scholarly journals SAT-676 Pembrolizumab Induced Worsening Glycemic Control and DKA in Type 2 Diabetes Mellitus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sarita Goud ◽  
Yu Yu Thar

Abstract INTRODUCTION Pembrolizumab(Keytruda) is a humanized IgG4 anti-programmed cell death-1 (PD-1) antibody serving as an immune-checkpoint inhibitor, now approved by FDA to treat several types of cancer. Although there are few reported cases of pembrolizumab induced new onset DKA in a non diabetic patients due to its autoimmune nature, its association in worsening glycemic control and DKA in pre-existing type 2 Diabetes mellitus is not well established. CASE 79 years old female with past medical hx of DM type 2 (Hba1c 7.4 was started on metformin), COPD(on chronic steroids and trilogy machine at home), recently diagnosed with poorly differentiated adenocarcinoma of the left lung, metastasis to liver, PDL 1 positive at 99%, started on palliative chemotherapy with Keytruda, 2 weeks after the third cycle of keytruda presented to the ED for AMS. Patient noted to be very dehydrated, somnolescent and tachypnea. Labs consistent with sugars > 600, potassium 6.8, Bicarb 5, Anion gap 33, beta hydroxybutyrate 11.5 (on 7/15/19 0.6), HbA1c 9.7,(On 12/15/16 7.3, 9/25/18 6.7, 1/22/19 7.4). PH 7.31, lactate 2.4. WBC count 21.5- no infectious source identified (CXR, CT brain, UA clean). Patient was admitted for DKA and treated with IV insulin and IV fluids. After medically stable patient was discharged with Insulin regimen. Within 5 days after being discharged, patient presented to ED again with DKA with PH 7.27, Bicarb 8, anion gap 22, sugars>600, beta hydroxybuterate 13.70. Patient was Rx for DKA- after a week of hospitalization was discharged to Hospice(due to metastatic cancer) and few weeks later expired.To summarize, pt with well controlled type 2 DM on metformin presented with frequent DKA 2 weeks after treatment with third cycle of keytruda leading to worsening glycemic control in-turn making patient Insulin dependent. CONCLUSION Incidence of Type 1 DM with pembrolizumab treatment is being increasingly recognized and reported, and DKA is a common initial presentation. However we need further studies to establish the mechanism of worsening glycemic control leading to Insulin dependent and DKA in patients with pre-existing type 2 diabetes. Also, physicians should counsel patients about this potential immune related adverse effect and educate them about the symptoms of hyperglycemia and DKA. REFERENCES Immune checkpoint inhibitors and type 1 diabetes mellitus: a case report and systematic review Jeroen M K de Filette1, Joeri J Pen2, Lore Decoster3, Thomas Vissers4, Bert Bravenboer1, Bart J Van der Auwera5, Frans K Gorus5, Bart O Roep6,7, Sandrine Aspeslagh3, Bart Neyns3, Brigitte Velkeniers1 and Aan V Kharagjitsingh1,2,5,8 Immune checkpoint inhibitors: an emerging cause of insulin-dependent diabetes. Anupam Kotwal1, Candace Haddox2, Matthew Block3, Yogish C Kudva1. BMJ open Diabetes and research, Vol 7, issue1.

1999 ◽  
Vol 46 (5) ◽  
pp. 425-435 ◽  
Author(s):  
Mary de Groot ◽  
Alan M Jacobson ◽  
Jacqueline A Samson ◽  
Garry Welch

Author(s):  
Ilda Maria Massano-Cardoso ◽  
Fernanda Daniel ◽  
Vítor Rodrigues ◽  
Ana Galhardo

Objective: The current study assessed depressive symptoms in Type 1 Diabetes Mellitus (T1DM) and Type 2 Diabetes Mellitus (T2DM) patients and explored whether these symptoms were associated with glycemic control. Methods: A cross-sectional design was used. Patients attending diabetes consultations participated in the study (N = 347). Participants completed the Beck Depression Inventory (BDI), and glycemic control was based on A1C criteria. Results: The mean score on the BDI, for either T1DM or T2DM, was not clinically significant and was not associated with diagnosis duration. The association between depression and glycemic control was significant in both DM types. T2DM participants presenting more depressive symptoms were those with greater glycemic control. T1DM and T2DM differences regarding depressive symptoms were in somatic symptoms. Conclusions: In T2DM depressive symptoms may be confounded with DM physical consequences. There is also the possibility that negative mood plays a mediating role in mobilizing survival strategies that promote glycemic control. Furthermore, the assessment of depressive symptomatology in patients with diabetes could benefit from the availability of a disease-specific measure.


