bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abducens Nerve Palsy as the First Manifestation of Type Two Diabetes Mellitus
Authors: Ibrahim Amira , Loseva Victoria 
Published: May 2021

Abstract
Introduction: Diabetes mellitus has varied presentations at different times from onset. One of the uncommon presentations is cranial nerve palsy secondary to microvascular ischemia. Approximately 20% of isolated abducens nerve palsies are secondary to vascular microangiopathy. Clinical Case: A 53-year-old female with no significant past medical history presented to the emergency department with concerns of double vision. The patient first noticed her symptoms five days prior to presentation. The patient endorsed blurry vision and stated that she has double vision in certain gazes that resolves with shutting either eye. Furthermore, she has also developed headaches during that period, described as a pressure-like sensation in her forehead and behind her eyes. She otherwise denied any tearing, redness, or pain. On review of systems, she denied numbness, tingling, changes in hearing, changes in speech, or extremity weakness. Due to the persistence of symptoms the patient presented to the emergency department. On exam, the patient’s vitals were normal. Pupils were equal and briskly reactive to light with no relative afferent pupillary defect. External examination was unremarkable without scalp tenderness, proptosis, or ptosis. Color vision was intact. Ocular motility testing revealed limited abduction of the left eye causing double vision on lateral gaze. Confrontation visual fields were full in each eye. Bilateral lower extremity exam revealed decreased sensation in the sole of the foot. The rest of the physical exam was unremarkable. Laboratory work revealed blood glucose level of 305 mg/dl (Reference range 70–99 mg/dl). HBA1C was 12.3% (Reference range 3.8–5.6%). CT head and CTA of the neck was performed and were unremarkable. Given the normal imaging and findings on examinations, her ocular motor findings were attributed to diabetes mellitus. The patient was started on insulin, aspirin, and received diabetic education for lifestyle modification, and was scheduled for outpatient follow up. The patient’s acute isolated left sixth cranial nerve palsy was most likely owing to microvascular ischemia from previously undiagnosed diabetes mellitus. A study of 59 patients with an isolated sixth cranial nerve palsy showed a 6-fold increase in the odds of having diabetes compared with controls.(1) Conclusion: Given the infrequent presentation of Diabetes with Abducens nerve palsy, diagnosis is usually delayed with the expense of ordering costly investigations that put a financial and psychological burden on patients. Thus, we urge clinicians’ awareness when encountering cases of isolated cranial nerve palsies. References: 1) Sanders SK, Kawasaki A, Purvin VA. Long-term prognosis in patients with vasculopathic sixth nerve palsy. Am J Ophthalmol. 2002;134(1):81–84.
Acute Sensorineural Hearing Loss - an Unusual Presentation of Uncontrolled DM
Authors: Arudkumaran Dharscika , Chang Albert , Umadat Deviani , Eschler Deirdre Cocks 
Published: May 2021

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 &gt;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.
Alpelisib-Induced Diabetic Ketoacidosis
Authors: Espinosa Luis Borges , Vendrame Francesco 
Published: May 2021

