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BackgroundNarcolepsy is an uncommon neurological disorder characterised by irresistible spells of sleep associated with abnormal rapid eye movement (REM) sleep. The association between narcolepsy and human leukocyte antigen HLA- DQB1*06:02 has been established elsewhere but remains to be investigated among Saudi Arabian patients with narcolepsy.MethodsA total of 29 Saudi patients with type I or type 2 narcolepsy comprising of 23 (79%) males and 6 (21%) females with a mean age of 17.2 ± 9.6 years were included in this study. Type 1 or type 2 narcolepsy was diagnosed by full polysomnography followed by a multiple sleep latency test in accordance with International Classifications of Sleep Disorders-3 criteria. HLA typing for DQB1 alleles was performed by polymerase chain reaction and hybridization with sequence-specific oligonucleotide probes. Differences in clinical and sleep parameters were compared by univariable analyses. HLA-DQB1*06:02 frequency was systematically compared with the published literature.ResultsType 1 narcolepsy was diagnosed in 19/29 (65.5%) patients, whereas 10/29 (34.5%) patients had type 2 narcolepsy. DQB1*06:02 was present in 25/29 (86.2%) patients; 15/19 (78.9%) narcolepsy type 1 patients and 10/10 (100%) narcolepsy type 2 patients harboured the DQB1*06:02 allele. REM latency was significantly lower in DQB1*06:02-positive patients compared to DQB1*06:02-negative patients (17.6 ± 32.3 min vs. 106.0 ± 86.0 min; p = 0.025). Epworth Sleepiness Scale scores were significantly higher among type 1 than type 2 narcolepsy patients (19.7 ± 3.2 vs 15.3 ± 3.6; p = 0.02).ConclusionsDQB1*06:02 allele frequencies among Saudi patients with narcolepsy were consistent with previously published data.

To determine the association between emergency department (ED) visits, glycemic control and the quality of preventive diabetes care among diabetic patients in a Saudi community. Methods: This study was an observational, cross-sectional study that collected data through interview-based surveys between February and April 2017. Data were collected from 530 diabetic patients in the diabetes clinics at King Saud Medical City, the tertiary center of Riyadh, Kingdom of Saudi Arabia.  Results: This study found statistically significant relationships (p less than 0.05) between ED visits and patient age, the glycated hemoglobin (HbA1c) and education level. Emergency department visits increased by 43% for each unit of increase in HbA1c (odds ratio [OR]=1.43, 95% confidence interval (CI)=1.26-1.62). Graduating from high school decreased the odds of visiting the ED by 43% (OR=0.57, 95% CI=0.34-0.94). Most of the participants were not followed for possible microvascular complications; the majority did not visit nephrology (96.2%), ophthalmology (78.3%) and neurology (97.9%) clinics within the 12 months prior to the interviews. Conclusion: Emergency department visits can indicate poor glycemic control in diabetic patients. Additionally, the current practices of preventive diabetes care in Saudi Arabia are not sufficient, according to the diabetic standards of care recommended by the American Diabetes Association.

Objectives: To determine the association between emergency department (ED) visits, glycemic control and the quality of preventive diabetes care among diabetic patients in a Saudi community. Methods: This study was an observational, cross-sectional study that collected data through interview-based surveys between February and April 2017. Data were collected from 530 diabetic patients in the diabetes clinics at King Saud Medical City, the tertiary center of Riyadh, Kingdom of Saudi Arabia. Results: This study found statistically significant relationships (p<0.05) between ED visits and patient age, the glycated hemoglobin (HbA1c) and education level. Emergency department visits increased by 43% for each unit of increase in HbA1c (odds ratio [OR]=1.43, 95% confidence interval (CI)=1.26-1.62). Graduating from high school decreased the odds of visiting the ED by 43% (OR=0.57, 95% CI=0.34-0.94). Most of the participants were not followed for possible microvascular complications; the majority did not visit nephrology (96.2%), ophthalmology (78.3%) and neurology (97.9%) clinics within the 12 months prior to the interviews. Conclusion: Emergency department visits can indicate poor glycemic control in diabetic patients. Additionally, the current practices of preventive diabetes care in Saudi Arabia are not sufficient, according to the diabetic standards of care recommended by the American Diabetes Association.

