Acute Pancreatitis Following a Lower Extremity Angioplasty

Introduction: Acute pancreatitis affects a significant population globally. Usual etiologies are gallstones, alcohol, hypertriglyceridemia, medications;less frequent are trauma, hypercalcemia, infections, toxins, ischemia, anatomic anomalies, vasculitis, and idiopathic. Pancreatitis post coronary intervention is an uncommon cause with only 19 published cases in the last two decades. Being cognizant of this etiology is important given the increasing number of patients undergoing angiography. Case Description/Methods: An 81-year-old female with hypertension, diabetes, peripheral arterial disease, prior cholecystectomy underwent left lower extremity angioplasty at an outside center. Within a few hours, she started having severe epigastric pain radiating to her back, nausea, vomiting and loose bloody stool. She presented to the emergency department 24 hours after symptom onset. Epigastric tenderness was present on exam. Labs revealed leukocytosis (24,450/muL), elevated lipase (1410 U/L), elevated creatinine (1.3 mg/dL), lactate (3.1 mmol/L), calcium 9.4 mg/dL and triglycerides 161 mg/dL. Incidentally, found to be positive for COVID-19. Normal common bile duct diameter seen on sonogram. CT angiogram of the abdomen/pelvis showed acute pancreatitis, duodenal and central small bowel enteritis (Figure). She was not on any medications known to cause pancreatitis and denied alcohol use. Patient improved with analgesics and intravenous fluids. She had no recurrence of bloody stools and hemoglobin remained stable. On day 4, she was able to tolerate a regular diet, and leukocyte count and creatinine normalized. Patient did not have any COVID respiratory symptoms, and was discharged. Discussion(s): Given the temporal association to angioplasty and no other identifiable cause, acute pancreatitis was presumed to be due to the contrast used during angioplasty. Other possibilities included cholesterol embolism but no peripheral signs of cholesterol embolism were seen. Patient was an asymptomatic COVID-19 case. Although, there are case series of pancreatitis due to COVID, those were found in very sick symptomatic patients. On review of literature, cholesterol embolism was identified as a definite cause only on autopsy or laparotomy (Table). Other possible mechanisms are: high viscosity of the contrast media leading to ischemia and necrosis, contrast causing NF-kB activation followed by epithelial damage, and vasospasm. Pancreatitis after coronary angiography is rare, nonetheless, an important differential especially if there is a temporal relationship.

Nirmatrelvir/ritonavir - A New Culprit of Acute Pancreatitis

Introduction: Nirmatrelvir/ritonavir is a new medication approved for the treatment of COVID-19 infection. It prevents viral replication by inhibiting the SARS-CoV-2 main protease. While mild adverse effects were described, including dysgeusia, diarrhea, hypertension and myalgia1, there were no reported cases of pancreatitis. Case Description/Methods: An 81-year-old female with a past medical history of hypertension and COPD presented to the hospital complaining of abdominal pain and nausea for one day. She had no history of alcohol, tobacco or marijuana use, recent travel, or trauma. Her medications included lisinopril and prednisone, and she had completed a 5-day course of nirmatrelvir/ritonavir for the treatment of COVID-19 infection 2 days prior to presentation. On abdominal exam, she had left upper and lower quadrant tenderness. Blood tests revealed an amylase of 1333 U/L, lipase of 3779 U/L, triglycerides of 297 mg/dL and calcium of 8.7 mg/dL. CT scan revealed an indurated pancreatic body and tail with peripancreatic fluid along the paracolic gutter. Ultrasound of the abdomen and MRCP did not reveal any acute findings. IgG subclasses 1-4 were normal. Discussion(s): According to the revised Atlanta criteria, the patient had clinical findings consistent with acute pancreatitis. Common causes such as gallstone, alcohol, autoimmune and hypertriglyceridemiainduced pancreatitis were ruled out. There were no masses or structural abnormalities on imaging that might have explained her diagnosis. There have been at least 2 reported cases of lisinopril and prednisone induced pancreatitis, however according to Badalov et al.2 both of these medications are class III drugs that lack any rechallenge in the literature. Moreover, the patient had been taking these medications for many years, making them an unlikely cause of the presenting diagnosis. There are no reports of nirmatrelvir/ritonavir associated pancreatitis or known pharmacologic interaction with her home medications, and a meta-analysis conducted by Babajide et al. revealed no association between acute pancreatitis and COVID-19 infection (3). Given the negative findings stated above and the recent initiation of a new medication, nirmatrelvir/ritonavir was the likely cause of acute pancreatitis.

What the Eye Cannot See: A Case of Persistent Altered Mental Status in a Patient With Cholestatic Liver Disease?

Introduction: Altered mental status (AMS) is a common symptom in patients with liver disease with a wide list of differential diagnoses. Knowledge of etiologies of AMS unique to patients with hepatic dysfunction is vital in order to help recognize, diagnose, and treat the underlying cause in a timely manner. Case Description/Methods: A 46-year-old man with a history of recent COVID infection was transferred to our hospital for further evaluation of acute liver injury and AMS. On arrival, his labs were notable for AST of 408 U/L, ALT of 620 U/L, ALP of 5942 U/L, TB of 11.0 mg/dL, and an INR of 1.1. His work-up included an MRCP that showed segmental biliary ductal dilation with associated restricted diffusion and peribiliary enhancement concerning for sclerosing cholangitis. ERCP revealed a 3cm biliary cast that was removed and noted diffuse rarefaction of ducts throughout the entire biliary tree. A liver biopsy revealed centrizonal cholestasis with portal-based bile ductular reaction and mild bile duct injury. Despite adequate treatment of suspected infection and hepatic encephalopathy, his AMS persisted. His basic metabolic panel (BMP) was notable for Na of 143 mEq/L. A send-out lipid panel that was obtained to work-up his dyslipidemia revealed a total cholesterol of 1018 mg/dL, triglycerides of 420mg/dL, and the presence of lipoprotein X. A venous blood gas (VBG) was obtained showing a Na of 157 mEq/L and serum osmolality was 322 mmol/kg, confirming true hypernatremia. He was slowly treated with hypotonic solutions with significant improvement in his mentation. On follow-up one year later, he has persistent cholestasis and is currently being considered for liver transplant. Discussion(s): The final diagnosis was COVID-related ischemic cholangitis and disappearing bile ducts with persistent cholangiopathy, presenting with severe cholestasis, accumulation of lipoprotein X, and pseudonormonatremia. When faced with severe cholestatic liver disease, clinicians should keep in mind the possibility of accumulation of lipoprotein X and its association with hyperviscosity and spurious electrolyte abnormalities. Clinicians should rely on obtaining blood gas analyses for accurate electrolyte measurement in such cholestatic patients as blood gas analyses utilize direct ion-sensitive electrodes (ISE) to measure electrolytes, whereas routine basic metabolic panels utilize indirect ISE that are liable to spurious results in the presence of hyperlipoproteinemia/lipoprotein X.

