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: COVID-19 has disproportionally affected communities of color in the US. These communities exhibit higher prevalence of chronic preventable disease including type 2 diabetes mellitus (DM2) and obesity. DM2 and obesity have been linked to higher morbidity and mortality in the setting of COVID-19 infection (1). Methods: We query data collected from 521 patients with laboratory-confirmed Covid-19 infection admitted to an inner-city community hospital in Brooklyn, New York between March 20 2020 and May 15 2020. Demographics, pre-infection medical comorbidities, laboratory data at admission and clinical outcomes including in-hospital mortality were analyzed. Results: Patients were 61 years on average (+/-17.2), 42.8% were female, 53.9% were Hispanic and 33% were African-American. Most common comorbidities included: hypertension (62%), chronic kidney disease (20.8%), diabetes (45 %). Mean BMI was 29.9 (+/- 8.2). Among patients with no prior diagnosis of diabetes mean A1c was 5.8% (+/-1.2) and 8.7 (+/-2.5) amongst those with a previous diagnosis of diabetes. Patients hospitalized with moderate to severe COVID-19 infection and a previous diagnosis of DM2 had significantly higher prevalence of CKD and HTN. Amongst those with T2DM, 19.1% presented with DKA. After adjustment for age, gender, race, BMI and creatinine obese patients, compared with normal-weight patients had significantly higher mortality rate (BMI > 30 kg/m2 [OR: 2.29, CI: 95%, P-value: <0.002]) however this association was not observed for DM2 ([OR: 1.25, CI: 95%, P-value: <0.002]). Conclusion: Our cohort represents a particular population affected by the first wave of Covid-19 infection in an urban inner-city community in NYC. The population studied had a larger proportion of African-American, Hispanic and younger patients compared to national averages; these differences are related to the demographics of the communities served by our hospital. Obesity is a negative prognostic factor in the course of Covid-19 infection in comparison to normal-weight patients. Obesity is a proinflammatory condition, associated with high levels of prothrombotic factors including angiotensin-II, also elevated in COVID-19. Understanding that link may yield valuable knowledge on the role obesity plays in numerous disease states beyond COVID-19. References:(1). Sabin ML, et al. Lancet. 2020;395(10232): 1243–44.(2). Hussain A, et al. Obes Res Clin Pract. 2020; 14(4): 295–300.

Background: Severe hyperglycemia due to insulin resistance is associated with increased mortality due to induction of pro-inflammatory cytokines, immunodepression, impairing cellular function and healing. We describe 6 patients admitted with COVID19 pneumonia complicated with DKA requiring high dose insulin infusion. # 1 19 yo African American (AA) male with history of pre-DM and obesity (BMI 41 kg/m2) presented with polyuria, polydipsia, obtunded and intubated in ER. Labs showed pH 7.35, serum sodium (Na) 138 mmol/L, potassium (K) 6.8 mmol/L, chloride (Cl) 85 mmol/L, bicarbonate (HCO3) 10 mmol/L, glucose 1140 mg/dL, lactate 1.4 mmol/L, anion gap (AG) 43, Beta Hydroxybutyrate (BOH) > 4.50 mmol/L. A1c 13.4%. Placed on insulin drip at 29.5 U/hr or 5.7 U/kg/hr. Discharged on Detemir 60 U TID and Novolog 20 U TID ac. # 2 55 yo female with T2DM and obesity (BMI 37.42 kg/m2) presented with shortness of breath, intubated for hypoxia in ER. Labs showed pH 7.21, serum Na 138 mmol/L, K 5.6 mmol/L, Cl 101 mmol/L, HCO3 13 mmol/L, glucose 557 mg/dL, lactate 5 mmol/L, AG 24, BOH > 0.27 mmol/L. A1c 7.8%. Placed on insulin drip at 23 U/hr or 5 U/kg/hr. Died from multiorgan failure on day 7. # 3 75 yo Hispanic female with T2DM, HCV, post liver-kidney transplant on