Disclosure: M. Alkhathlan: None. A. Siddiqui: None. Background: Pregnancy is well known to be a diabetogenic and ketogenic state. When coinciding with an acute illness like COVID-19 infection, it can lead to full-blown DKA requiring intervention to reverse ketoacidosis. Complete restoration of normal glycemic status can be achieved after treatment of COVID-19 infection. Clinical case: A 34-year-old, G3 P2 woman who was at 26 weeks gestation with triplet pregnancy presented to the ED with fever, shortness of breath, nausea and vomiting for 3 days. She had gestational hypertension and impaired glucose tolerance during her previous pregnancy, but none during her current pregnancy. She had tested positive for COVID-19 infection at an outpatient evaluation for mild upper respiratory symptoms, two days prior to her presentation. Vital signs in the ER were T 35.3 °C, RR 22, HR 103, BP 121/70, and O2 sat 95% on 4 L/min nasal cannula. Initial laboratory testing showed sodium 132 (135-145), potassium 4.4 (3.5-5.5), bicarb 9 mmol/L (22-29), anion gap 18 mmol/L (5-14), BUN 3 mg/dL (6-23), creatinine 0.43, eGFR > 60, glucose 113 mg/dL (74-109), serum ketones 3.13 mmol/L (0.02-0.27) and lactate 1.6 mmol/L (0.5-2.5). ABG confirmed acidosis with pH of 7.29, and PCO2 was 22. She was diagnosed with euglycemic DKA after ruling out other possible etiologies of high anion gap metabolic acidosis. She received betamethasone by the Obstetrics team and fetal monitoring was initiated. DKA treatment was started with IV insulin, dextrose and close glucose monitoring. She had complete resolution of metabolic acidosis after 34 hours and did not require subcutaneous insulin treatment post-DKA resolution. She was able to tolerate oral diet with significant improvement of all her symptoms. She required only supportive treatment for COVID-19 infection and tested negative on the third day of hospitalization. Conclusion: Pregnancy is a ketogenic state and when superimposed with a significant acute illness of COVID-19, can lead to euglycemic DKA even in the absence of gestational diabetes. Early detection and treatment of ketoacidosis with COVID-19 is critical to avoid fetal and maternal complications or premature delivery. Presentation: Thursday, June 15, 2023

INTRODUCTION:Obstructive jaundice is a known cause of sinus bradycardia. It is usually attributed to the effect of bile salts on the electrophysiology of the heart and mainly on the SA node. But can Primary biliary cirrhosis cause bradycardia? Here, we are presenting a case of sinus bradycardia with a junctional rhythm that could be secondary to primary biliary cirrhosis.CASE DESCRIPTION/METHODS:A 65-year-old female with a history of primary biliary cirrhosis complicated by esophageal varices and recurrent ascites. The patient presented with a syncopal episode. The patient had a history of episodes of lightheadedness for several days before admission. Upon arrival at the hospital, the patient was bradycardiac with heart rate around 30 and she was hypotensive. She was given several doses of atropine and then she was started on dopamine drip. Initial EKG showed that the patient has a junctional rhythm. After reviewing the patient cardiac history, we found that the patient didn't have any heart issues before and she had a coronary angiogram done one year ago and showed normal coronaries. Medications were reviewed and showed that the patient was on Metoprolol 25 mg twice daily for anxiety and she was on it for more than 10 years and there were no recent changes in the dose. Labs showed that the patient had mild elevation is AST 41 IU/L and ALT 62 IU/L. Total serum bilirubin was 1.7 mg/dl (mildly elevated) and direct bilirubin was 0.7 mg/dl (mildly elevated). After beta-blocker was held, the patient heart rate improved, and dopamine drip was discontinued.DISCUSSION:This is a case of primary biliary cirrhosis who presented with symptomatic bradycardia. This patient was on beta-blockers for a long period of time and she didn't have any heart issues given her last coronary angiogram and echocardiogram were normal. We believe that one of the contributors of the patient bradycardia is the primary biliary cirrhosis itself as it can cause bradycardia which is believed to be secondary to bile salts. In conclusion, primary biliary cirrhosis should be considered as a cause of bradycardia and the use of metoprolol in those patients should be closely monitored as Metoprolol is primarily metabolized by the liver and can intensify the bradycardia.

