duration https://doi.org/10.3389/fimmu.2022.877022.The B-chain of insulin (amino acid sequence B:9-23) has been considered a predominant autoantigen in T1D. Wenzlau and Haskins present exciting new data about a post translational modified (PTM) hybrid insulin peptide (HIP) called HIP6.3 that results from the fusion of insulin B:9-23 with a ProSAAS sequence (ProSASS is an endogenous inhibitor of prohormone convertase). When used in a stimulation assay with the highly diabetogenic T cell clone BDC-6.9, this neoantigen generated a 4 to 5-fold increased interferon-gamma response. This neoantigens generates more inflammation and immunity in T1D than conventional antigens https://doi.org/10.3389/fimmu.2022.926650.Under appreciated is the role of lymphotoxins (LTs) in immune inflammatory disease. Liu and Wang provide a comprehensive overview of LTs and their indirect role in cytotoxicity towards pancreatic beta cells. LTs mediate formation of tertiary lymphoid organs that are seen in NOD mice and perhaps play a role in T cell recruitment to the pancreatic islets https://doi.org/10.3389/fimmu.2022.917577.In addition, Yang and colleagues present an elegant and comprehensive review of post-translational modification (PTM) of proteins in autoimmunity and beta cell metabolism. This detailed publication provides a fundamental roadmap for understanding metabolic changes that create neo-antigens, alter Tcell metabolism, and improve biomarker sensitivity in T1D and autoimmune conditions. Highlights include detailed explanations of peptide citrullination, T-cell transition from oxidative phosphorylation to glycolytic metabolism, and PTM of novel T1D biomarkers. This is a must read https://doi.org/10.3389/fimmu.2022.1028130.Turning to clinical correlates between effector T cells and T1D progression, T cell metabolism was assessed in T1D subjects over 36 months. Complex interactions occur between cellular metabolism of glucose or fatty acid and T cell function. Simplistically stated, effector T cells have increased autoreactivity when their metabolic program uses glucose rather than fatty acids. Tang and associates evaluated glucose and fatty acid metabolism in CD4 + and CD8 + T cells from 86 Chinese T1D subjects and 45 non-diabetic controls and followed them for 3 years. T1D subjects with low T cell glucose uptake at entry maintained higher c-peptide levels and beta cell function compared to those individuals with high glucose uptake. Therefore, T-cell metabolism now appears to be an important component of sustained autoimmunity in T1D https://doi.org/10.3389/fimmu.2022.897047.Last, the bacterial flora in the gut plays an important role in T1D susceptibility through host-microbe interactions. Studies in monozygotic twins show discordance in T1D development which suggests that non-genomic factors play a role in the disease. It is proposed that altered microbiome in the gut leads to proinflammatory responses through numerous mechanisms including direct signaling from bacterial metabolic products to receptors that regulate immune responses in the human host. Therefore, one twin might have a different microbiome than the other twin and perhaps, a different immune system response. Host-microbiota interactions in T1D is extensively reviewed by Majumdar and Bettini as a capstone for this special edition https://doi.org/10.3389/fimmu.2022.974178.

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• Abstract #1399358: Treatment of Familial Tumoral Calcinosis with Acetazolamide Plus a Phosphate Binder

  Endocrine Practice · 2023-05-01

  article
  PublisherDOI

Recent grants

• NIH Grant R21DK063351

  NIH · $821k · 2006

Frequent coauthors

• Melissa Scollan‐Koliopoulos

  Sacred Heart University

  30 shared

• Heberth Moran

  Rutgers New Jersey Medical School

  24 shared

• William C. Gause

  Rutgers, The State University of New Jersey

  21 shared

• George S. Eisenbarth

  20 shared

• Simge Yuksel

  Rutgers New Jersey Medical School

  20 shared

• Richard A. Jackson

  University of Liverpool

  18 shared

• Maya Raghuwanshi

  18 shared

• Kenneth J. Rapp

  Rutgers, The State University of New Jersey

  18 shared

Education

• M.D.

  New York Medical College

  1983

• B.A.

  Haverford College

  1979

Awards & honors

• American Diabetes Association leadership roles
• Juvenile Diabetes Research Foundation International leadersh…
• Department of Defense Diabetes Grant Review