The Complexities of Managing Hypertriglyceridemia-Induced Pancreatitis in a Critically-Ill COVID-19 Patient

Introduction: Hypertriglyceridemia-induced pancreatitis (HTP) is a variant of pancreatitis requiring unique management. The complications of COVID-19 and its treatments can make HTP therapy more nuanced. This case describes a patient who presented in diabetic ketoacidosis (DKA) with HTP, and COVID-19. The patient developed renal and respiratory failure, necessitating hemodialysis (HD) and extracorporeal membrane oxygenation (ECMO), complicating an otherwise straightforward medical management plan. Case Description: A morbidly obese (BMI 38.9 kg/m2) 43-year-old male presented to an outside hospital with abdominal pain, and vomiting, and was found to have HTP with triglycerides (TG) >2000 mg/dL (<149 mg/dL) and presumed new-onset type 2 Diabetes (HbA1c 10.9%) with DKA. Treatment with fluids, intravenous (IV) insulin infusion and plasmapheresis were initiated. He developed hypoxia after receiving over 17 liters of fluids and was intubated, subsequently developing renal failure and was transferred to our tertiary center for HD and ECMO. On admission, he tested positive for COVID-19, rhabdomyolysis [creatinine kinase 5600 U/L (30-200 U/L)], HTP [TG 783 mg/dL (<149 mg/dL), lipase 461 U/l (7-60 U/L)], glucose 269 mg/dL (not in DKA), transaminitis [AST 184 U/L (4-40 U/L), ALT 61 U/L (4-41 U/L)] and renal failure (GFR 10 ml/min/1.73m2). IV insulin infusion was initiated for hyperglycemia worsened by COVID-19 dexamethasone treatment. Plasmapheresis was performed twice with minimal effect at maintaining a low TG. Fenofibrate was not initiated due to renal failure;Lovaza could not be given via oral gastric tube;Atorvastatin was attempted once rhabdomyolysis resolved, with subsequent worsening of liver function tests. Heparin infusion was initiated for deep vein thrombosis treatment and HTP but was stopped after development of heparin induced thrombocytopenia. The patient developed worsening hypoglycemia requiring cessation of IV insulin, hypotension requiring maximum pressor support, and worsening sepsis leading to his death. Discussion(s): This case illustrates the challenges of managing a patient with HTP and COVID-19. It demonstrates how a normally straightforward treatment algorithm can become increasingly complex when factoring the patient's comorbid conditions. The case highlights the importance of knowing both treatment indications and contraindications for HTP. In this case, HTP may have been the initial diagnosis, straightforward for most endocrinologists, but its treatments and comorbid conditions ultimately made the landscape more challenging, limiting effective management and ultimately leading to this patient's demise.Copyright © 2023

X-Linked Inhibitor of Apoptosis (XIAP) deficiency presenting as hemophagocytic lymphohistiocytosis triggered by drug allergy

X-linked inhibitor of apoptosis (XIAP) deficiency is a primary immunodeficiency associated with recurrent hemophagocytic lymphohistiocytosis (HLH) episodes. The clinical phenotypes of XIAP deficiency vary, ranging from splenomegaly to life-threatening inflammation. We report a case of XIAP deficiency with unusual late-onset HLH presentation likely triggered by a drug allergy. A previously healthy adolescent boy presented to the hospital with fever and rash seven days after starting antibiotics for a neck abscess. Laboratory evaluation demonstrated cytopenias, elevated liver enzymes, and increased inflammatory markers. Initially, antibiotics were discontinued due to concern for drug rash. He continued to deteriorate clinically and became hypotensive. Additional testing revealed decreased NK cell function, as well as elevated ferritin, triglycerides, and soluble IL-2 receptor. SLAM-Associated Protein (SAP) and XIAP evaluation by flow cytometry demonstrated decreased XIAP expression. Subsequently, genetic testing revealed a known pathogenic mutation in BIRC4 (c.421_422del), confirming the diagnosis of XIAP deficiency.Copyright © 2023