immunosuppressants, HTN presented with weakness. Intubated on day 6 for hypoxemia. Placed on stress dose steroids for transplant failure. BMI 30 kg/m2. Labs on day 6 showed pH 6.98, serum Na 140 mmol/L, K 3.5 mmol/L, Cl 100 mmol/L, HCO3 20 mmol/L, glucose 590 mg/dL, AG 20, BOH 1.40 mmol/L. A1c 6.6% a year ago. Placed on insulin drip at 34 U/hr or 10.9 U/kg/hr. She developed ESRD requiring CRRT dialysis. She was made comfort care. Died on day 7. # 4 38 yo AA male with obesity (BMI 59.5 kg/m2) presenting with confusion, polyuria, polydipsia. Labs showed pH 7.22. serum Na 133 mmol/L, K 6.8 mmol/L, Cl 81 mmol/L, HCO3 15 mmol/L, glucose 1760 mg/dL, lactate 3.8 mmol/L, AG 37, BOH > 4.50 mmol/L. A1c 12.6%. Placed on insulin drip at 36 U/hr or 6 U/kg/hr. Discharged on Detemir 20 U qhs. # 5 27 yo AA female with T2DM, HTN and obesity (BMI 51 kg/m2), pituitary adenoma presented with seizures. Labs showed pH 7.15, serum Na 133 mmol/L, K 7.0 mmol/L, Cl 84 mmol/L, HCO3 7 mmol/L, serum glucose 951 mg/dL, lactate 1.6 mmol/L, AG 24, BOH >2.45 mmol/L. A1c >15%. Placed on insulin drip at 24 U/hr or 5 U/kg/hr. Died on day 5 from multiorgan failure. # 6 74 yo Hispanic female with T2DM, HTN and asthma presented with altered mental status. BMI 28 kg/m2. Labs showed pH 7.25, serum Na 155 mmol/L, K 4.6 mmol/L, Cl 125 mmol/L, HCO3 17 mmol/L, serum glucose 779 mg/dL, lactate 2.6 mmol/L, AG 13, BOH >2.45 mmol/L. A1c > 15%. Placed on insulin drip at 24 U/hr or 3.5 U/kg/hr. Died on day 5. Conclusion: Patients with DM and obesity admitted with Covid19 infection presented with severe insulin resistance and poor outcomes. Cconsideration should be given to assessing therapeutic interventions to enhance insulin sensitivity and improve outcomes.

The coronavirus disease 2019 COVID-19 pandemic is a major public health crisis. Obesity has emerged as a significant comorbidity for COVID-19 severity. To study the association of both pandemics, we conducted an observational, retrospective cohort study involving 521 patients admitted with Covid-19 to an inner city, community hospital in Brooklyn, NY in the period March 20 to May 2, 2020. Of the cohort, 57.6% was men, mean age was 61.6±17.2 years, and mean BMI was 29.0 ± 8.2 kg /m2. 11% had BMI > 40 kg/m2. 53.9% was Hispanic, 33.3% was African American, 7.1% was White, with a predominance of type 2 diabetes (99%). Diabetes, hypertension, coronary artery disease and chronic kidney disease were found in 45%, 41.5%, 15%, and 20.1% cases, respectively. Mean HbA1c was 5.8%± 1.1 in patients with no history of diabetes, 3% presented with diabetic ketoacidosis, mortality rate was 30.6%. Non-survivors were significantly older (median age 68 vs 56, p < 0.03) and had higher rate of microvascular and macrovascular diseases. In patients with diabetes, mortality rate was 40.1%. HbA1c was similar between survivors and non-survivors. Older age and hyperglycemia on admission were the risk factors for mortality. Only 30% of the cohort had normal weight (BMI<25), 30% was overweight and 40% was obese. In univariate analysis, the characteristics at admission significantly associated with mortality were age, BMI, hyperglycemia, diabetes and DKA in patients with or without diabetes. In age- and sex-adjusted multivariable analysis only BMI 30–39 kg/m2 (OR = 1.63; 95% CI, 1.10, 2.43; p = 0.015), BMI >40 kg/m2 (OR = 2.05; 95% CI, 1.22, 3.44; p = 0.007) and DKA (OR = 1.77; 95% CI, 1.18, 2.64; p = 0.005) remained positively associated with higher mortality. In summary, BMI, and DKA but not diabetes, were positively and independently associated with mortality in patients hospitalized with Covid-19. Reference: (1) Popkin et al., Obesity Reviews 2020 August;21(11):e13128. (2) Cariou et al., Diabetologia 2020 May;63(8): 1500–1515.