Background: A patient on chronic methadone therapy presented following a suicide attempt, was noted to have recurrent episodes of non-fasting symptomatic hypoglycemia and was diagnosed with opioid induced adrenal insufficiency (OIAI). Opioid induced endocrinopathies are underappreciated, particularly in the midst of a growing opioid epidemic in the United States. We believe this is the first reported clinical case of OIAI associated with non-fasting hypoglycemia. Clinical Case: A 33-year-old female with history of depression and heroine abuse on methadone therapy presented after a suicide attempt by methadone overdose. Home medications included 170mg of methadone daily for the past 5 years. She was afebrile, heart rate of 68, blood pressure 102/72, respiratory rate of 10, oxygen saturation 92%. On exam she was lethargic with altered mental status and had pinpoint pupils. Labs showed a normal complete blood count and metabolic panel. Urine toxicology was positive for methadone. Clinical picture improved temporarily after Narcan administration however 1 hour later she was confused again, with a fingerstick glucose of 50mg/dL and she was admitted to ICU for monitoring. In the ICU she continued to be lethargic with dizziness, nausea and headaches. She continued to have approximately 4 spontaneous episodes of hypoglycemia per day, despite having a good appetite and increased parenteral glucose administration. Blood pressure continued to be marginal, ranging from 85–100/50–60. There was no obvious source of infection. Urine sulfonylurea screen was negative. Investigations showed a morning cortisol of 2.23 ug/dL. A 250 µg ACTH stimulation test showed an inadequate response. The am basal plasma cortisol was 2.25 ug/dL with 15.28 ug/dL and 15.13 ug/dL at 30 and 60 minutes respectively (6.20–19.40ug/dL). She was diagnosed with hypoglycemia secondary to OIAI. Given the patient’s critical condition she was initially started on stress dose of hydrocortisone 80mg every 8 hours. Attempts to down titrate the methadone dose were unsuccessful. Patient’s symptoms improved and hypoglycemia subsided. She was discharged home on hydrocortisone 10mg qam & 5 mg qpm and she was continued on Methadone 170mg daily. Conclusion: OIAI is an under-recognized clinical entity with potentially serious adverse outcomes. Currently, 3% to 4% of US adults receive long-term opioid treatment. OIAI is present in 9—29% of individuals on chronic opioids. Opioids act through suppression of the HPA axis, primarily at the level of the hypothalamus, mediated through either delta or kappa receptors leading to a decrease in ACTH and cortisol secretion. Management should include decreasing and ideally discontinue opioids, along with glucocorticoid replacement until documented recovery of the HPA axis. Reference: Reference: (1)Donegan, Diane et al. Opioid-Induced Adrenal Insufficiency. Mayo Clin. Proc. 2018 93(7), 937–944.
Background: Primary aldosteronism (PA) is a renin-independent hypersecretion of aldosterone that remains an underdiagnosed etiology of hypertension. Less than 50 cases of primary hyperaldosteronism in pregnancy have been reported in literature that are associated with pregnancy complications including preeclampsia. Clinical Case: A 41-year-old female G9P4 at 32 weeks gestation was admitted for suspected preeclampsia due to elevated blood pressure during a routine prenatal visit. Her comorbidities include type 2 diabetes, uncontrolled hypertension, and preeclampsia in a previous pregnancy. Home medications included Lisinopril 10 mg once daily which was discontinued upon pregnancy and switched to Labetalol 400 mg twice daily and Nifedipine ER 30 mg daily. She was on a total of 220 units of insulin daily. On presentation, patient complained of anxiety but denied any headache, nausea, visual disturbances, chest pain, palpitations, muscle cramps, or fatigue. Her blood pressure was 180/100 mmHg with heat rate of 73. Laboratory values was notable for potassium: 2.8 mmol/L (n 3.5–5 mmol/L), bicarbonate: 28 mmol/L (n 24–31 mmol/L), and magnesium: 1.4 mEq/L (n 1.3–1.9 mEq/L). Liver function test and platelet count were normal. Spot protein-creatinine ratio was 0.3 (n 0–0.2). ECG was normal sinus rhythm with a heart rate of 82 without decreased T wave amplitude or U waves. She received three doses of oral 40 mEq potassium chloride over twelve hours and potassium level post repletion was 3.0 mmol/L. Initially, her hypokalemia was attributed to high insulin dose requirements. Despite down titration of insulin, patient continued to have hypokalemic episodes (nadir 2.7 mmol/L) refractory to oral and parenteral potassium supplementation. She remained hypertensive despite Labetalol 600 mg every 8 hours, Nifedipine ER 30 mg every 12 hours, with as needed hydralazine 10 mg IV pushes, and underwent urgent cesarean delivery. Uncontrolled hypertension persisted postpartum with recurrent episodes of hypokalemia. Further investigations revealed a plasma aldosterone concentration (PAC) and plasma renin activity (PRA) levels of 43.5 ng/dL (n <10 ng/dL) and 1.67 ng/mL/hr (n 0.17–5.38 ng/mL/hr) respectively, potassium at time of testing was 3.6 mmol/L. PAC to PRA ratio was greater than 20:1 with an absolute PAC greater than 15 ng/dL, which is highly suggestive of PA. Conclusion: We present a case of suspected PA with spontaneous hypokalemia potentially masked by the use of ACE inhibitors uncovered during pregnancy. Given the changes to the renin-angiotensin-aldosterone system (RAAS) during pregnancy, the diagnosis of PA is difficult to establish during gestation. Still, little is known on how to optimally treat these patients. Reference: Morton, A., 2015. Primary Aldosteronism and Pregnancy. Pregnancy and hypertension. An International Journal of Women’s Cardiovascular Health, Volume 5 Issue 4, 259–262.