COVID-19: A CONFOUNDING MIMICKER OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome involving pathologic immune activation that is often fatal. The link between the cytokine storm related to COVID-19 and development of HLH has been reported since the onset of the pandemic, but little is known about clinical manifestations of HLH, thereby delaying treatment. CASE PRESENTATION: A 50 year-old male presented with a several day history of progressive weakness in the setting of missed dialysis session. Medical history was significant for ESRD on dialysis and diastolic heart failure (EF 35%). Initial vitals were unremarkable. Physical exam was notable for peripheral edema bilaterally. Laboratory studies were consistent with hyperkalemia, elevated ferritin (28,383) and elevated liver function tests. COVID-19 PCR was positive upon admission. Chest x-ray, CTA chest and a right upper quadrant ultrasound were unremarkable. He was admitted to the medical ICU for emergent dialysis. Soon after arrival to the ICU, he became lethargic and confused with increasing oxygen requirements and a subsequent a code blue was called. Cardiopulmonary resuscitation was immediately initiated, with a first rhythm consistent with ventricular fibrillation. He was shocked and placed on an amiodarone infusion with return of spontaneous circulation. TTE revealed a severely reduced EF <10%. Despite initiation of advanced COVID-19 therapies with Solu-Medrol and tocilizumab he remained ventilator dependent. Due to hemodynamic instability and persistent metabolic acidosis, he was transitioned to continuous renal replacement. Further blood work showed worsening inflammatory markers (ferritin 33,500, LDH 6981). Because of the significantly elevated ferritin, there were concerns for possible HLH. Triglycerides and IL-2 receptor were 395 mg/dL and 9300 pg/mL respectively. Total NK cells were decreased to 1.2%. He remained persistently unstable despite aggressive measures. He suffered a second cardiopulmonary arrest, which was unable to achieve return of spontaneous circulation and he ultimately passed away. DISCUSSION: HLH is characterized by uncontrolled activation and proliferation of benign macrophages in reticuloendothelial organs. This results in histiocytic hemophagocytosis, worsening peripheral blood cytopenia(s), cytokine storm, and cytokine mediated biochemical alteration ultimately culminating in multiorgan dysfunction and disseminated intravascular coagulation. Although a distinctive constellation of features has been described for HLH, diagnosis remains challenging as patients have diverse presentations associated with a variety of triggers. CONCLUSIONS: As HLH is a medical emergency with poor prognosis, prompt recognition and early treatment is crucial for improving clinical outcomes. We hope this case will create increased awareness and timely diagnosis of cytokine storm syndromes in patients with severe COVID-19 infection. Reference #1: Meazza Prina M, Martini F, Bracchi F, Di Mauro D, Fargnoli A, Motta M, Giussani C, Gobbin G, Taverna M, D'Alessio A. Hemophagocytic syndrome secondary to SARS-Cov-2 infection: a case report. BMC Infect Dis. 2021 Aug 13;21(1):811. doi: 10.1186/s12879-021-06532-7. PMID: 34388982;PMCID: PMC8361241. Reference #2: Schnaubelt, Sebastian MDa,*;Tihanyi, Daniel MDb;Strassl, Robert MDc;Schmidt, Ralf MDc;Anders, Sonja MDb;Laggner, Anton N. MDa;Agis, Hermine MDd;Domanovits, Hans MDa Hemophagocytic lymphohistiocytosis in COVID-19, Medicine: March 26, 2021 - Volume 100 - Issue 12 - p e25170 doi: 10.1097/MD.0000000000025170 DISCLOSURES: No relevant relationships by Garrett Fiscus No relevant relationships by Niala Moallem No relevant relationships by Resham Pawar

PLASMAPHERESIS FOR HYPERTRIGLYCERIDEMIA-INDUCED PANCREATITIS

SESSION TITLE: Critical Renal and Endocrine Disorders Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: About 7% of acute pancreatitis (AP) cases are caused by hypertriglyceridemia (HTG). In such cases bowel rest, IV fluids, symptomatic therapy, and triglyceride (TG) lowering interventions are initiated. Plasmapheresis is one of the treatment options, but it has specific indications. We present a case of severe hypertriglyceridemia-induced pancreatitis that required plasmapheresis. CASE PRESENTATION: A 30 y/o man with type 2 diabetes, hyperlipidemia, multiple previous admissions for HTG-AP, presented with severe abdominal pain, nausea, and vomiting x 1 day. On admission, he was tachycardic, hypotensive, afebrile, SpO2 > 96% on RA. Labs: Glu 491 mg/dL, TG > 1000 mg/dL, Cholesterol 509 mg/dL, Lipase 987 U/L, Cr/BUN 2.4 mg/dL /20 mg/dL, VBG pH 7.25/PCO2 36.2 mmHg/PO2 19.4 mmHg/Ca 0.8/lactate 5.6;WBC 13.07 K/cm;COVID PCR positive. CXR: diffuse patchy opacities. CTAP with contrast was deferred because of AKI. He was admitted to the ICU and started on insulin drip with no improvement over 24hrs. He was still acidotic, Ca persistently low, TG still >1000, and kidney function worsened. Plasmapheresis was initiated. After one session his TG lowered to 700. He was restarted on insulin drip and in the next 24hr TG decreased to < 500 and metabolic acidosis resolved. Once AKI resolved, CT abdomen/pelvis with contrast confirmed acute pancreatitis, with focal hypodensities within the uncinate process and the proximal body, concerning infarcts as well as large phlegmon surrounding the pancreas, but no evidence of necrotizing or hemorrhagic pancreatitis. His hospital course was complicated with sepsis and DVT, which resolved with therapy. He was discharged home with TG lowering agents, Apixaban, and his previous T2DM regimen. DISCUSSION: Plasmapheresis is indicated in patients with severe HTG (>1000- 2000 mg/dl), severe HTG-AP, and when standard treatment options are inadequate. It lowers the lipid levels and removes proinflammatory markers and cytokines stopping further inflammation and damage to the pancreas and other organs faster compared to conservative therapy. Most patients need only one session which lowers TG level by 50-80%, as seen in our patient. CONCLUSIONS: Plasmapheresis should be considered in cases of HTGP with worrisome features such as lactic acidosis, hypocalcemia, worsening inflammation, and multi organ failure. Reference #1: Rajat Garg, Tarun Rustagi, "Management of Hypertriglyceridemia Induced Acute Pancreatitis", BioMed Research International, vol. 2018, Article ID 4721357, 12 pages, 2018. https://doi.org/10.1155/2018/4721357 Reference #2: Pothoulakis I, Paragomi P, Tuft M, Lahooti A, Archibugi L, Capurso G, Papachristou GI. Association of Serum Triglyceride Levels with Severity in Acute Pancreatitis: Results from an International, Multicenter Cohort Study. Digestion. 2021;102(5):809-813. doi: 10.1159/000512682. Epub 2021 Jan 21. PMID: 33477149. Reference #3: Gavva C, Sarode R, Agrawal D, Burner J. Therapeutic plasma exchange for hypertriglyceridemia induced pancreatitis: A rapid and practical approach. Transfus Apher Sci. 2016 Feb;54(1):99-102. doi: 10.1016/j.transci.2016.02.001. Epub 2016 Feb 20. PMID: 26947356. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Vaishali Geedigunta No relevant relationships by Zinobia Khan No relevant relationships by Jelena Stojsavljevic

Triglyceride levels in COVID-19 patients during admission in intensive care correlate with disease severity and mortality