Disclosure: M. Alkhathlan: None. Y. Li: None. A. Siddiqui: None. S. Goud: None. Background: Hypercalcemia is a common condition with a variety of etiologies. In general, it can be categorized as either parathyroid hormone (PTH) dependent or independent. In those with non-PTH mediated hypercalcemia, elevated 1, 25 vitamin D is one of the causes and among pathologies behind it are sarcoidosis, malignancy, and to less extent infectious process. An important determinant in the management of elevated 1,25vitD is to identify the source of 1,25vitD overproduction as the choice of treatment can affect the outcomes and increase the risk of mortality. Clinical Case: Our patient is an 81-year-old man who had been admitted to the hospital for nonspecific fatigue and weakness for two months. He was discharged from another hospital with similar complaints without resolution. At the time of admission, he was noted to have elevated total calcium 12.5 mg/dL (8.4-10.2) with albumin 3.0 g/dL (3.5-5.2), subacute kidney injury with creatinine 3.46 mg/dL (0.7-1.3), suppressed parathyroid hormone (PTH) and markedly elevated 1,25-dihydroxy vitamin D (1,25OH2D) 128 pg/mL (19.9-79.3). His calcium and kidney function were normal 4 months ago. The hypercalcemia was refractory to intravenous fluid, loop diuretic or calcitonin administration. Extensive workup eventually revealed disseminated histoplasmosis infection with blood and urine positive for histoplasmosis antigens. Bone marrow aspiration showed scattered non-necrotizing granulomas. With antifungal treatment, his calcium level returned to the normal range in two weeks (8.9 mg/dL) and was maintained in the normal range. Conclusion: Hypercalcemia is a rare presentation of histoplasmosis. Pubmed keyword search of hypercalcemia and histoplasmosis returned 18 clinical case reports from 1977 to 2021. The case review showed a striking similarity in atypical clinical presentation and diagnosis challenges. Hypercalcemia is most developed in histoplasmosis disseminated cases with elevated 1,25vitD levels and pathology identification of granulomas in some of the cases. With successful antifungal treatment, patients will have prompt recovery of hypercalcemia. Steroid treatment is a well know and effective treatment by suppressing 1-alpha hydroxylation of 25-vitD. However, treatment with steroids before establishing diagnosis due to Inconspicuous presentations or delay in diagnosis may lead to mortality quickly. Presentation: Saturday, June 17, 2023

Disclosure: S.G. Goud: None. A. Siddiqui: None. M. Alkhathlan: None. C.Y. Fan: None. Introduction: Immune checkpoint inhibitors such as pembrolizumab (Keytruda) used in the treatment of various cancers are associated with immune mediated endocrinopathies, among which thyroid dysfunction and pituitary hypophysitis are common, whereas hypoparathyroidism is rare. We report a case of primary hypoparathyroidism and hypocalcemia with pembrolizumab. Clinical Case: 58-year-old male with metastatic urothelial cell carcinoma, status post neoadjuvant chemotherapy with gemcitabine and cisplatin in 2017, followed by radical cystectomy with recurrence of metastasis in 2018, who was started on Keytruda every three weeks. After 10 months, he developed immune mediated hypothyroidism treated with levothyroxine. After 33 months on Keytruda, he developed hematochezia with constipation and intermittent abdominal pain. Colonoscopy showed findings consistent with autoimmune colitis; Keytruda was held and colitis was treated with tapering steroids. Surveillance imaging showed stable disease, so Keytruda continued to be held. After 7 months of holding Keytruda, on routine blood work he had a critically low calcium level of 5.5 mg/dl (8.4-10.2 mg/dl) with tingling and numbness in his hands, muscle spasms, generalized weakness, and fatigue for the past few weeks. On exam there was no Trousseau’s sign, Chvostek's sign, or gait ataxia. Hemodynamically stable. Labs showed lowest corrected calcium of 5.5, normal renal function, low vitamin D of 8 ng/ml (30-100 ng/ml), elevated phosphorus of 6.3 mg/dl (2.5-4.5 mg/dl), and normal magnesium. PTH was frankly low at 12.7 pg/ml (15-65 pg/ml), indicating primary hypoparathyroidism. ACTH stimulation test was normal. Retrospective review of the labs from oncology office records showed gradual, progressive hypocalcemia for a few months prior to presentation, with calcium levels ranging between 6.7 to 7.7 mg/dl. Of note, calcium prior to pembrolizumab was normal at 9.4 mg/dl. He was treated with IV calcium gluconate and then transitioned to calcium carbonate (CaCO3) 500 mg TID, calcitriol 0.5 mg BID, and Vit D 50,000 IU twice weekly. Hydrochlorothiazide (HCTZ) added as calcium remained low. After three days calcium improved to 7 mg/dl range and he was discharged. Calcium levels checked periodically after discharge ranged from 8 to 9 mg/dl (8.4-10.2 mg/dl), and phosphorus levels normalized. CaCO3 dose was adjusted accordingly, Vit D was changed to 50,000 IU weekly based on a level of 71 ng/dl after 3 months, and HCTZ was discontinued after 6 months. PTH was still low at 9.7 pg/ml (15-65 pg/ml) 6 months after discharge, off pembrolizumab for over a year. Calcium sensing receptor (CaSR) activating antibody was not checked in our case. Conclusion: It is important clinicians be aware of the risk for hypocalcemia and its unpredictable presentation to help with timely recognition and management. Presentation: Saturday, June 17, 2023