suMMuRY A case of primary haemangiosarcoma of the liver with secondary deposits in the pericardium is described. The patient presented most unusually with cardiac tamponade. There was no association with vinyl chloride, thorium dioxide, or arsenic.Primary haemangioendothelial sarcoma of liver is remarkable. A diagnosis of pericardial tamponade rare and usually presents with abdominal pain and was made. After aspiration of 350ml bloodweight loss (MacSween et al., 1973; Ludwig and stained fluid the patient became conscious, the Hoffman, 1975). Most patients die of hepatic failure heart rate fell to 80 per minute, blood pressure rose or exsanguination from the hepatic tumour (Lud-to 130/80 mmHg, and the central venous pressure wig and Hoffman, 1975). Metastases are reported fell to + 8 cm. The patient was now able to give a in less than half of the cases and are rare in the history of long-standing indigestion, recent malaise, pericardium (Ludwig and Hoffman, 1975). We and weight loss. As a plumber he had been exposed describe a patient with primary haemangio-to platinum and asbestos. endothelial sarcoma of the liver who presented withThe pericardial fluid had a packed cell volume cardiac tamponade from a haemopericardium of 28 (blood PCV 32) and did not clot. Neoplastic resulting from secondary deposits in the right atrial cells were not found and the fluid was sterile on wall.culture. The electrocardiograms varied showing sinus rhythm and occasionally atrioventricular Case history dissociation or atrial fibrillation. There were no changes of myocardial infarction. Echocardiography A 58-year-old plumber developed bronchospasm disclosed no evidence of aortic dissection. On in March 1976. A chest x-ray film in July 1976 admission haemoglobin was 11-8 g/dl, ESR 3 mm/ showed an enlarged heart shadow. While awaiting a hour, SGOT 1960 U/1, HBD 2245 U/1, SGPT referral appointment, the patient suddenly 1230 U/1, and alkaline phosphatase 236 U!/ (normal developed severe epigastric pain, had a haema-<92 U/1). There was no bleeding diathesis. temesis, and collapsed.Alpha-fetoprotein was negative and alpha-I-antiOn admission to hospital he was unconscious and trypsin normal. shocked. On examination he was apyrexial, jaunForty-eight hours after admission the patient diced, and centrally cyanosed. He had a sinus developed peritonitis caused by a perforated peptic tachycardia of 140 per minute, an unrecordable ulcer and died before an operation could be blood pressure, and a raised jugular venous pressure. attempted.The apex beat was not palpable but cardiac dullness to percussion was increased. Heart sounds were Pathology inaudible. The abdomen was soft with epigastric tenderness. A smooth, firm liver edge was palpable At necropsy, the immediate cause of death was a 6 cm below the costal margin. Central venous perforated peptic ulcer. The liver was enlarged pressure was then recorded as + 35 cm H20. A (1174 g) and contained numerous purple nodules chest radiograph showed a large pericardial (up to 2 cm in diameter) which on se...

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INTRODUCTION:Gemcitabine is a nucleoside analog and pyrimidine antimetabolite that inhibits RNA synthesis and is currently approved to treat a variety of cancers. It is considered relatively safe and is generally well tolerated. The most common side effects include myelosuppression and gastrointestinal side effects. Cardiac side effects from this medication are rare. A prior meta-analysis involving gemcitabine showed incidence estimates of ~1% for overall cardiovascular adverse events which includes myocardial ischemia, supraventricular arrythmias, heart failure and pericardial disease. Of all the possible cardiac toxicities, cardiomyopathy appears to be the least reported. In one estimate, out of 13,900 patients reporting any side effects with gemcitabine, only 30 patients (0.22%) had cardiomyopathy. CASE PRESENTATION:A 67-year-old lady with history of metastatic pancreatic adenocarcinoma presented to the emergency department with new onset dyspnea and lower extremity edema for the past week in the setting of recent completion of sixth cycle of adjuvant chemotherapy with gemcitabine. She was hypoxic on arrival with oxygen saturation of 70% on room air. Physical exam was significant for accessory muscle use, bibasilar crackles and 2þ lower extremity edema. Her labs on admission were: Hb 9.6 g/dl, WBC 18.8 k/ul, Platelets 70 k/ul, Sodium 138 mmol/l, Potassium 4.8 mmol/l, Glucose 195 mg/dL, Cr 1.7 mg/dL and pro-BNP 38,400 pg/mL. Chest x-ray showed extensive pulmonary edema with bilateral pleural effusions. EKG showed sinus tachycardia with nonspecific ST changes. Serial troponins were unremarkable. 2D Echocardiogram revealed diffuse hypokinesis and an ejection fraction of 36% which was markedly reduced from baseline of 67%, a month earlier. Acute onset of cardiomyopathy with volume overload was managed with aggressive diuresis. Gemcitabine was indefinitely held for concern of cardiotoxicity. The symptoms improved after this treatment.DISCUSSION: Gemcitabine induced cardiomyopathy is an uncommon condition and requires a high index of suspicion. Mortality rate can be as high as 17%. Evidence of normal ejection fraction prior to initiation of gemcitabine therapy proves a temporal relation between gemcitabine use and subsequent development of acute cardiomyopathy.CONCLUSIONS: This case highlights the significance of early recognition and prompt diagnosis of gemcitabine induced cardiomyopathy. Here, we describe a patient with no known cardiac history receiving gemcitabine for pancreatic cancer who developed rapid onset of cardiomyopathy. Symptoms improved with discontinuation of gemcitabine and aggressive diuresis.