Introduction: It has been established that plasma triglyceride levels are raised during infection and inflammation, due to increased adipose tissue lipolysis, fatty acid synthesis and suppressed fatty acid oxidation.1 Increased triglycerides have also been linked to the 'cytokine storm' underlying the pathophysiology of coronavirus disease 2019 (COVID-19).2 Severe outcomes in COVID-19 patients have been found to be associated with higher triglyceride levels before the infection.3 Another study found triglycerides to be significantly higher after recovery than during the acute phase of infection.4 There is limited data on the trajectory of triglyceride levels in COVID-19 patients during admission in intensive care. Investigating whether triglyceride levels are a useful predictor of disease severity and mortality would enable earlier detection of high-risk patients. While triglyceride levels in COVID-19 patients with mild or severe infections were found to be elevated, this was not the case in those with critical illness which included respiratory or multiple organ failure and septic shock.5 The differences in lipid metabolism between COVID-19 patients and patients with critical illness are yet to be elucidated. Objectives: In this study, triglyceride levels of COVID-19 patients during admission in the general intensive care (GICU) were examined in relation to disease severity and mortality. Triglyceride levels at the beginning of hospitalisation were compared between GICU patients with COVID-19, acute respiratory distress syndrome (ARDS) and critical illness, and healthy controls. Methods: Data was obtained from medical records of 93 patients with COVID-19 admitted to GICU at University Hospital Southampton, between March 2020 and May 2020. Triglyceride levels were recorded for each day of hospitalisation. Data was also obtained from medical records of 8 critically ill patients, 10 patients with ARDS and 10 healthy volunteers. Results: The trajectory of triglyceride levels in this cohort of COVID-19 patients started low, then increased over the course of admission (Figure 1). Increased average triglyceride levels correlated with increased risk for severe disease outcome, as indicated by the Sequential Organ Failure Assessment (SOFA) score calculated at the beginning of GICU admission (p<0.05) (Figure 2). Increased triglyceride levels in the first week of GICU admission also correlated with mortality (p<0.05). When compared with healthy controls and patients admitted to GICU with ARDS, patients with COVID-19 and critical illness had raised triglycerides (Figure 3). Conclusions: Increased triglyceride levels in COVID-19 patients over the duration of GICU admission are associated with worse disease outcomes and increased mortality. This provides further evidence for the role of dyslipidaemia in the progression of COVID-19.

Correlation of Lipid Profile with Inflammatory Markers among COVID-19 Positive Patients: A Retrospective Study

Introduction: Lipids are fundamental biomolecules of the body. Infections like COVID-19 with intricate immune response in some patient’s leads to acute complications by affecting metabolic pathways at multiple levels. Metabolism of cholesterol, triglyceride and High Density Lipoprotein (HDL)-Cholesterol is deranged by cytokines and multiple inflammatory mediators. The sex differences in lipid metabolism may contribute in susceptibility, severity and outcome of Coronavirus Disease 2019 (COVID-19). Performing lipid profile in COVID-19 patient may help in assessing severity and prognosis of disease. Aim: To assess the relationship between lipid profile and inflammatory markers in COVID-19 patients and also to evaluate the gender wise differences in lipid parameters and their correlations with inflammatory markers. Materials and Methods: This retrospective study was conducted in Department of Biochemistry at SHKM, GMC, Mewat, Haryana, India (tertiary care health centre) on COVID-19 positive patients attending Outpatient Department (OPD) and Inpatient Department (IPD), from October 2020 to December 2020. The data of 85 patients with COVID-19 positive, confirmed by Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and who were prescribed for lipid profile along with C-Reactive Protein (CRP) and serum ferritin were included in the study. Serum total cholesterol, triglyceride, HDL-Cholesterol, CRP and ferritin were measured in the subjects. Data was statistically analysed using Student’s t test and Pearson correlation coefficient. results: Total 85 (46 males and 39 females) COVID-19 patients were included in the study. Mean age in male and female patients were 43.02±15.52 years and 42.02±15.25 years, respectively with a range of 5-82 years. Mean value of Serum triglycerides, HDL-C and total cholesterol was 204.94±141.27 mg/dL, 42.97±13.38 mg/ dL and 187.058±45.75 mg/dL, respectively. Serum triglycerides were statistically significantly higher in males than females (p-value=0.0413). The HDL-C however was significantly higher in females than males (p-value=0.0006). In male patients, r-value between cholesterol and CRP was -0.3538, and p-value was 0.016. Ferritin had a significant negative correlation with HDL-C (r-value=-0.3578, p-value=0.00079). Weak Positive correlation was noted between triglyceride and ferritin (r-value= 0.2285, p-value=0.035). conclusion: High levels of serum triglycerides, low total cholesterol, and low HDL-cholesterol correlates with inflammatory markers like CRP and ferritin in COVID-19 patients. Lipid profile may be used as a potential marker in all COVID-19 patients in assessing prognosis of disease.

Hemophagocytic Lymphohistiocytosis after COVID-19 Vaccination: A Case Report

Aim and background: Cases of thrombotic thrombocytopenia induced by coronavirus disease 2019 (COVID-19) vaccines have been reported recently. Herein, we describe hemophagocytic lymphohistiocytosis (HLH) following COVID-19 vaccination. Case report: A 35-year-old male, chronic alcoholic, 3 years into abstinence received first dose Covishield vaccine. He started developing a fever, testicular pain, diminished sensorium requiring invasive ventilation, and decreased urine output 4 days after getting vaccinated. Initial workup for NCCT brain and HRCT chest was normal, tropical fever panel was negative, cultures for blood and endotracheal aspirate were sterile, liver and renal functions showed mild derangement, CSF study was normal. Ultrasound examination of the abdomen revealed mild hepatosplenomegaly, mild testicular swelling, and suprainguinal lymphadenopathy, with no focus of infection. Subsequently, he developed bicytopenia with haemoglobin 9.0 g/dL and platelet counts 50 × 109/L, ferritin 2130 μg/L, triglyceride 353 mg/dL, and decreased fibrinogen 1.41 g/L. Bone marrow as well as lymph node biopsy showed haemophagocytosis with engulfment of neutrophils, lymphocytes, and normoblasts making HLH a likely diagnosis. Soluble CD25 and NK cell function could not be performed. Extensive evaluation was done to look into the etiology of HLH. SARS-CoV-2 reverse transcriptase-polymerase chain reaction (RT-PCR) test was negative. RT-PCR test for Epstein-Barr virus (EBV), influenza A (H1N1, H3N2), influenza B, cytomegalovirus (CMV) performed from endotracheal aspirate (ETA) was negative. Similarly, the RT-PCR test from serum samples for EBV, Parvo B-19, CMV, and from CSF sample for EBV, Parvo B-19, CMV, and HSV-1 was negative. Hepatitis B, C, and HIV serologies were negative. Culture and sensitivity repeated from blood, ETA and urine was sterile. Autoimmune panel including complements levels were negative. Peripheral smear, bone marrow, and lymph node biopsy were normal and did not reveal abnormal or malignant cells. He had persistent fevers to 38.6°C during the first 6 days of his admission, with a rise in his ferritin to 1950 μg/L. The patient received steroids but not etoposide. By the 8th day, his fevers resolved, with improvement in his lethargy and malaise. Two weeks later, his ferritin had reduced to 510 μg/L, platelet count rose to 180 × 109/L, and repeat ultrasound abdomen demonstrated resolution of his splenomegaly. In our patient, there was no clear precipitant of HLH other than the Covishield vaccine. There was no evidence of an infection or malignancy. Due to our patient's clinical stability, resolution of symptoms, and improvement of HLH parameters he did not require HLH specific therapy. It is unclear if he had a pre-existing genetic predisposition to HLH as genetic testing is pending, however, it is unlikely as he has reached the age of 35 and suffered from previous viral infections without developing HLH.