Background Sellar and parasellar plasmacytoma is a rare tumor that often poses a diagnostic challenge as it can often be misdiagnosed as a nonfunctioning pituitary adenoma. Here we present a case of sellar plasmacytoma and point to clues helping establish the diagnosis. Clinical case 60-year-old male presented with two weeks of worsening morning headache followed by eyelid drooping. A physical exam was notable for left-sided ptosis, mydriasis, poor pupillary light reflex, and otherwise normal eye movement in cardinal positions . Head CT revealed 33×32×30 mm sellar mass; thus endocrinology team was consulted for evaluation. Further workup revealed normal TSH, free T4, ACTH and morning cortisol, FSH, LH, and IGF-1. He had a minimal elevation of prolactin levels at 33 ng/ml after serial dilutions (reference range: 2-17.7 ng/ml). We noticed the patient had an elevated serum protein concentration of 10.6 g/dl (reference range: 6.4-8.3 g/dl) with an albumin level of 4 gm/dl with an elevated gamma gap at 6.6 g/dl, suggestive of elevated gamma globulins. Serum protein electrophoresis showed an M-spike of 3.8 g/dl, and urine was positive for Bence Jones protein. Brain MRI with and without contrast showed homogeneously enhancing mass mainly within the sphenoid sinus extending down to the clivus, isointense on T1, hyperintense on T2 with no diffusion restriction, encasing the left internal carotid artery with intact pituitary and optic chiasm. Transsphenoidal biopsy showed sheets of plasma cells. Immunohistochemistry showed lambda light chain only and negative for kappa light chain. Flow cytometry was positive for CD38, CD138, CD200, and CD56, confirming a diagnosis of plasmacytoma. Fluorescent in situ hybridization was positive for FGFR3-IGH t(4;14) translocation, indicating a higher risk. Otherwise, beta-2-microglobulin, lactate dehydrogenase, and albumin were within normal. Initial management included pulsed dexamethasone of 40 mg for four days, followed by a taper with skull base radiotherapy, a total of 3500 cGy. Ptosis and eye movement gradually improved. The patient was discharged to start bortezomib-based treatment by the oncology team. Clinical lesson: Based on large case series, sellar plasmacytoma often presents as headache (70%), visual changes (77%), and hyperprolactinemia (38%). Imaging shows clinal invasion (74%), cavernous sinus invasion (49%), encasement of the internal carotid artery (17%) [1]. The differential diagnosis for such findings on imaging includes nonfunctioning pituitary adenoma, chordoma, and meningioma. Special attention to gamma gap, urinary, and serum protein electrophoresis can urge to perform a biopsy to prove the diagnosis of plasmacytoma and avoid delay in therapy. Reference: 1. Lee J, Kulubya E, Pressman BD, et al. Sellar, and clival plasmacytomas: case series of 5 patients with systematic review of 65 published cases. Pituitary. 2017;20(3): 381-392. doi: 10.1007/s11102-017-0799-5 Presentation: No date and time listed
Introduction Hyperosmolar crisis, which includes diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), is a severe and acute complication of diabetes. The estimated mortality rates of DKA and HHS are 6.8% and 10%, respectively (Benoit, Zhang, Geiss, Gregg, & Albright, 2018) (Pasquel & Umpierrez, 2014). There is limited evidence regarding the clinical characteristics, hospital complications, and mortality rate of patients with combined DKA and HHS. Therefore, we aim to compare hospital outcomes between patients with DKA, HHS, and combined DKA and HHS in a community hospital in Brooklyn, NY. Methodology We performed a retrospective analysis from the patients admitted for DKA and/or HHS at Health+Hospitals / Woodhull from 2019 to 2021. Descriptive statistics