ResearchPad - diabetes-complications-ii Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[MON-667 Prevalence and Predictors of Diabetic Retinopathy Among Type 2 Diabetes Patients at a Tertiary Care Center]]> Objective: Diabetic retinopathy (DR) is one of the most common microvascular complications of type 2 diabetes (T2D). The reported prevalence of DR from different populations in the last decade was 13 - 38.1%. A report from our center 17 years ago showed that DR prevalence was 43.6%. With the all accumulated evidence showing that diabetes control decreases DR risk and the introduction of new drugs that helped better T2D control, we aimed to assess the current prevalence and predictors of DR among patients with T2D attending out-patient department at our tertiary care center. Methods: We conducted a cross-sectional study involving 638 patients. We collected information about their baseline characteristics, confirmed DR with its severity and maculopathy diagnosis, age at T2D diagnosis, duration of T2D, and averages of HbA1C, blood pressure (BP), cholesterol, and vitamin D levels over the previous year. A statistical analysis was performed using the software SPSS 23.0. A multivariate logistic regression analysis examined the independent predictors of DR development. Results: The mean age of the patients was 55.8 ± 10.3 years, and 42.8% were males. The mean BMI was 32.4 ± 12.4 kg/m2 with 58% had obesity. The mean duration of T2D was 11.5 ± 7.7 years, and the mean age at T2D diagnosis was 44.0 ± 9.98 years. The mean HbA1C was 8.3 ± 1.6 % with 77% had average HbA1C above 7% and 51.3% had average HbA1c above 8%. The mean systolic and diastolic BP were 136.37 ± 15.01 mmHg and 74.12 ± 8.078 mmHg, respectively. DR was diagnosed in 223 cases (35%). Of the 638 patients, 24.5% had non-proliferative DR, 9.2% had proliferative DR, and 4.2% had maculopathy. There was no significant difference in DR prevalence between males (36%) and females (34.1%) (P = 0.59). Predictors of DR development were age above 40 years, duration of T2D more than 10 years, early age of T2D diagnosis, average HbA1C more than 8%, and hypertension. Discussion: T2D is a major health challenge to our community with its very high prevalence. The prevalence of DR in T2D patients attending our institution was significant (more than one-third, 35%) in comparison to reports from other centers. However, we showed an improvement in DR development in our patients from 43.6% to 35%, probably due to better T2D and BP control. Similar to previous reports, T2D patients with older age, long T2D duration, younger age at T2D diagnosis, uncontrolled diabetes, and uncontrolled BP were more likely to develop DR. Conclusion: Physicians treating T2D patients should ensure regular retina screening especially for those with risk factors for DR. Also, they should fix the modifiable risk factors of DR; diabetes and BP control. References: (1) Alaboud et al. Saudi Med J 2016; Vol. 37 (12): 1408–1411.doi: 10.15537/smj.2016.12.17062. (2) Lim MC et al. Ann Acad Med Singapore. 2008 Sep;37(9):753–9. (3) Hammes H-P et al. PLoS ONE 10(7): e0132492. doi:10.1371/journal. pone.0132492

<![CDATA[MON-689 Diabetes Mellitus---Hypoglycemic Response---Empyema]]> Diabetes mellitus---hypoglycemic response---empyema

Case report

A 65-year-old woman was admitted to our department due to high blood glucose for two days on February 29, 2016. Fasting blood glucose was 12.53mmol/L on February 28 without polydipsia, polyuria, polyphagia and weight loss.

In the past medical history, she started to cough in January 2016. On February 2, the routine blood examination showed that white blood cells and neutrophils were higher than normal. Chest X-ray was normal. Moxifloxacin was given and symptoms were relieved slightly.

On examination, the temperature was 36.9℃. Auscultation of the chest was normal. On the evening of admission, body temperature rose to 37.8 C. On March 1st, white cell, neutrophil, erythrocyte sedimentation rate and C-reactive protein were increased. FBG was 10.5mmol/L, and HbA1c was 10.5%. Chest CT was normal. Piperacillin Tazobactam Sodium and Moxifloxacin were given, and insulin was used to lower blood glucose.

On March 2, body temperature was normal. And palpitation, tremor, sweating, fatigue and cold extremities appeared several times. Blood glucose test ruled out hypoglycemia. The above symptoms appeared again at around 4 pm, more serious than before. Gas analysis at 5:12pm showed PH 7.403 and lactic acid 19.27mmol/L. At 6:00pm, blood pressure started to drop. Vasoactive drug was given. In gas analysis at 6:27pm, PH was 7.237, lactic acid 21.05mmol/L. 5% NaHCO3 solution was given to buffer acidosis. Cardiac and respiratory arrested during transferring to ICU. Undergoing cardiopulmonary resuscitation, vasoactive drugs and ventilator-assisted breathing were applied. Hemodialysis was used to counteract lactate acidosis. The bedside chest radiograph showed that the transmittance of left lung was decreased. On March 3, the transmittance of left lung was lower. Doctors prescribed Tylenol and Vancomycin. On March 4, left thoracic puncture and catheterization were performed. The pus was drained out and bacterial cultures were made. Klebsiella pneumoniae was cultured. Sensitive antibiotics therapy was chosen according to pleural cultures. On March 9, left empyema was removed and pericardial fenestration was performed by thoracoscope under general anesthesia. Nutritional support had been given. The patient gradually recovered and was discharged on April 9.