Severe Hypertriglyceridemia as a Cause of Arterial Thrombosis with Peripheral Embolic Complications

Lead Author's Financial Disclosures: Nothing to disclose. Study Funding: None. Background/Synopsis: Extensive evidence exists in support of a causal association of elevated triglyceride-rich lipoprotein (TRL) levels with the risk of atherosclerosis progression. Hypertriglyceridemia has been established as a risk factor for venous thrombosis, including a 2- fold increase in the risk of venous thrombosis in postmenopausal women. However, there is limited data on the role of hypertriglyceridemia in the arterial thrombosis. Objective/Purpose: Not Applicable. Methods: Case description: A 51-year-old white female with hypertension and type 2 diabetes (hemoglobin A1C, 7.4%) was transferred for further management of newly diagnosed bilateral renal and splenic infarcts. No risky habits were elicited except for the use of combined hormonal contraceptives over the past two years to control menorrhagia. Family history was significant for hypertriglyceridemia. Her physical exam was unremarkable. Testing for COVID-19 was negative. An extensive hypercoagulable and autoimmune work-up was unremarkable. Fasting lipid profile was significant for elevated levels of triglycerides, 1,274 mg/dL (replicated on two separate occasions), very low-density lipoprotein-cholesterol, 255 mg/dL, and non-high-density lipoprotein-cholesterol, 214 mg/dL, directly measured low-density lipoprotein cholesterol, 39 mg/dL and lipoprotein(a), 6 mg/dL. There was no structural pathology on the echocardiogram, including no interatrial shunt or intracardiac thrombus. Her whole-body computed tomography angiography revealed a focal calcified protruding thrombus in the distal thoracic aorta. No significant plaque was seen elsewhere in the aorta. Results: Decision-making. The posterior thrombus in the distal thoracic and proximal abdominal aorta was determined as a culprit for the visceral organ infarcts. Over the course of the hospital stay her abdominal pain gradually resolved. Treatment with low dose aspirin and therapeutic dose of low-molecular weight heparin was initiated followed by apixaban and aspirin on discharge. She was started on atorvastatin 40 mg, fenofibrate 145 mg, icosapent ethyl 4 g, resulting in a 70% reduction in the triglycerides levels (306 mg/dL). In 3 months, her repeat CT angiography showed significant resolution of the aortic atherothrombosis with no signs of aortic wall inflammation. At the 6-month follow-up visit she was switched to dual antiplatelet therapy with a plan to repeat imaging in 6 months. Conclusions: This case illustrates challenges in managing patients with arterial thrombosis in the setting of familial hypertriglyceridemia. Apart from severely elevated triglycerides no other etiology was evident. We propose further investigation of the prothrombotic properties of TRL and the role of targeted triglyceride-lowering therapies on atherothrombotic outcomes.

Lipid profile of patients with arterial hypertension who underwent COVID-19: possibilities of drug therapy/ LEADER

Aim. To study the dynamics of the lipid profile of hypertensive patients with dyslipidemia who underwent COVID-19. Material and methods. Hypertensive patients with dyslipidemia who underwent COVID-19 [n=126;58 men and 68 women;median age 60 (56.0;65.5) years] examined. Patients were included into two groups: group 1 (n=64) received a single pill combination of lisinopril + amlodipine + rosuvastatin;2 groups (n=62) continued the previous drug treatment. Clinical, demographic, office blood pressure (BP), total cholesterol (TC), low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol, triglycerides, C-reactive protein (CRP) levels were assessed in all patients in 3 visits within 24 weeks. Results. The groups did not differ in prior antihypertensive therapy (except for more frequent use of angiotensin II receptor blockers in group 2, p<0.05), lipid profile and blood pressure parameters at study entry. A decrease in systolic (by 9.5%) and diastolic blood pressure (by 12.1%) after 24 weeks was found in group 1 compared with 4.29% and 5.56%, respectively, in group 2 (p<0.05). A decrease in the level of total cholesterol by 14.5% and LDL-c by 31.4% after 24 weeks was found in group 1 compared with 11.2% and 9.7%, respectively, in group 2 (p<0.05). The level of CRP during the observation period decreased by 53.7% in group 1 versus 43.4% in patients of group 2 (p<0.05). Conclusion. The single pill combination of lisinopril/amlodipine/rosuvastatin in hypertensive patients with dyslipidemia who underwent COVID-19 led to an improvement in lipid profile and blood pressure control.