were used to determine the frequency of patients in each hyperglycemic group and their clinical characteristics. Using one-way ANOVA and Chi-square test, we compared the demographics and clinical outcomes between subgroups. Multivariate regression analysis and log-rank test were used to assess the influence of multiple variables on hospital mortality and the difference in survival between groups, respectively. Results We studied 263 patients admitted for a hyperglycemic crisis, DKA (58%), HHS (14%), and DKA+HHS (28%). Baseline characteristics of the population include male (60%), African American (42%), Hispanic (32%), and mean BMI of 28±8 kg/m2. No difference was found in mean admission HbA1c (DKA 12±2.6%, HHS 12.7±3%, DKA+HHS 12.7±2.5%, p: 0.08). Patients with HHS were older (mean age 56±15) compared with DKA (47±17) and DKA+HHS (49±18). Patients with DKA+HHS had higher mean admission blood sugar (893±330 mg/dL), compared with DKA (497±206 mg/dL) and HHS (808±346 mg/dL) (p <0.001). There was no difference in the frequency of hypokalemia, K+ <3.5 mEq/L (DKA 26.9%, HHS 6.3%, DKA+HHS 12.6%, p: 0.8); hypoglycemia (DKA 12%, HHS 4.6%, DKA+HHS 7%, p: 0.2); or cerebral edema (DKA 0.8%, HHS 0.4%, DKA+HHS 1.5%, p: 0.1) between the groups. However, the frequency of acute kidney injury (AKI) was higher in DKA (24.7%) than in HHS (7%) or DKA+HHS (16.7%) (p: 0.034). There was no difference in the mean days of hospital stay (DKA 8.5±28, HHS 7±8, DKA+HHS 8±10, p: 0.9) and in-hospital mortality (DKA 3.4%, HHS 3.5%, DKA+HHS 4%, p: 0.069) among the groups. In all subtypes of hyperglycemic crisis, the mortality rate was significantly higher with older age, presence of AKI, cerebral edema, and vasopressor requirement. Conclusions There was no significant difference in mortality, length of admission, prevalence of hypoglycemia, hypokalemia, and cerebral edema between the three groups. The prevalence of AKI was significantly higher in DKA compared with HHS and DKA+HHS. Older age, presence of AKI, cerebral edema, and vasopressor requirement were mortality predictors among hyperglycemic crisis. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
Evidence shows that people with poor glycemic control are at greater risk of mortality due to Covid19. It is important to achieve and maintain good glycemic control to prevent negative outcomes during this pandemic (1). To study the effect of lockdown on glucose control we conducted an observational, retrospective cohort study involving 98 patients followed at endocrine clinic at an inner city, community hospital in Brooklyn, NY in the period February to May 2020. Of the cohort, 60% were women, mean age was 54.1 + 15.3 years, 70% was Hispanic, 24% was African American with a predominance of type 2 diabetes (86%). Mean HbA1c of prelockdown and lockdown phase was 9.77 ± 2.26% and 9.49 ± 2.17 % respectively and the difference was statistically significant (p < 0.001) both in patients with Type 1 and Type 2 diabetes. Mean BMI of prelockdown and lockdown phase was 30.5 ± 6.8% and 30.1 ± 6.05% respectively and the difference was not statistically significant (p = 0.33). Despite no significant change in BMI, the factors responsible for improvement in HbA1c might be a result of refined eating patterns (increased consumption of homemade food), increased adherence to medication and time to cope with the daily challenges of diabetes management (1). Reference: Maddaloni E, Coraggio L, Pieralice S, Carlone A, Pozzilli P, Buzzetti R. Effects of COVID-19 Lockdown on Glucose Control: Continuous Glucose Monitoring Data From People With Diabetes on Intensive Insulin Therapy. Diabetes Care Aug 2020, 43 (8) e86-e87; DOI: 10.2337/dc20-0954
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