Palpitation, tremor, sweating and fatigue were the first manifestations of the condition change in this diabetic patient. The condition rapidly developed into septic shock and empyema. After active treatment, she was cured and discharged from hospital. Besides hypoglycemia, other diseases such as septic shock also may cause the symptoms of sympathetic excitation, which should be considered in order to avoid delaying the time of treatment. Furthermore, diabetic patients complicating with infection should be actively treated with effective antibiotics.

<![CDATA[MON-668 The Content of Serum Clusterin in Patients with Diabetic Macular Edema Depending on the Kind of Glucose Lowering Therapy]]> Relevance. Insight into the pathophysiology of diabetic macular edema (DME) has led to novel treatments, including anti-VEGF, corticosteroid-based treatment strategies and novel therapies, such as a clusterin blood retina barrier (BRB) cytoprotection. It has been shown the protective effect of clusterin on oxidative stress-induced cell death and its emerging roles in reduction of both BRB breakdown and neural retina damage. Goal. To assess the content of serum clusterin in patients with type 2 diabetes (T2D) and diabetic macular edema depending on the type of glucose lowering therapy. Material and methods. This study was conducted in 82 patients with T2D and DME. The average age of patients was 65.25 ± 10.85 years (±SD) [25; 84], the average duration of diabetes was 14.0 ± 7.05 years (±SD) [1; 35], the average level of HbA1c was 8.40 ± 1.58% (±SD). The criteria for inclusion in the open study was voluntary informed consent, age 18 years and more, the presence of T2DM. Non-inclusion criteria were the presence of endocrine diseases, which can lead to type 2 diabetes, T1D, acute infectious diseases, cancer, decompensation of comorbid pathology, mental disorders, antipsychotics, antidepressants, neurodegenerative diseases of the central nervous system, proteinuria, damage to the optic nerve, glaucoma and mature cataracts. 43 patients received oral glucose lowering drugs (OGLD: sulfonylureas, biguanides), 39 patients received insulin therapy. All patients had instrumental ophthalmological examinations. The concentration of serum clusterin was measured by «Human Clusterin ELISA» kits. Statistical analysis was performed by one-way ANOVA analysis. Results. A study of level variability of blood clusterin in patients with DME showed its dependence from the type of glucose lowering therapy. Comparison of mean values of strum clusterin in patients with DME and T2DM revealed the following statistically significant differences: OGLD 87,08 ± 3,15 mcg/ml [95% CI 82,63 - 91,54 mcg/ml]; insulin therapy 74,79±2,98 mcg/ml [95% CІ 70,58 - 78,99 mcg/ml] (р=0,006). Apparently, clusterin is involved in the pathogenesis of DME and may have a potential in reducing of the pathogenic effect of diabetes on the neurovascular unit. The data obtained make it possible to discuss the neuroprotective role of clusterin in DME with the use of voiced oral hypoglycemic drugs, which usually prescribe for patients with mild form of T2D or for the patients with moderate severity T2D (i. e. at the initial stages of development of diabetes). Conclusion. Against the background of glucose lowering drugs in patients with type 2 diabetes and diabetic macular edema statistically significant (р=0,006) increases the content of serum clusterin compared to insulin therapy.

<![CDATA[MON-701 Uncontrolled Diabetes Presenting as Isolated Sixth Nerve Palsy]]> BACKGROUND Our case report demonstrates acute onset of diplopia due to Isolated Sixth Nerve Palsy (ISNP) secondary to uncontrolled T2DM, presenting as an ophthalmoplegia. The most frequent one, is ISNP with an incidence of 11.3/100.000 1. Vasculopathic ISNP is associated with atherosclerosis in patients older than 50 years 1.

CASE PRESENTATION A 63 year-old male with history of T2DM, HTN, HL, came for evaluation of acute onset double vision 3 days prior. He noted diplopia while attempting to park his car; he saw that tracking to the left with his eyes would elicit double vision. Denied recent travel, trauma, headache or dizziness. He was awake and alert, BP 200/110mmHg, BMI 33. No pathologic murmur. He had PERRLA bilaterally but impaired lateral rectus muscle movement on the left side. Otherwise, EOMI on the right side. No facial asymmetry or ptosis. Overall, findings positive for ISNP. BMP only remarkable for a glucose of 297, HA1c was 10.0. Head CT was negative for any acute intracranial abnormality. Orbital MRI did not show acute infarction or masses. Patient was admitted for acute diplopia due to ISNP. Differential diagnoses were neoplasm, migraine, MS and diabetic neuropathy. Based on the aforementioned data, we suggested that T2DM was the probable cause. Counseling on improving glycemic control was given. Unfortunately, patient was lost to follow up. DISCUSSION ISNP remains an elusive entity; atherosclerotic risk factors such as DM, HTN, HL, hyperhomocysteinemia 2 or viral infections 3 have been reported in association. This type of palsy seems to be more frequent in children and can be recurrent in nature.