ENDOTHELIAL COMPLICATIONS IN HYPERTENSIVE PATIENTS WITH OBESITY OR NORMAL BODY WEIGHT AFTER COVID-19

Objective: To study the contribution of a COVID-19 to endothelial dysfunction in hypertensive patients with obesity or normal body weight. Design and method: 59 hypertensive patients, male and female, aged 20-50 years (40.2 ± 6.7 years), with blood pressure (BP) under control, without diabetes, non-smokers were included in the study. All of them were divided into three groups: I (n = 13) - patients with obesity (body mass index (BMI) > 30 kg/m2) and 1 month after COVID-19;II (n = 11) - patients with normal body weight (BMI < 25 kg/m2) and 1 month after COVID-19;III (n = 25) - patients with obesity (BMI > 30 kg/m2) without COVID-19. Patients of Ith and IIIth groups were comparable in BMI and BP levels. LDL-cholesterol and triglycerides levels, office systolic BP and diastolic BP, flow-mediated dilation (FMD) study to assessed endothelial function, were performed in all groups. Calculation was done with software STATISTICA 6.0. Results: Post-COVID-19 patients with obesity had significantly higher levels LDL-cholesterol and triglycerides, systolic BP and diastolic BP then in post- COVID-19 patients with normal body weight: 3.5 ± 0.7 mmol/l vs 3.02 ± 0.62 mmol/l (p < 0.05), 3.5 ± 2.9 mmol/l vs 1.10 ± 0.3 mmol/l (p < 0.05), 141 ± 9.6 mmHg vs 123 ± 10.3 mmHg (p < 0.05), 89.5 ± 10.01 mmHg vs 76 ± 8.8 mmHg (p < 0.05) respectively. FMD were significantly lower in patients with obesity and COVID-19 (3.6 ± 2.9%, p < 0.05) then in patients with normal body weight and COVID-19 (8.7 ± 3.4%, p < 0,05) and in patients with obesity without COVID-19 (4.2 ± 3.6%, p < 0.05). Conclusions: Our study highlights that chronic impairment of systemic vascular endothelial function in patients with obesity, when intensified by the detrimental effects of SARS-CoV-2 over the endothelium, may explain their worse outcomes in COVID-19. However, obesity itself is one of important factors contributing to deterioration of endothelial function.

Ezetimibe Evaluation as a Treatment of Hyperlipidemia in Patients with Covid-19: A Case Report

The current coronavirus disease known as (COVID-19) which has been declared by the World Health Organization (WHO) in December 2019 as a global health emergency and then after as a pandemic, represents a big challenge to all healthcare systems worldwide specially for managing the infection among patients who are hospitalized, acutely ill or elderly. The death rate caused by COVID-19 is not predictable but is increased by many factors including age, dyslipidemia, diabetes mellitus, obesity, and cardiovascular disorders. Since a lot of patients with these conditions are under lipid-lowering therapy, we carried out this case report study to understand the effectiveness, safety, and potential interactions between Ezetimibe, and patients with acute COVID-19 infection. In this study, the lipid profile, kidney functions, and glycated hemoglobin has been measured baseline and then after 25 days for patient with hyperlipidemia and suffers from acute COVID-19 infection. Serum cholesterol level, HDL, LDL and HDL risk factor were decreased in COVID case by 17%, 10%, 21%, and 7%, respectively. Interestingly, we observed a considerable increase in triglycerides concentration by 13.5%. These findings reveal that Sars-CoV-2 might be a factor interacting with hyperlipidemia-reducing therapy, and lower ezetimibe efficacy. However, larger cohort studies are required to confirm these findings.

DE NOVO DOUBLE GLOMERULOPATHY (MEMBRANOUS NEPHROPATHY, MN AND COLLAPSING FOCAL SEGMENTAL GLOMERULOSCLEROSIS, CFSGS) ASSOCIATED TO POSITIVE MYELOPEROXIDASE-O (MPO) ANTIBODY FOLLOWING PFIZER - BIONTECH MRNA VACCINATION COVID 19

BACKGROUND AND AIMS: In the COVID 19 pandemic era, anti SARS-CoV-2 vaccination showed high efficacy at preventing the infection and its most severe complications. The aim of this report is to describe an unusual double glomerulopathy related to anti SARS-CoV-2 vaccination and the good results obtained with the immunosoppressive treatment. METHOD: An 80-year-old caucasian woman developed a nephrotic syndrome, progressive renal insufficiency and microhematuria. The patient presented a medical history of thrombocytopenic purpura treated and resolved by steroids in 2013, hypothyroidism, hypertension, ischaemic heart disease treated with surgical bypass in 2019 and pacemaker in 2020 for atrial ventricular block. Due to pandemic COVID 19 status, she received two doses of the Pfizer BioNTech mRNA COVID-19 vaccine in March 2021. Two weeks after the second dose her weight increased of 23 kg. The family physician added furosemide to her therapy for generalized edema with no diuretic effect. In April, creatinine was 1.38 mg/dL (versus 0.8 mg/dL 1 year before);urinalysis showed proteinuria (300 mg/dL) and microscopic hematuria;serum total cholesterol level was 218 mg/dL and triglycerides 178 mg/dL;then it was suggested to increase the doses of furosemide. In May 2021, creatinine resulted 2 mg/dL, serum albumin 2 g/dL, and urinalysis confirmed proteinuria and microscopic hematuria;proteinuria was 10 g/day. Abdomen ultrasound showed normal liver, kidneys and spleen, not ascites. Lower limb eco-Doppler showed right superficial femoral artery stenosis of 60% and absence of venous thrombosis. The physical examination evidenced anasarca. The patients were admitted to the nephrology unit;hepatitis B surface antigen, hepatitis C antibody and human immunodeficiency virus antigen and antibody were negative. Both complement C3 and C4 levels resulted within the normal range. Cryoglobulins were absent. Urinary Bence Jones, antinuclear antibody (ANA), anti-extractable nuclear antigen (ENA), anti-double stranded DNA (nDNA) antibodies were negative. Antineutrophil cytoplasm antibodies (ANCA) were 1:2560 with Perinuclear pattern and anti-MPO positivity (716 UA/mL);anti-proteinase-3 antibodies (PR3) were negative. Antiphosholipase A2 receptor antibody (PLA2R Ab) was positive with high titre. A kidney biopsy was performed showing a double nephropathy: a focal segmental glomerulosclerosis (FSGS) with some collapsing features, superimposed on membranous glomerulonephritis (Fig. 1). RESULTS: We started the Ponticelli regimen (alternate months steroids and cyclophosphamide). After the first month of therapy, blood tests revealed creatinine 1.7 mg/dL, haemoglobin 11.7 g/dL;serum albumin 2.7 g/dL and urinalysis without microscopic haematuria. At the third month of therapy, the patient developed atrial fibrillation and started anticoagulation;blood tests were as follows: creatinine 1.1 mg/dL, serum albumin 3.0 g/dL, Ab anti-MPO 7 UA/mL and PLA2R Ab was absent. A left ocular, frontal and parietal herpes zoster induced a short discontinuation of therapy and responded well to Acyclovir;then we concluded the fourth month of therapy. At the fifth month, a SARS CoV 2 RT PCR unexpectedly resulted positive;the patient remained asymptomatic, but we stopped definitively the therapy. One month later, blood tests showed: creatinine 1 mg/dL, serum albumin 4 g/dL, proteinuria 0.7 g/die, MPO 2 UA/mL and PLA2R Ab absent. CONCLUSION: To our knowledge, this is the first case of nephrotic sindrome secondary to a De novo MN and FSGS, associated with positive MPO antibody, following Pfizer-BioNTech mRNA vaccination COVID 19;the patient responded well to immunosoppression going in remission and regaining renal function. (Figure Presented).