Abstract
Introduction: Alpelisib is a alpha-specific phosphoinositide 3-kinase inhibitor (PI3K) recently approved for patients with advanced or metastatic breast cancer with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, and activating mutations in the PIK3CA gene. PI3K is involved in the insulin receptor signaling pathway that leads to glucose uptake. Hyperglycemia is a frequent adverse effect of Alpisilib but diabetic ketoacidosis (DKA) is considered a rare occurrence.
Case ReportA 53 year-old woman with metastatic breast cancer presented with 5 days of worsening polydipsia, fatigue, nausea, vomiting, slurred speech and altered mental status. She was started on Alpelisib 300 mg daily two weeks prior to admission and instructed to check glucose twice weekly but did not follow directions. Family history was significant for type 2 diabetes. On physical exam blood pressure was 150/90, heart rate 120 beats/minute, respiratory rate 120 breaths/minute; BMI was 27 Kg/m2. The neurological exam was significant for a lethargic state with the patient arousable to verbal stimuli. The skin exam was negative for acanthosis nigricans or skin tags. Laboratory tests showed glucose at 1425 mg/dl, bicarbonate 11 mEq/l (19–34), anion gap 39 (6–22), sodium 138 mmol/l (135–146), potassium 5.0 mmol/l (3.5–5.5), serum osmolality 378 mosm/kg (275–295), Cr 3.99 mg/dl (0.4–1.1), lactic acid 3.5 mmol/l (0.5–2.0), ketonuria and glucosuria. No arterial blood gas was performed. HbA1c was 5.9% before starting Alpelisib. Results were consistent with DKA and hyperosmolar hyperglycemic state. Additional tests showed HbA1c 10.5 %, c-peptide 1.2 ng/ml (1.1–4.4) with glucose 183 mg/dl; type 1 diabetes autoantibodies were negative. Alpesilib was held and the patient managed with insulin drip and then insulin basal/bolus regimen. Patient was discharged on basal insulin and metformin with the plan to resume alpelisib at a lower dose and monitor.
ConclusionIn the SOLAR-1 trial hyperglycemia was reported in 63% of patients taking alpesilib and two cases of DKA were observed. A case of a patient who developed DKA with Alpesilib was also recently reported. The mechanism underlying DKA in these patients is unclear. PI3K inhibitors may prevent the transcription of the insulin gene in response to high concentrations of glucose and the combination of impaired peripheral glucose uptake with impaired insulin secretion trigger DKA. Further studies are needed to identify which patients on Alpelisib are at increased risk of developing DKA. Clinicians should be aware of this life threatening complication.
References: F André, et al. Alpelisib for PIK3CA-Mutated, Hormone Receptor-Positive Advanced Breast Cancer. N Engl J Med 2019; 380.SJ. Farah, et al. Diabetic ketoacidosis associated with alpelisib treatment of metastatic breast cancer. AACE Clinical Case Reports 2020; Vol. 6, No. 6.
An Atypical Presentation of Hyperosmolar Hyperglycemic State Induced by SARS CoV 2
Authors: Rivera Nazario Ivan Augusto , Ortiz Arnaldo Nieves , Rivera Jose Ayala , Moya Kyomara Hernandez , Rojas Arnaldo , Lopez Zahira Marie Lugo , Torres Marina Torres , Cintron-Colon Hector R , Fonseca Vanessa , Bisono Nicolas Cabrera , Miranda Maria De Lourdes 
Published: May 2021

Abstract
Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2.
We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms.
SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.
An Unusual Case of Latent Autoimmune Diabetes in Adult and Pancreatic Neuroendocrine Tumor in a Patient Presenting With Diabetes
Authors: Baral Neelam , Gubbi Sriram , Al-Naqeeb Ghadah , Verbalis Joseph G 
Published: May 2021

Abstract
Introduction: Latent autoimmune diabetes in adults (LADA) and pancreatic neuroendocrine tumors (PNETs) are rare causes of adult-onset diabetes mellitus (DM). The existence of both LADA and a PNET in a single patient has not been previously reported.
Clinical Case: A 65-year-old female with history of type 2 DM diagnosed 15 months ago, on metformin 500mg twice a day presented with fatigue, dry mouth, polyuria, and blurry vision for one week and weight loss of 12 pounds over 3 months. Plasma glucose was 599 (nl 65–144 mg/dL) with an elevated anion gap (17; nl 5–15 mmol/L), low bicarbonate (19; nl 21–32 mmol/L) and elevated beta hydroxybutyrate (4.79; nl 0.02–0.27 mmol/L). Diabetic ketoacidosis was diagnosed, and intravenous fluids and insulin were administered. Work up revealed HbA1C of 14% (nl 4.2%-5.6%) which had increased from 7% noted three months ago. glutamic acid decarboxylase antibodies (GAD65 Ab) was &gt;250 (0.0–0.5 IU/mL) and C peptide was 0.42 (0.81–3.85 ng/mL). A computed tomogram of the abdomen performed to evaluate the acute worsening of her HbA1C revealed a 1.4 x 1.3 cm poorly defined hypoenhancing pancreatic head lesion, which on magnetic resonance imaging was 1.6 x 1.2 cm. Further evaluation showed normal levels of glucagon (127; nl &lt;=208 ng/L), somatostatin (26; nl &lt;=30ppg/mL) and vasoactive intestinal peptide (&lt;13; nl 0–60 pg/mL), and an elevated chromogranin A (155; nl 0-95ng/mL). An endoscopic ultrasound guided fine needle aspiration of pancreatic head mass revealed a well differentiated NET with Ki-67 proliferation index of &lt;1%. She underwent pylorus preserving pancreaticoduodenectomy and histopathology showed a 2 cm grade one NET on pancreatic head with no involvement of the 23 tested lymph nodes. Immunohistochemistry was positive for chromogranin and synaptophysin and negative for insulin, somatostatin and gastrin, confirming diagnosis of well-differentiated pancreatic NET Stage Ib (T2N0M0). Whole body PET CT scan done 2 months following surgery did not reveal any focal radiotracer uptake to suggest metastasis. Given the presence of GAD65 Ab, age of onset of DM, and an initial non-requirement of insulin, the patient was diagnosed with LADA and insulin therapy was initiated.
Conclusion: We report a unique case of a patient with LADA who was incidentally found to have a non-functioning pancreatic NET. Although functional PNETs such as glucagonoma and somatostatinoma cause hyperglycemia, DM associated with non-functioning NETs is rare, but has been reported with gastrointestinal NETs (1). Our patient likely developed uncontrolled hyperglycemia from LADA but was incidentally found to have a PNET which may have contributed to the worsening of hyperglycemia. This highlights the importance of thorough evaluation for the causes for acute worsening of hyperglycemia.
Application of the S (AD) SAD System as a Prognostic and Evaluation Tool for the Multidisciplinary Treatment of a Diabetic Foot Ulcer
Authors: de Oliveira Izabela , Baldissera Vilmar , Souza Gabriella S 
Published: May 2021