In adults, the most likely cause of ISNP seems to be ischemic mononeuropathy or more aggressive etiologies such as temporal arteritis 4. Inconclusive images prove even a higher diagnostic challenge 3. Of note, we found a case demonstrating evidence for Eicosapentaenoic Acid in the improvement of ISNP with recovery in as shortly as 8 weeks. The basis of this treatment lies in the recovery of endothelial function focusing on the anti-platelet and anti-inflammatory effects of the drug2,4. REFERENCES (1). Elder, Christopher, et al. “Isolated abducens nerve palsy: update on evaluation and diagnosis.” Current neurology and neuroscience reports 16.8 (2016): 69. (2). Takenouchi, Yasuhiro, et al. “Eicosapentaenoic acid ethyl ester improves endothelial dysfunction in type 2 diabetic mice.” Lipids in health and disease 17.1 (2018): 118. (3). Azarmina, Mohsen, and Hossein Azarmina. “The six syndromes of the sixth cranial nerve.” Journal of ophthalmic & vision research 8.2 (2013): 160. (4). Yanai, Hidekatsu, and Mariko Hakoshima. “Eicosapentaenoic Acid for Diabetic Abducens Nerve Palsy.” Journal of Endocrinology and Metabolism 7.4 (2017): 131–132.

<![CDATA[MON-683 Assessment of Features Associated with Diabetic Foot Risk in General Hospital in Lima-Peru]]> Objectives: To determine the frequency of diabetic foot risk of ulceration and associated factors in patients with type 2 diabetes mellitus.

Methods and materials: We used a cross-sectional descriptive design. Data collection was performed in the foot at risk office at Maria Auxiliadora hospital over a period of 3 years, dating from the october 2016 to september 2019.

Foot risk assessment was based on the International Working Group of Diabetic Foot (IWGDF) system, which evaluates peripheral neuropathy (with monofilament or tuning fork), biomechanical deformity, peripheral arterial disease (altered pulse or ankle branchial index) or a history of foot ulcer1,2. Foot risk frequency was found according to epidemiological characteristics, and the prevalence ratios with 95% confidence interval were calculated to association analysis, we perform bivariate and multivariate analysis using a generalized linear model. This study has the approval of the María Auxiliadora HospitaĹs Ethics Committee.

Results: a total of 402 subjects were included in this study, 63.3% were women, average age 62 yo and diabetes duration <10 years in 56%. 76.6% presented risk to develop ulcer, of which 54.7% presented biomechanical deformation, 37.3% Peripheral Neuropathy (NP), 35.4% Peripheral Arterial Disease (PAD), and 12.7% history of foot ulcer. Patients with foot at risk were associated with older age (RP 1,006, 95% CI 1,001-1.01), and with a score> 5 with respect to <5 in the Total Symptom Score (RP 1.26, 95% CI 1.05-1.51).

Conclusions: 3 of 4 patients have a foot at risk of ulceration, predominantly due to biomechanical deformation and peripheral neuropathy, and this risk was associated with older age and greater pain symptomatology.


1. Bakker K, Apelqvist J, Schaper NC. Practical Guidelines on the management and prevention of the diabetic foot 2011. International Working Group on the Diabetic Foot Guidelines. Diabetes Metab Res Rev. 2012; 28(1):225-231

2. Peters E, Lavery L. Effectiveness of the Diabetic Foot Risk Classification System of the International Working Group on the Diabetic Foot. Diabetes Care. 2001 24:1442–7.

<![CDATA[MON-693 Strongyloides Stercoralis Hyper Infestation Syndrome in Type 2 Diabetes: An ANCA Positive Case Report from India]]> A 53-year old male patient with T2D and hypertension for 13 years, presented to Apollo Sugar Clinic, Raipur with recurrent abdomen pain, but no vomiting, constipation, diarrhea or fever. The patient has a past history of asthmatic bronchitis, recurrent eosinophilia, and one month prior to hospitalization, recovered from erythematous maculopapular serpentine rash measuring 6.0 x 1.5 cm over the abdomen post anti-allergic treatment. The patient was neither suffering from immunosuppressive condition nor was on immunosuppressant therapy, had normal vitals but the laboratory findings revealed high total leukocyte count and raised absolute eosinophil count (52%). The provisional diagnosis was made as hypereosinophilic enteritis in a long-standing T2D and hypertension. Immunological tests antinuclear antibody (ANA) and antineutrophil cytoplasmic antibodies (ANCA) resulted in positive ruling out vasculitis. Stool examination detected rhabditiform larvae of S Stercoralis and diagnosed as Strongyloides hyper infestation syndrome. The patient was managed with IV antibiotics, IV fluids, IV insulin and when abdomen pain reduced started with the oral diet. To remove larvae load, unlike routine treatment, the patient was put on albendazole and ivermectin for three consecutive days. After 15 days follow-up patient was completely asymptomatic; at 6 weeks TLC, stool test, ANCA and ANA titer were negative indicating no parasite load. These antibodies detected could be due to molecular mimicry triggered by parasite antigens which may help in diagnosing and monitoring the disease course. ANA and ANCA positive results have been rarely reported in the past for S stercoralis. This unique case of S stercoralis infestation in T2D may enlighten the health care physicians to investigate for this infestation in immunocompromised T2D patients with pain abdomen. Precise diagnosis with timely management can prevent steroid therapy due to eosinophilic enteritis which can be harmful to the patients.