IMPACT of COVID OUTBREAK on PREVENTION and CARE for HIV and STIs at A LARGE HOSPITAL

Background: Routine medical care was drastically affected by the overwhelming irruption of COVID-19 pandemic. We comprehensively assessed the impact of the COVID-19 pandemic on the prevention and care for HIV and other sexually transmitted infections at a large reference hospital providing preventive and clinical services for HIV infection and other sexually transmitted infections. Methods: We retrospectively compared clinical and laboratory data from March to December 2020 (first ten months of the SARS-CoV-2 epidemics in Spain) vs. the same period 2019 in the setting of Hospital Clínic of Barcelona which provides preventive and clinical services for HIV infection and other sexually transmitted infections for the region of Catalonia and is the largest of its kind in Spain. Monthly clinical data on HIV pre-exposure and post-exposure prophylaxis users and on adults with HIV infection were retrieved from the administrative hospital database. Monthly tests for HIV, hepatitis B and C, Treponema pallidum, Neisseria gonorrhoeae, and Chlamydia trachomatis, and plasma lipids and glucose were recovered from the laboratory database. De novo HIV, hepatitis B, or hepatitis C diagnosis were considered whenever a person had a first known positive laboratory test. Results: There were less (28% reduction) but more advanced (mean [SD] CD4 cell counts per mm3 at HIV diagnosis 305 [167] vs. 370 [170], P<0.001;26 (18%) persons had AIDS-defining conditions at HIV diagnosis vs. 20 (10%), P=0.03) HIV cases and more gonorrhea (39% increase, P<0.001) and chlamydia (37% increase, P<0.001) infections in 2020 vs. 2019. In people with HIV, rates of viral load above the level of detection remained stable (11% vs 11%, P=0.147) despite less scheduled visits (25% reduction, P<0.001). However, they had less antiretroviral prescription changes (10% reduction, P=0.018), worse plasma lipids (mean total cholesterol 190 vs 185 mg/dL, P<0.001;mean LDL cholesterol 114 vs 110 mg/dL, P<0.001;mean triglycerides 136 vs 125 mg/dL, P<0.001;mean HDL cholesterol 47 vs 48 mg/dL, P=0.006), and an excess of mortality (29 deaths vs 11, 264% increase, P=0.006) due in great part to COVID-19 (n=11) but also to other non-COVID-19 causes. Conclusion: In the setting of a large Spanish reference hospital, SARS-CoV-2 epidemics was associated with an increase of some prevalent sexually transmitted infections, with less but more advanced de novo HIV infections, and with worse non-virologic healthcare outcomes and higher mortality in people living with HIV.

Lipid profile alteration in sars coronavirus 2 (SARS-CoV-2) affected patients and its association with inflammatory markers

Introduction Coronavirus disease 2019 (COVID-19) caused by the SARS coronavirus 2 has challenged the global healthcare system since 2019. Lipids are integral component of this enveloped virus that play an essential role in in its life cycle starting from fusion of viral membrane to host cell, viral replication and exocytosis. It also disrupts metabolic profile due to the release of pro-inflammatory cytokines leading to systemic inflammation reaction. Aim and Objective Therefore, it was aimed to find association between human host serum lipid levels and its association with inflammatory markers. Materials and Methods It was a retrospective study conducted from June 2020 to December 2020, included 500 COVID-19 admitted patients tested positive by Oral/Nasopharyngeal swab by Real time PCR. Total Cholesterol, Triglycerides (TG), Low Density Lipoprotein (LDL-C), High Density lipoprotein (HDL), Ferritin, Procalcitonin (PCT), High sensitive C Reactive protein (hsCRP) estimated in Vitros XT 7600 Autoanalyzer and Interleukin-6(IL-6) by ELISA. Results A significant increase in Serum Triglycerides(185mg/dL) and decrease in HDLC(30mg/dL) was observed with no remarkable finding in other lipid parameters. A statistically significant (p<0.05)positive correlation was observed between TG and inflammatory markers such as hsCRP, PCT, Ferritin, IL-6. Likewise, a negative correlation was detected between HDL-C and hsCRP, PCT, Ferritin, IL-6. Conclusion Lipid profile and host cell metabolism is altered in COVID 19 patients either by cellular infection or by systemic inflammation. Hence it is important to study lipid profile alterations in synergism with inflammatory markers. It may act as guiding step in management and prognosis of this disease.

