INTRODUCTION: Hypereosinophilic Syndrome (HES) is defined by the presence of peripheral eosinophilia of 1.5 x 10*9 /L for at least one month resulting in end organ damage in the absence of secondary causes of eosinophilia [1]. The most common organs involved at presentation are skin and lungs. Early cardiovascular and cerebrovascular involvement is rare [2]. CASE PRESENTATION:A 59 year old female with Diabetes Mellitus and hypertension presented with non-ST segment elevation myocardial infarction of the inferior wall. A few days later the patient developed acute right cerebral and cerebellar infarction confirmed by MRI of the brain.She had leukocytosis with an eosinophil count 79 x 10*3/mcL. Tests for parasitic infection, drug allergy, mast cell dyscrasias, and autoimmune process were negative. Bone marrow biopsy showed hypercellular bone marrow with dysplastic eosinophils suggestive of HES. In the absence of skin disease, negative PDGFRA 2 translocation, and normal vitamin B12 levels, a diagnosis of Idiopathic HES was made. She was treated with high dose steroids, hydroxyurea, and leukapheresis followed by imatinib, with no benefit.Over the next week MRI revealed multiple new bilateral infarcts in the cerebellum and cerebrum. Concomitantly she developed STEMI of the inferior wall. Echocardiogram on day three was normal. On days 6, 11, and 23, echocardiogram revealed worsening restrictive cardiomyopathy with infiltrative disease in both ventricles extending from apex to lateral wall and obliterating the left ventricular cavity resulting in cardiogenic shock and pulmonary edema. Rapidly progressing neurologic, as well as cardiac complications, were attributed to HES. Interleukin-5 receptor antibody, Benralizumab, was started without benefit and the patient died.DISCUSSION: In primary HES, eosinophilic expansion occurs due to underlying stem cell, myeloid, or eosinophilic neoplasm. In secondary HES, polyclonal eosinophilic expansion is driven by eosinophilopoietic cytokines. Neurological and cardiovascular involvement is well described but rare and presents usually in the form of parenchymal involvement and not vascular occlusive disease as in our patient [2].CONCLUSIONS: HES syndrome typically presents with features of gastrointestinal, pulmonary, and skin involvement [1]. Neurological involvement, when seen, is in the form of parenchymal involvement and later in disease course. Our patient instead had arterial occlusive disease involving coronary, cerebral, and vertebral basilar system as the primary manifestation of the disease, which is unique. Similarly, cardiac involvement occurs as a restrictive/infiltrative cardiomyopathy not as coronary artery occlusion. A striking feature was the rapid progression of infiltrative disease of the left ventricle leading to near occlusion of the LV cavity resulting in cardiogenic shock and death within 2 weeks.

Introduction: Colorectal Cancer (CRC) is the 3rd most diagnosed cancer worldwide with a high incidence in the USA. Most common sites of involvement with metastatic colorectal cancer (mCRC) are liver and lungs. Brain metastasis (BM) and osseous metastasis (OM) are rarely seen, let alone as the initial presentation of CRC. BM confers poor prognosis among patients with CRC. Diagnosing BM remains critical, as early surgical intervention improves outcome. This is an unusual case of mCRC presenting with neurological deficits as a feature of atypical metastatic sites -brain and bone, with concurrent lung metastasis. Case Description/Methods: A 62-year-old healthy female presented with 3 days of right upper extremity weakness. She denied any other neurological or GI complaints. Her mentation was intact but motor deficit of 2/5 in the right upper extremity was present. Labs were consistent with microcytic anemia (Hg 7.6 g/dL, MCV 71.5 fL), and elevated CEA level (36 ng/mL); transaminases were normal. CT head showed left frontal and right temporoparietal masses with vasogenic edema and mass effect upon left lateral ventricle. MRI brain was deferred due to claustrophobia. CTA chest revealed multiple nodules in bilateral lung fields and NM bone scan showed increased tracer uptake in bilateral ribs concerning for metastatic disease in lungs and bones, respectively. Concurrently, irregular wall thickening of the rectosigmoid colon suspicious for neoplasm was noted on CT abdomen. Dexamethasone was initiated and patient underwent right craniotomy with tumor resection. Pathology was positive for APC, tp53 and kras mutations, consistent with metastatic adenocarcinoma of colorectal origin. Patient was ultimately discharged home with hospice care and colonoscopy was deemed futile. Discussion: Most common sites of mCRC are liver (50%) and lungs (36%), whereas metastasis to brain and bone is very rare and is often a late presentation. Increased risk of BM and OM is associated with known lung metastasis and KRAS mutation in a patient with primary CRC. The average time between detection of OM and diagnosing CRC is reported to be 21 months. We did not find any case describing simultaneous metastasis to lung, brain and bones from primary CRC at the time of diagnosis especially in the absence of hepatic lesions. Lastly, neurological deficit, as seen in our patient, is an uncommon presentation for CRC. Increased awareness of BM and OM in mCRC is crucial for early diagnosis and intervention.

Introduction: Severe acute respiratory syndrome coronavirus, a novel coronavirus that was declared a pandemic in 2019 is now known to affect multiple organ systems. While the primary organ affected has been the lungs, as time elapses, this virus finds victims in multiple organ systems. This case describes the clinical course and histopathological findings of a rare SARS-CoV-2 induced cholangiopathy. Case Description/Methods: A 37-year-old male presented with 5 days of sharp, 10/10, periumbilical pain radiating to the RUQ with no exacerbating or alleviating factors. He had RUQ, and epigastric tenderness to palpation, jaundice and scleral icterus. Labs showed lipase .3000, total bilirubin 12.5, direct bilirubin 9.6, ALP 281, ALT 144, AST 70, and positive SARS-CoV-2 PCR. Previous liver chemistries were normal. Autoimmune and viral hepatitis work-up was negative. US was concerning for acute cholecystitis with CBD 9mm. Antibiotics, IVF and morphine were initiated for presumed gallstone pancreatitis/ acute cholecystitis/choledocholithiasis. ERCP was pursued due to worsening biliary chemistry despite medical management. It revealed non-dilated CBD, but Mirizzi Syndrome was suspected due to a notably distended gallbladder compressing the common hepatic duct during cholangiogram. Sphincterotomy, sludge removal and biliary stent placement were done. Post-ERCP, ALT, AST, and ALP improved but total bilirubin remained elevated. MRCP failed to reveal intraductal filling defects or abnormalities to suggest sclerosing cholangitis. Cholecystectomy and liver biopsy were done which showed hepatocellular and canalicular cholestasis, lymphocytic inflammation, arterialization of central venules, hypocellular bridging fibrous septa connecting adjacent central areas. Patient was discharged with outpatient follow up after clinical improvement. Discussion: Hepato-biliary complications from COVID-19 remain an area of research. Some of the complications reported include cholangiopathy, acalculous cholecystitis and secondary sclerosing cholangitis. Cases of cholangiopathy are described as a late complication of COVID-19 with diagnosis up to 118 days post infection. Though the time of COVID -19 infection is unclear, intrahepatic cholestasis due to pancreatitis/medication and COVID -19 are all contributing factors in our patients' disease progression. Making an accurate diagnosis of COVID-19 cholangiopathy is prudent as it may progress to cirrhosis, especially if a patient has underlying liver pathology.

Figure 1. The image on the left shows whitish nodular mucosa in the second portion of the duodenum in Case 1. The image on the right shows abnormal duodenal mucosa in Case 2.

No abstract