<![CDATA[MON-707 Improving Screening for Diabetic Retinopathy in a Resident Based Clinic]]> Introduction Diabetic retinopathy is the leading cause of blindness in US Adults. In order to improve screening rates, we partnered with the Division of Ophthalmology and installed an onsite retinal camera at our primary care clinic. This led to an improvement in EMR reported screening rates from 20.5% to 44% over the first 3 months. We noticed that any fundus photo, whether gradable or not, led to an automatic annotation in EMR (EPIC) health Maintenance that screening had been completed. Abnormal or ungradable (quality too poor to interpret) retinal photos must be followed up with a complete ophthalmologic evaluation. We designed a chart audit to investigate further whether ungradable retinal photos were being followed up appropriately. Methods A retinal camera was installed in the clinic, and patients obtained DR screening during their routine visits from May through October 2018. The nursing staff received training on using the camera and ensuring image quality. These images were then sent to an Ophthalmologist and resulted within the work week. Patients with an abnormal or poor-quality retinal photo were contacted by their resident PCP. We did a retrospective chart review of patients with ungradable photos evaluating whether patients were contacted and whether they followed up with Ophthalmology in the 3 month period after the initial intervention. Results Of the 131 patients who received fundus photos in the study period, 29 (22%) had ungradable photos. Twenty-four of these patients were contacted and ophthalmology consults were placed for 22 patients. Eleven (38%) of these patients went on to complete screening with Ophthalmology within 3 months of the ungradable photo. Eighteen patients, or 62% of ungradeable photos, remained incorrectly identified as having completed retinopathy screening by EMR. Discussion Over reliance on EMR reporting features can lead to incorrect assumptions about DR screening. Based on this analysis, we need to design better interventions for following up on ungradable photos and ensuring appropriate follow up. One such intervention may be changing how EMR reports ungradable photos. EPIC is a widely used EMR in outpatient settings and other practices may be facing similar issues.

<![CDATA[MON-700 Protective Effects of Smoking? Improved In-Hospital Mortality in Smokers Admitted for Diabetic Ketoacidosis]]> PURPOSE: To determine the relationship between tobacco smokers and the rate of hospital readmission within 30 days, mortality, morbidity, and health care resource utilization in patients admitted to the hospital in the United States with diabetic ketoacidosis (DKA). METHOD: A retrospective study was conducted using the AHRQ-HCUP National Inpatient Sample for the year 2014. Adults (≥ 18 years) with a principal diagnosis of DKA and a secondary diagnosis of tobacco dependence or active smokers were identified using ICD-9 codes as described in the literature (1). The primary outcome was in-hospital mortality. Secondary outcomes include readmission rate, length of hospital stay (LOS), total hospitalization costs. Propensity score (PS) using the next neighbor method without replacement with 1:1 matching was utilized to adjust for confounders (2). Independent risk factors for readmission were identified using multivariate logistic regression model (3). RESULTS: In total, 186,824 hospital admissions with a primary diagnosis of DKA were identified, of which 32.44% (47,382) had TD. In-hospital morality among the smoking cohort (0.39%, SD 0.03) was lower than the non-smoking cohort (0.32%, SD 0.04) during the first hospitalization. Similar effects were observed after propensity match - 0.33% (SD 0.18) vs 0.27% (SD 0.03). The mortality rate during next hospitalization was also lower in the smoking cohort (0.72%, SD 0.03) in comparison to their counterpart (1.16%, SD 0.01). Smokers had a higher readmission rate of 17.6% (SD 0.57) than non-smokers (9.6%, SD 0.25). The length of stay among smokers and non-smokers were similar after propensity match - 3.12 days (SD 0.03) vs 3.06 days (SD 0.09), p=0.42, respectively. Total hospital cost was also similar between the two groups, $6,898 (SD $82) vs $7,100 (SD $203), p=0.32, respectively. Based on multivariate logistic regression, female and high Charlson comorbidity index were associated with higher 30-day readmission rate; whereas private insurance and high household income were associated with reduced readmission rate. CONCLUSION: Smoking has been associated with improved survival in patients with DKA (4). Previous studies have shown that glucose concentration were significantly lower at fasting and 120 min in current smokers than non-smokers. However, the effects of cigarette smoking on glucose metabolism and insulin resistance are still disputed.

<![CDATA[MON-685 Lipodystrophy, a Forgotten Syndrome]]> Background: Lipodystrophy comprises a group of heterogenous congenital and acquired disorders. These disorders may present as a complete or partial loss of adipose tissue. The magnitude of lipoatrophy correlates with the severity of the associated metabolic disturbances, which include severe insulin resistance, progressive liver disease, severe dyslipidemia, among others. The most prevalent form of lipodystrophy is related to antiviral use in patients with HIV. However, lipodystrophy occurring unrelated to medication side effect is often missed due to the heterogeneity and rarity of this disorder.