Abstract
Introduction: Foot ulcers combined with infection is one of the main complications of type 2 diabetes mellitus (DM2), and when not diagnosed and treated, amputation is the most frequent outcome. Thus, patients with DM2 are ten times more likely to be hospitalized for infections when compared to normal ones. For this reason, it is indisputable that diabetic foot ulcers have a major impact on health and the early approach can reduce the chances of amputations. Case Report: A 48-year-old woman, admitted with an ulcer on her right foot for 30 days, reports worsening and pain for 7 days. Previous history of DM2 diagnosed 2 years ago, using metformin irregularly. On physical examination, he had edema, flushing, impaired tibial pulses and ulcer in the calcaneus with exudate in the right lower limb. In addition, he had a BMI of 32.5, showing overweight. Having considered the hypothesis of a diabetic foot associated with hyperglycemia, the S (AD) SAD system (SEPSIS, ARTERIOPATY, DENERVATION) was applied, in order to assess the prognosis of foot ulcer (healing), setting a score of 10 due to the presence of an affected area greater than 3 cm², affected depth up to the joint capsule, presence of osteomyelitis, reduced pulses, and reduced sensitivity at the site. In this sense, the system suggested an expectation for cure in a period greater than 6 months and with a high risk for limb amputation. The exams were consistent with the hypothesis of hyperglycemia, revealing decompensated diabetes mellitus. Thus, he presented elevated glycated hemoglobin (11.8%), estimated mean glycemia (292 ml / dL), and elevated basal glucose (191 mg / dL). Treatment with antibiotic therapy was initiated for 30 days and the patient was asked to go to the health service three times a week to perform debridement with SF 0.9% and apply the ionic silver dressing to treat the ulcer. In addition, the patient received guidance related to dietary reeducation, and started treatment with empagliflozin to control DM2. The patient progressed with progressive ulcer healing and weight reduction. After 3 months of treatment, after monitoring and multidisciplinary intervention, the patient had an adequate glycated hemoglobin rate (6.9%) and the patient achieved total healing of the ulcer, with improved sensitivity and peripheral circulation of the affected limb. Conclusion: Although ulcers are a frequent problem, there are difficulties not only in choosing the most appropriate approach, but also in a system that provides a prognosis and that makes it possible to assess the risk of amputation. Therefore, the S (AD) SAD system, a reproducible tool that favored decision making, provided a prognosis for slow healing and a high risk for amputation. Thus, the multidisciplinary team was able to measure the severity of the condition, choose a treatment, and evaluate the success of the approach adopted, which configured the total healing in 3 months.
Diabetes and Tuberculosis: Challenge of Modern Medicine
Authors: Kostitska Iryna Oleksandrivna , Ostrovskyi Mykola Mykolayovych , Makoida Iryna Yaremivna , Molodovets Olga Bogdanivna , Babliuk Lyudmyla Antonivna , Maniv Lesya Yaroslavivna 
Published: May 2021