2021 ◽  
pp. 875512252110557
Author(s):  
Anna Kabakov ◽  
Andrew Merker

Objective: The various basal insulin products possess differences in pharmacokinetics that can significantly impact glycemic control and total daily basal insulin dosing. In addition, there will be instances where transitions between the different long-acting insulins will need to be made. Because every basal insulin product is not interchangeable on a 1:1 unit-to-unit basis, it is important for health care providers to understand the expected dose adjustments necessary to maintain a similar level of glycemic control. Data Sources: A Medline and Web of Science search was conducted in September 2021 using the following keywords and medical subjecting headings: NPH, glargine, detemir, type 1 diabetes mellitus, and type 2 diabetes mellitus. Study Selection and Data Extraction: Included articles were those that followed adult patients with type 1 diabetes mellitus and/or type 2 diabetes mellitus and compared the following types of insulin: “NPH and glargine,” “NPH and detemir,” and “glargine and detemir” for at least 4 weeks, had documented basal insulin (BI) doses, and excluded pregnant patients. Data synthesis: Twenty-five articles were found that include adult type 1 and/or type 2 diabetes mellitus patients. Once daily NPH can be converted unit-to-unit to glargine or detemir. Twice daily NPH converted to glargine or detemir requires an initial 20% reduction in BI dose. An increase in dose of BI is recommended when transitioning from glargine to detemir. Glargine and detemir consistently resulted in improved glycemic control with lower incidence of hypoglycemic events compared with NPH. Conclusions: When transitioning between long-acting insulins, the doses are not always interchangeable on a 1:1 basis. Unit dose adjustments are likely if transitioning between BIs and can influence short-term parameters in the acute care setting and long-term parameters in the outpatient setting.


2010 ◽  
Vol 16 (4) ◽  
pp. 264-275 ◽  
Author(s):  
Joseph Menzin ◽  
Jonathan R. Korn ◽  
Joseph Cohen ◽  
Francis Lobo ◽  
Bin Zhang ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A363-A363
Author(s):  
Bakr Swaid

Abstract Introduction: Diabetes mellitus have been reported in around 1% of patients receiving immune checkpoint inhibitors (ICI) resultingin immune checkpoint inhibitor induced diabetes mellitus (ICI-DM). 4 phenotypes of ICI-DM exist: acute autoimmuneinsulin-dependent diabetes, decompensation of prediabetes or type 2 diabetes, autoimmune pancreatitis, andautoimmune lipoatrophy. Clinical Case: A 52-year-old man was diagnosed with stage IIIb malignant melanoma. Two months following local excision, he wasstarted on nivolumab every 4 weeks planned for 1 year. His past medical history was significant for prediabetes,hypertension, obesity (BMI 33.27 kg/m²), primary hypogonadism, adult attention deficit disorder, obstructive sleepapnea, gastric ulcer, and gastroesophageal reflux disease. He denied tobacco use but reported semi-daily use ofmarijuana and alcohol. His baseline HbA1c was 6.0%. After the 8th cycle of nivolumab, he reported several bloodglucose readings in the 200 mg/dL range. He was thought to have progressed to type 2 diabetes and metformin wasstarted. Glipizide was added shortly thereafter due to persistent hyperglycemia. At the 9th cycle of nivolumab, hisHbA1c was 8.2%. In 1 week from this time, the patient developed abdominal pain, nausea, and persistent vomiting. Hewas found to be in DKA with blood glucose of 278 mg/dL, bicarbonate of 9.3 mmol/L, anion gap of 21, and arterial pHof 7.22. He was treated in the ICU per standard DKA care. His C-peptide was 0.5 ng/mL (reference 0.8–3.5) withconcomitant plasma glucose of 229 mg/dL. Autoantibody screening was negative including glutamic aciddecarboxylase antibody (anti-GAD), insulin antibody, insulin antigen-2 (IA-2) autoantibody, and zinc transporter 8antibody. The patient was discharged home on multiple daily injections of insulin but he struggled with diabetes carewhich proved to be of brittle nature requiring CGM use. Two months after completion of nivolumab treatment, thepatient reported epigastric abdominal pain with frequent nausea and occasional vomiting of few weeks duration. He wasdiagnosed with subacute pancreatitis based on symptoms and elevated lipase. There was no evidence of gallstones. Although immunotherapy-related pancreatitis was considered, we decided to try alcohol cessation first hoping to avoidthe need to use prednisone. Over several weeks, lipase normalized and his symptoms completely resolved. Conclusion: In this case, nivolumab resulted in progressive beta-cell failure and complete insulin dependence in a person with ahistory of prediabetes. Not all pancreatitis cases in the settings of immunotherapy use are immune-related adverseevents (irAE). Usual causes, e.g. alcohol, should still be considered. With cessation of alcohol, pancreatitis fullyresolved leading to avoidance of prednisone which would likely have worsened diabetes management in this patientwith brittle diabetes.


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