Clinical Case: 31 year old female with medical history of type 2 diabetes mellitus, hypertension, mixed dyslipidemia and polycystic ovarian syndrome who was referred to our clinics due to difficult to control hyperglycemia. Family history was limited. She was diagnosed with diabetes mellitus at 12 years old after presenting with polyuria, polydipsia and polyphagia requiring oral antidiabetic therapy. Following poor response, she was started on insulin therapy. At 23 years old, the patient had an episode of pancreatitis associated with hypertriglyceridemia and eruptive xanthomas. Insulin pump therapy with regular U-100 insulin, total daily dose of 308 units, was initiated but failed to improve glycemic control. The patient was referred to our Endocrinology clinics due to high insulin resistance and a glycosylated hemoglobin (A1C) at 12% (n < 6.5%). Physical examination revealed a body mass index of 23 kg/m2, abnormal fat distribution predominantly over the neck and face, and acanthosis nigricans. Abdominal ultrasound revealed fatty liver infiltration consistent with intrabdominal fat deposition. Due to the constellation of the aforementioned findings, the diagnosis of partial lipodystrophy syndrome was presumed. She was started on antidiabetic therapy with metformin, pioglitazone and insulin pump therapy with U-500 insulin, and high-dose statin therapy plus fenofibrate for dyslipidemia. At follow up, the patient showed improvement in glycemic control and an improved lipid profile. She was referred to a geneticist for evaluation.

Conclusion: Lipodystrophy syndromes are a group of heterogenous disorders, which may often be overlooked due to their rarity and lack of familiarity by physicians. The diagnosis of lipodystrophy is based on history, abnormal body fat distribution, and metabolic profile. The metabolic disturbances seen in these patients are mainly due to the lack of adipose tissue, which results in impaired energy storage. Early recognition of these syndromes is important because intensive treatment of hyperlipidemia and diabetes prevents development of severe complications. In this case we highlight this rare condition and the successful use of new therapeutic technology with insulin pumps and U-500 insulin in the glycemic control of a patient with lipodystrophy.

<![CDATA[MON-695 Multiple Recurrent Lipomatoses with Thiazolidinedione Therapy in Familial Partial Lipodystrophy, Dunnigan Variety (FPLD2)]]> Background: FPLD2, a rare autosomal dominant disorder due to heterozygous missense mutations in LMNA, is characterized by gradual loss of subcutaneous (sc) fat from the limbs starting during late childhood and predisposition to metabolic complications, such as diabetes, dyslipidemia and hepatic steatosis. Some patients, especially females, accumulate excess sc fat in the chin, neck, supraclavicular and perineal regions. We report disfiguring and disabling lipomatoses in unusual locations with thiazolidinedione therapy in two women with FPLD2.

Clinical Cases: A 57-year-old white female with FPLD2, due to heterozygous p.R482Q LMNA mutation, developed recurrent large lipomatoses in the axillae at age 33 years, and later in the posterior neck (buffalo hump), mons pubis and above sacrum. She developed diabetes at age 30 and was started on pioglitazone 45 mg daily, which was switched to rosiglitazone 8 mg daily at age 43 years. Supra-sacral lipomatoses were approximately 40 cm X 20 cm bilaterally and continued to grow despite lipectomy and multiple liposuctions. Rosiglitazone was stopped at age 56 years, and she reported no further increase in the size of lipomatoses. Her other medications included colesevelam, atorvastatin, metformin, glimepiride, lisinopril, losartan, hydrochlorothiazide, aspirin, insulin and dulaglutide. Her 54-year-old younger sister with FPLD2 (heterozygous p.R482Q LMNA mutation) was treated with lisinopril, metoprolol, atorvastatin, liraglutide, and insulin glargine and aspart, but no history of taking thiazolidinediones, and she never developed any lipomatoses. Another 43-year-old white female with FPLD2, due to heterozygous p.S583L LMNA mutation, was noticed to have lipomatous deposits in the axillae, medial gluteal region, labia and perineal regions. She developed diabetes mellitus at age 36 years and took metformin for 6 years and pioglitazone 30 mg daily for one year before she noticed the lipomatoses. Her other medications included atorvastatin, aldactone and vitamin D3. Pioglitazone was stopped and after one year, she reported reduction in the size of lipomatoses.

Conclusion: Thiazolidinediones are selective peroxisomal proliferator-activated receptor-γ agonists and induce weight gain by increasing fat mass, especially subcutaneous depots. Our cases suggest that thiazolidinediones can cause undesired growth of non-lipodystrophic adipose tissue in patients with FPLD2 and thus should be avoided.

<![CDATA[MON-679 What’s in a Bottle? the Importance of Careful Medication Review to Prevent Life Threatening Hypoglycemia]]> Background: Over 1 in 9 emergency department (ED) visits are due to drug-related adverse events (1) and careful medication review is essential for patient safety.