SARS-CoV-2 induced pancreatitis

Case Report SARS-CoV-2 Induced Pancreatitis Introduction SARS-CoV-2 is responsible for the ongoing pandemic and has been the cause of 4.7 million deaths and 233 million infections worldwide. Although it primarily attacks the respiratory system, the extrapulmonary targets of the virus include the gastrointestinal tract and hepatobiliary system, among others. We present a case of acute pancreatitis in a patient with SARS-CoV-2 infection without any other known causes. Case presentation A 55-year-old male with a past medical history of coronary artery disease, hypertension, 0.5 pack per day tobacco use for 30 years, and hyperlipidemia presents to the emergency department with a chief complaint of left precordial and epigastric sharp pain radiating to the back associated with nausea and vomiting. He denied shortness of breath, cough, fever, or chills. COVID PCR testing was positive on admission, and the patient had not received the COVID vaccine. Heart Rate- 82 beats per minute, Respiratory Rate- 22 per minute, Blood Pressure- 154/95 mmHg, 100% Oxygen Saturation on Room Air. Physical examination was significant for epigastric tenderness. Laboratory results: Lipase- 395U/L, Triglycerides-152 mg/dL, LDL-103 mg/dL, D-dimer- 0.67 mcg/mL. Normal troponin. CXR on admission showed mild patchy bibasilar infiltrates suggestive of developing pneumonia. Right upper quadrant abdominal ultrasound showed no gallstones or other abnormalities within the pancreatobiliary system. CT abdomen and chest with and without contrast showed evidence of acute pancreatitis and no other abnormalities. He was managed with intravenous fluids, pain management, and DVT prophylaxis and transitioned to a full liquid diet on hospital day four with lipase at 37U/L. He was discharged on hospital day five with full resolution of pancreatitis and COVID symptoms. Conclusion There is a limited but growing amount of literature supporting the diagnosis of SARS-CoV-2 induced viral pancreatitis. We worked up common causes of pancreatitis, and we do believe the patient presented with SARS-CoV-2 induced pancreatitis. About 1-2% of non-severe and 17% of severe cases of COVID have exhibited pancreatic injury. Angiotensin-converting enzyme 2 (ACE2) is the main target receptor of SARS-CoV-2. ACE2 is most abundantly expressed in the pulmonary sytem, but is also expressed in pancreatic cells as well as other cells in the gastrointestinal tract. This could explain a correlation between the virus and pancreatitis and other gastrointestinal symptoms. Although there is growing evidence of COVID-induced pancreatitis, the causal relationship is still debated between the two presentations.

Association of serum lipid levels with COVID-19 infection, severity and mortality

Purpose of Study Coronavirus disease (COVID-19) can range from asymptomatic infection to severe illness with multiorgan failure. Recent studies demonstrated an association between lower serum lipid levels namely high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total cholesterol (TC) and COVID-19 disease severity. But the results lack consistency, and the magnitude of the association is currently unknown. Methods Used We conducted a systematic review and metaanalysis on the difference in HDL, LDL, TC, and triglycerides (TG) levels between 1) COVID-19 patients and healthy controls 2) COVID-19 patients with and without severe disease 3) COVID-19 patients who died and who survived. We included articles from PubMed and Embase up to September 1, 2021. We analyzed the pooled mean differences (pMD) in lipid levels (mg/dL) for the above-mentioned groups using random effects meta-analysis and assessed publication bias using funnel plots. Summary of Results Among the 441 articles retrieved, 29 articles (26 retrospective and 3 prospective cohorts) met the inclusion criteria with an aggregate of 256,721 participants. Patients with COVID-19 had lower HDL (pMD = -6.95), and TC (pMD = -14.9) levels (table 1 and figure 1). There was no difference in LDL and TG levels among patients with and without COVID-19. Patients with severe COVID-19 had lower HDL (pMD = -4.4), LDL (pMD = -4.4), and TC (pMD = -10.4) levels compared to non-severe COVID-19 patients. Patients who died had lower HDL (pMD = -2.5), LDL (pMD = -10.6) and TC (pMD = -14.9) levels. TG levels did not differ with COVID-19 severity or mortality. None of the above analyses showed statistically significant publication bias. Conclusions Our analysis demonstrated lower lipid levels in COVID-19 patients compared to healthy controls. Among COVID-19 patients, lower HDL, LDL, and TC levels were associated with severity and mortality. We believe that reduced lipoprotein levels are secondary to systemic inflammation and hepatic dysfunction. Lipid levels could be explored as potential prognostic factors in patients with COVID-19. (Table Presented).

An atypical presentation of hemophagocytic lymphohistiocytosis secondary to toxoplasmosis in an immunocompetent 10-yearold boy

Case Report Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening condition that can occur as primary disorder or secondary to a variety of infections, rheumatic diseases, or malignancies. It is usually diagnosed among patients who are hospitalized with shock-like multiorgan dysfunction and unremitting fevers. It is associated with high mortality and morbidity. HLH secondary to toxoplasmosis is not uncommon in immunocompromised patients. However, it is rarely reported in immunocompetent patients. We herein, report a case of HLH triggered by toxoplasmosis in an immunocompetent patient. Case description A previously healthy 10-year-old male, who lives on a farm, presented with acute onset abdominal pain, vomiting, subjective fever, generalized myalgia, lymphadenopathy, and hepatosplenomegaly. Initial labs revealed thrombocytopenia, neutropenia, abnormal hepatic panel, and significantly elevated ferritin, which worsened upon recheck. Further workup revealed increased triglyceride and soluble IL-2 receptor and decreased fibrinogen, which confirmed the diagnosis of HLH. Toxoplasma testing showed positive IgM and IgG with low IgG avidity, indicative of a recent infection. Brain MRI and fundoscopy were unremarkable. Other infectious workup including hepatitis A, B, and C viruses, CMV, and respiratory pathogen panel including Covid-19 were negative. EBV serology was consistent with previous infection. Immunologic work up showed increased CD8 T cells and increased IgM. Treatment for HLH was not initiated since patient remained well-appearing and afebrile throughout the hospital stay. Treatment for toxoplasmosis was not indicated due to the absence of brain and retinal involvement. Subsequently, laboratory parameters started to improve on day 6 of hospitalization. The patient was discharged the following day. Five days later, platelet count, ANC, ferritin, and fibrinogen levels were normalized. Discussion Although meeting HLH-2004 diagnostic criteria, the course of illness was not typical, as this patient remained afebrile and clinically well with spontaneous recovery. This is in contrast to 95% of typical HLH cases that have high unremitting fever. The initial suspicion of HLH was low due to the atypical features. We proceeded with the HLH investigations due to hyperferritinemia on repeat testing, which has a 90% sensitivity for HLH. Soluble IL-2 receptor test further confirmed our suspicion. To our knowledge, there have been only a few pediatric case reports of HLH secondary to acquired toxoplasmosis without an underlying condition. No underlying immune deficiency disorder was found. Conclusion This case highlights the fact that toxoplasmosis can trigger HLH in immunocompetent children. Early diagnosis and prompt treatment are crucial in avoiding a fatal outcome.