Abstract
The world medical community is strongly concentrated on the fight COVD-19, HIV/AIDS, tuberculosis. The combination of two or more concurrent nosologies is a major problem in patient management. Thus considering the abovementioned facts, we would like to focus your attention on such comorbidities as diabetes and tuberculosis. Patient M., 49 y.o., type 2 diabetes during 10 years. In July 2018, she consulted her physician and complained of non-productive mild cough, low-grade fever, fatigue, reduced workability. After the follow-up examination which involved chest X-ray and complete blood cell count, she was diagnosed with an abscess forming pneumonia in the right lower lobe and prescribed treatment with the use of broad-spectrum antibiotics according to the protocol. After the treatment, the patient’s condition has slightly improved, though the labile diabetes with frequent episodes of hypoglycemia and hyperglycemia, and cough still persisted. The level of HbA1C was 7.8%. At the patient’s request, she continued to receive: glimepiride 6 mg/day, metformin 1000 mg/day. Considering the patient’s general condition as gradual recovery the doctor has discharged the patient. In January 2019, the patient consulted a tuberculotherapist, because the cough persisted, the body temperature markers sometimes attained feverish indices, the general weakness increased. After the follow-up examination: complete blood cell count, chest X-ray, sputum smear microscopy, genetic-molecular study with GeneXpert-test and culture test on the BACTEC system, the patient was diagnosed with disseminated tuberculosis with bacterial excretion, susceptible. The patient received treatment according to the 2HRZE 4HR scheme. Results: the treatment was completed, whereas the cavern was preserved, the patient refused to undergo surgical treatment. After 7 months, the previous symptoms reappeared, after additional examination the patient was diagnosed with multi-drug resistant tuberculosis and was prescribed treatment with second-line agents for 20 months, and the patient was given insulin degludec/aspart at a daily dose of 64 IU. The therapy resulted in patient’s recovery, the cavern was closed, and compensation of diabetes was achieved: no episodes of hypoglycemia were recorded; the HbA1C - 6.5%. Analyzing the previous data it is necessary to note the mistakes that were made. The mismatch of clinical symptoms with the established diagnosis, the absence of a sputum smear for acid-resistant bacteria, apical localization of tuberculosis which is typical for patients with diabetes was not characteristic in this case, all these factors have led to an incorrect diagnosis at the primary level. At the beginning of tuberculosis treatment, the patient should be transferred to the correction of blood glucose levels with insulin and, if the cavern preserves, the patient should be prepared for its surgical removal.
Diabetic Ketoacidosis Presenting in Major Thalassemia With Pancreatic Hemosiderosis: A Case Report
Authors: Mulyadi Calvin Kurnia , Effendi Bonita , Pratomo Robby , Kesuma Pratiwi , Tahapary Dicky Levenus 
Published: May 2021

Abstract
Introduction: Iron overload is a common complication of thalassemia, responsible for multiple organ damage, including pancreas. The prevalence of diabetes in thalassemia was 9.7–29%,1 while the incidence of diabetic ketoacidosis (DKA) is only 0,3%.2
Case Illustration: A 26 year-old male with thalassemia major (TM) admitted due to dyspnea, which later revealed as first episode of DKA. No prior history of hyperglycemia, but the patient has unexplained weight loss. He receives combination of chelators (deferiprone, desferroxamine, deferriprox) with ferritin level 8,387 μg/mL. Serum glucose was remarkably high (690 mg/dL), with ketosis (4.2 μg/dL) and metabolic acidosis (pH 7.2; bicarbonate 5.6 mEq/L). No single insult was identified, but recurrent ventricular tachycardia was documented. T2* MRI demonstrates severe cardiac and mild pancreatic hemosiderosis. Echocardiography shows reduced ejection fraction (25.6%), atrioventricular dilatation, and hypokinetism.
Discussion: Impaired glucose metabolism in TM is initially mediated by insulin resistance, but later, the interplay between defect in insulin secretion and resistance determines the various clinical picture of diabetes in TM.3 Several mechanisms have been linked: oxidative stress, induction of autoimmunity, and zinc deficiency; yet, current evidence remains inadequate.4 The T2* MRI provides the most reliable tool to predict the development of glycemic dysregulation, whereas relying solely on ferritin could lead to imprecise measurement of iron deposits.5 The presence of cardiac abnormality might responsible for the DKA and suggests the need of rescue chelation for this patient.
Conclusion: DKA is a rare endocrine complications which can be prevented by routine T2* MRI screening and has wide spectrum of clinical characteristics.