Clinical Case: A 73-year-old male presented to the ED after his family found him to be tremulous with a blood glucometer reading of 30 mg/dL. He was given glucagon and oral glucose however this did not help his blood glucose and he was brought in for further evaluation. He had a history of chronic kidney disease, hepatocellular carcinoma (HCC) and diabetes mellitus type 2 for which he was on no medication at the time of presentation. He reported being on Glipizide nine months ago. In the ED, he had a temperature of 98.3°F; pulse of 76 beats/min; respiratory rate of 18 breaths/min and blood pressure of 166/71. On physical examination, he was in no acute distress with normal neurologic, cardiac and respiratory exam. Laboratory workup was notable for glucose 40 mg/dL, HbA1c 5.0%, Cr 2.55 mg/dL, eGFR 24, ALT 7 IU/L and AST 23 U/L. CT abdomen and pelvis was consistent with known diagnosis of HCC. The patient was given 4 boluses of D50W and started on a continuous dextrose infusion along with octreotide infusion due to persistent hypoglycemia. Patient’s blood glucose improved one day later and he remained stable off the dextrose and octreotide infusions. Further laboratory evaluation revealed ACTH 9 pg/mL (ref 6-50), Random Cortisol 16.1 at 1:36pm, TSH 1.40uIU/ml, Free T4 1.09 ng/dL, Cosyntropin stimulation test at baseline 15.4 ug/dL; at 30 min 22 ug/dL; at 60 min 28.3 ug/dL and Beta-Hydroxybutyrate 0.11 mmol/L. With a blood sugar level of 32 mg/dL, he was found to have Insulin level 35.9 (ref 3.0-25.0mU/L), Pro-insulin 55.6 (ref &lt 18.8pmol/L) and C-peptide 9.21 (ref 0.8-3.85ng/mL). The patient’s family brought his medications for review with no clear discrepancies noted. Closer inspection of the tablets inside each pill bottle revealed that the pills inside the Docusate-Senna container did not match the description for the same but instead matched the description for Glipizide. The patient disclosed that he had emptied the Glipizide tablets into the bowel regimen container for “safe keeping” when it was discontinued. He was inadvertently taking two Glipizide tablets twice a day as the VNA had mistakenly used these pills to fill his pill box. This serious error in confirming the patient’s medications resulted in his severe hypoglycemia. His Sulfonylurea screen returned positive for Glipizide.

Conclusion: Sulfonylureas, an essential component of diabetes management, have a dangerous side effect of hypoglycemia and errors in its administration can be fatal. Therefore, thorough medication reconciliation and review of the actual pills is essential to prevent such errors.

Reference: Zed PJ, et al. Incidence, severity and preventability of medication-related visits to the emergency department: a prospective study. Can Med Assoc J. 2008;178(12):1563-1569.

<![CDATA[MON-705 Islet Auto-Transplantation Following Partial Pancreatectomy Improves Glycemic Outcomes and Reduces Length of Hospital Stay: Multi-Center, Case-Control Study]]> Introduction: Islet auto-transplantation (IAT) is increasingly being performed to prevent brittle diabetes following pancreatic resection in patients with benign pancreatic diseases. While patients undergoing total or completion pancreatectomy clearly benefit from IAT, the glycemic benefit of IAT in patients undergoing partial pancreatic resection is not known. We aimed to determine if IAT improved glycemic outcomes in patients undergoing partial pancreatectomy for benign pancreatic diseases. Methods: We performed a multicenter, retrospective case-control study of patients who underwent partial pancreatic resection with IAT at two tertiary care centers. Case patients were compared to controls who underwent partial pancreatic resection without IAT at one center prior to offering IAT. The primary outcome was the mean change in pre vs. post-operative HgA1c following transplant as well as the development of new post-operative diabetes. Results: 9 patients requiring partial pancreatectomy for benign disease underwent IAT and were compared to 13 historical controls without IAT. Baseline characteristics were similar between groups including age, etiology of pancreatitis, the presence of diabetes and pre-operative HgA1c (5.7 vs. 5.2, p=0.448). With a median follow-up of 22 months, those who received an IAT had a smaller increase in their pre- vs. post-operative HgA1c (0.42 vs 2.83, p=0.004) and one case patient (14.3%) vs. three control patients (23.1%) developed new post-operative diabetes (p=0.581). Patients who underwent IAT had a shorter length of stay (6 days vs 11 days, p=0.039) compared to control patients. Conclusions: Patients undergoing partial pancreatic resection for benign pancreatic disease should be considered for IAT, as long-term glycemic outcomes are improved in those undergoing transplant. The shorter length of hospital stay is likely related to less brittle glucose control after the surgery with some endogenous insulin production by auto-islet graft function.

<![CDATA[MON-LB126 A Benign and Favorable Diagnosis: Glycogen Hepatopathy Causing Transient Transaminitis During Diabetic Ketoacidosis in Type 1 Diabetes Mellitus]]> Background: Transient transaminitis is a rarely discussed complication of uncontrolled diabetes mellitus (DM). Known as glycogenic hepatopathy (GH), it is belived to be caused by build-up of glycogen in hepatocytes. Recognized as benign and reversible, GH is associated with hepatomegaly (>90% cases) and primarily seen in patients with type 1 DM during periods of inadequate hyperglycemic control. Differential diagnoses include glycogen storage diseases, nonalcoholic fatty liver disease, hepatosclerosis, autoimmune hepatitis, hemochromatosis, Wilson disease, and acute viral hepatitis.1

Case Report: A 26-year-old African American female with type 1 DM and sickle cell presented on multiple occasions to the emergency department with abdominal pain associated with nausea, vomiting and diarrhea. Initial labs consistently included glucose levels >600 mg/dL (70-105 mg/dL), elevated anion gap ranging 20-40s mEq/L (5-15 mEq), and severe metabolic acidosis reflective of diabetic ketoacidosis (DKA). Labs were also significant for repeated mild transaminitis despite adequate fluid hydration.

After several admissions, we observed a distinct pattern of mild transaminitis that directly fluctuated with her levels of blood glucose. With some minor lag, the patient’s liver enzymes normalized when her glucose levels normalized and DKA resolved.

Further work-up ruled out more common etiologies of liver injury. Multiple abdominal ultrasounds and CT scans showed a normal sized liver without obvious structural abnormalities. Labs were significant for negative hepatitis B and hepatitis C; several negative anti-smooth muscle, anti-nuclear antibody, centromere antibody, and liver kidney microsomal type 1 antibody; normal levels of ceruloplasmin and alpha 1 anti-trypsin; low iron levels 23 ug/dL (60-180 ug/dL); borderline low IgG 627 mg/dL (700-1600 mg/dL).

We hypothesized that the patient likely had GH by exclusion of other liver pathologies and given the context of transient transaminitis during DKA.

Conclusion: GH is a benign and favorable diagnosis in diabetic patients with elevated transaminases.1 Given the small number of cases of GH reported, there is a need to record and analyze more patients with likely GH in order to better understand the condition. Appropriate clinician awareness of GH can also eliminate the need for time consuming and costly workup.

References:1. Sherigar, Jagannath M et al. “Glycogenic Hepatopathy: A Narrative Review”. World Journal Of Hepatology, vol 10, no. 2, 2018, pp. 172-185. Baishideng Publishing Group Inc., doi:10.4254/wjh.v10.i2.172.

<![CDATA[MON-687 Diabetic Muscle Infarction (DMI) a Rare Under-Recognised Complication of Diabetes Mellitus (DM): A Series of Three Cases]]> Background: Diabetic muscle infarction (DMI) also known as diabetic myonecrosis is an acute, rare, microangiopathic complication of long-standing poorly controlled Diabetes Mellitus (DM). DMI presents as severe pain and swelling of the affected muscle group, usually of the lower extremities. It generally occurs in patients with established vasculopathy from uncontrolled diabetes including retinopathy and nephropathy. However, a clear association of DMI to long term mortality has not yet been defined. Proposed pathophysiologic mechanisms for DMI are microvascular endothelial damage complicated by thromboembolic events triggering an inflammatory cascade, leading to local tissue ischemia and eventual infarction. Alterations in the coagulation-fibrinolysis system and vasculitis have also been invoked. About 50% of the cases have DMI recurrence in the setting of uncontrolled DM.

Clinical Case: We report 3 cases of DMI diagnosed in patients with long-standing poorly controlled DM with at least two established micro-vascular complications. The lower extremity muscle group was affected, especially the thigh muscles and paraspinal muscle in one case. Biochemical parameters were significant for normal white blood cell counts, elevated erythrocyte sedimentation rate (112, 105, 145 mm/hr respectively; n 0–15 mm/hr) and C-reactive protein (CRP) (54.3, 260, 162 mg/L respectively; n 0–5.0 mg/L) and elevated creatine kinase in two cases (539 and 379 U/L; n 5–150 U/L). Infectious work-up including blood cultures were negative. Lower extremity doppler was negative in all three cases. Diagnosis was established with the help of MRI in two cases showing diffuse hyperintensities of the muscle groups involved and muscle biopsy in the third showing neutrophilic and eosinophilic inflammation and areas of necrosis, fibrosis and hemorrhage. Treatment involved adequate pain management and anti-platelet therapy along with tight glycemic control. No recurrence thus far was noticed in all three patients.

Conclusion: DMI should be considered in the differential diagnosis of patients with the aforementioned risk factors who did not show a response to antibiotics, as administered for presumed cellulitis. Though self-limiting, studies have shown a long term temporal correlation with increased all-cause mortality in patients with DMI. Hence DMI is considered as another cardiovascular risk equivalent. Further studies are needed to explore strategies aimed at preventing DMI and its recurrence.

<![CDATA[MON-LB122 Psychiatric Medication Induced Diabetes Mellitus]]> AbstractPsychiatric medications are well established cause of diabetes. Our case had similar presentation. 67-year-old African-American male with history of hypertension and dementia was brought to the ER for auditory hallucination and bizarre behavior. His home medications were Hydrochlorothiazide, Nifedipine and Spironolactone. Psychiatry was consulted and he was admitted to psychiatric floor. He was diagnosed for first time with psychosis and depression. He was treated with citalopram 20 mg for depression; donepezil 10 mg for dementia and risperidone 0.5 mg twice a day for psychosis. 2 weeks later he developed difficulty swallowing and weakness, blood glucose level of 1263 mg/dl. All of his psychiatric medications were stopped except for citalopram 10 mg daily and patient was transferred to ICU. In the ICU, pH was 7.28 (normal 7.34-7.45), normal anion gap, bicarbonate 29mmol/L (normal 20-24), plasma osmolality 428 mOsm/kg (normal 280-320), HbA1c 10% (normal 4-5.6). He was intubated and managed as Hyperosmolar Hyperglycemic Non-Ketotic coma (HONK). He was started on insulin drip and later transitioned to Lantus and short-acting insulin. He improved and was then extubated. After 40 days, repeat A1C was 7.4%. The patient moved to another state and follow-up was lost.Discussion While the patient was on thiazide for a long time, he had a fairly good glucose control; his A1C ranged from normal to prediabetic (A1c 5.7%-6.4%). This makes thiazide unlikely cause of diabetes mellitus for him. The fact that right after 21 days of starting psych medications caused him to land in ICU for HONK, with A1c of 10% and glucose of 1273 mg/dl, strongly suggests that this is a case of psych medications induced T2DM. This is also supported by the fact that discontinuation of those medications lowered the A1c to 7.4% in 40 days. 3 weeks before the hospitalization his A1c was 5.1%. Metformin is demonstrated to be most promising long term medication in cases like this.Conclusion Psychiatric medications are important cause of drug induced diabetes and should always be thought as a cause of acute new onset diabetes. Stopping the offending drugs ensues good glycemic control. ]]> <![CDATA[MON-688 Emphysematous Gastritis and Diabetes]]> <![CDATA[MON-678 Worsening Diabetes Control in Breast Cancer Patients Treated with Alpelisib]]> <![CDATA[MON-LB127 Pulmonary Embolism in the Setting of Diabetic Ketoacidosis. an Under-Recognized Complication]]> <![CDATA[MON-LB123 Diagnosis and Management of Euglycemic DKA in the Setting of SGLT2 Inhibitor Use and Prostate Abscess]]> <![CDATA[MON-LB121 New Onset Insulin Dependent Diabetes Mellitus Secondary to Treatment With Immune Checkpoint Inhibitor]]> 100 mIU/L (Normal 0.27-4.2) and FT4 5.4 pmol/L (Normal 12.0-22.0), subsequently patient was started on Levothyroxine 50 mcg once daily.Patient presented to emergency department with polyuria and polydipsia last 5 days and also blurred vision for last 3 weeks. Patient did not notice any recent weight loss and had widespread pain, worse on skin lesions and hip joints but did not had any other specific complaints.Patient was current smoker with more than 40 pack year history and was taking 25 units of Alcohol per week for many years. Patient did not had any significant family history including any history diabetes in the family.On examination, patient was clinically dry with capillary refill time was 5 seconds.Investigations showed-Venous blood gas-Blood Glucose - Hi (mmol/L out of range), later 22.7 mmol/LPh- 7.291, PCO2 6.14 kPa, HCO3 19.3 mmol/L, Lactate 2.2 mmol/LBlood ketones- Hi (mmol/L out of range), later >7 mmol/LOther investigations showed-Na 131 mmol/L (Normal 135-145), K 5.4 mmol/L (Normal 3.5-5.1), Urea 7.1 mmol/L (Normal 1.7-8.3)Creatinine 139 umol/L (Normal 49-92)Bilirubin 12 umol/L (Normal 0-20), ALT 56 IU/L (Normal 10-35), ALP 157 IU/L (Normal 35-104)Amylase 59 IU/L (Normal 28-100), Albumin 48 g/L (Normal 34-50), Adjusted Calcium 2.56 mmol/L (Normal 2.2-2.6)9 am Cortisol 826 nmol/L (Normal 133-537), ACTH 28 ng/l (Normal 7.2-63.3)FSH 78.7 IU/L (Normal 25.8-134.8), LH 37.6 IU/L (Normal 7.7-58.5)IGF1 9.6 nmol/L (Normal 3.5-32.0), Prolactin 476 mIU/L (Normal 102-496)HbA1C 10.6% / 93 mmol/mmol (Normal 20-42)Serum Anti-GAD titre- 5 IU/L (Normal 0-10)Patient was started on treatment for Diabetic Ketoacidosis (DKA) with intravenous fluid and also fixed rate Insulin infusion according to protocol. Patient responded well to treatment and biochemical profile improved with initial treatment, subsequently patient was started on regular basal bolus Insulin regime with the help from the diabetes team. Discussion:Here we have presented a case with new onset Insulin dependent Diabetes Mellitus induced by immune checkpoint inhibitor. This kind of Diabetes progress rapidly to severe insulin deficiency compared to spontaneous Type 1 Diabetes, frequently patient present with DKA and do not go into remission. As this condition can develop rapidly, it is suggested that glucose level is to be monitored regularly and also to check HbA1C prior to initiating the immunotherapy. Their management requires complex Insulin regime to get good glycaemic control and add significant comorbidity along with the underlying cancer. The exact pathophysiologic mechanism and predictive biomarkers have not yet been established. The end result is permanent Insulin dependence. In future better characterization and further study is required to improve diagnosis and management, also to follow the natural history of this condition.Reference:1) Kotwal A, Haddox C, Block M, et alImmune checkpoint inhibitors: an emerging cause of insulin-dependent diabetesBMJ Open Diabetes Research and Care 2019;7:e000591. doi: 10.1136/bmjdrc-2018-0005912) Immune checkpoint inhibitors and type 1 diabetes mellitus: a case report and systematic Filette JMK1, Pen JJ2, Decoster L3, Vissers T4, Bravenboer B1, Van der Auwera BJ5, Gorus FK5, Roep BO6,7, Aspeslagh S3, Neyns B3, Velkeniers B1, Kharagjitsingh AV1, ]]>