Background: Losartan has been shown to attenuate symptomatic and hormonal responses to hypoglycemia in prior studies. This results predominantly from blocking AT-II receptors blunting the hypoglycemia-induced rise in plasma epinephrine predisposing them to hypoglycemia unawareness. To our knowledge, however there are no case reports describing losartan induced hypoglycemia in a nondiabetic patient. This abstract is the first description of a patient without diabetes mellitus experiencing severe hypoglycemia induced by the ARB, Losartan. Clinical Case: A 51- year old nondiabetic female was found to be somnolent and in acute respiratory failure. Blood sugar was 34 mg/dL. She received D10 by EMS while coming to the hospital. She was intubated and treated for atypical pneumonia based on bilateral interstitial infiltrates. She remained persistently hypoglycemic around 62 mg/dL. Her most recent A1c was 4.4%. Thyroid function was within normal limits. AM cortisol was 16.8 mcg/dL so there was no concern of adrenal insufficiency. She had no history of gastric bypass surgery. She underwent a 72-hour fast and developed symptomatic hypoglycemia. Her venous blood glucose at this time was 49 mg/dL. Her hypoglycemia panel obtained at this time showed C-peptide 0.7 ng/mL, total insulin 2.9 microU/mL, proinsulin 3.1 pmol/L, IGF 45 ng/mL and BHOB 13.5 mmol/L. Her oral hypoglycemic agent screen was negative. Based on levels that were obtained during the hypoglycemic episode, this correlated to a non-diagnostic study for conventionally described causes of hypoglycemia including exogenous insulin, insulinoma, NIPHS, PGBH, oral hypoglycemic agent, insulin autoimmune or IGF-mediated. Her medication list was analyzed again. We learnt that she had recently been started on losartan about a month prior to this admission for her heart failure management. On further review, the patient mentioned that she was noticing these hypoglycemic events in the last month and that seemed to coincide with when she was started on losartan. We subsequently held losartan which resulted in profound improvement in her glycemic control and her blood sugars improved to a range of 110–140 mg/dL consistently. She was discharged from hospital off losartan. Blood sugar was stable on repeat testing outpatient after discharge. Conclusion: This is the first case that demonstrates the role of losartan in causing severe hypoglycemia in patients without a history of diabetes mellitus. Discontinuation of losartan resulted in prompt improvement of hypoglycemia. Reference: (1) Deininger E, Oltmanns KM, Wellhoener P, Fruehwald-Schultes B, Kern W, Heuer B, Dominiak P, Born J, Fehm HL, Peters A. Losartan attenuates symptomatic and hormonal responses to hypoglycemia in humans. Clin Pharmacol Ther. 2001 Oct;70(4):362–9. PMID: 11673752.

Background: Insulinomas are rare tumors with an incidence of approximately 4 cases per million person per year. Only 39 cases of pancreatic neuroendocrine tumors have been reported in pregnancy. We report a case of pregnancy protecting the mother from manifesting the symptoms of insulinoma. Clinical Case: This case describes a 25-year old female who initially noticed symptoms of generalized weakness and oral tingling sensation in Fall 2018. She became pregnant in March 2019. She noticed an immediate reduction of the intensity of her symptoms during pregnancy. Her pregnancy was uneventful, and she delivered a healthy newborn in November 2019. Two months postpartum, she had worsening symptoms including syncopal episodes, confusion, difficulty ambulating and visual changes that improved with PO intake specifically carbohydrate intake. She was evaluated in March 2020 and labs showed the following: venous glucose 32 mg/dL, C-peptide 1.7 nmol/L, BOHB 0.4 mmol/L, Insulin 6.1 microU/ml, Proinsulin 25.8 pmol/L, IGF-2 354 ng/mL, negative insulin antibodies and negative oral hypoglycemic agent screen. TSH was unremarkable and AM cortisol was 16.1 mcg/dL. She was started on diazoxide twice a day. She underwent MRI of abdomen, which was negative followed by an EUS which was also negative. She had run out of her diazoxide and became severely symptomatic resulting in an ER visit where she was found to be hypoglycemic. Further evaluation was done with a Triple Phase spiral CT which showed a 1 cm arterial enhancing focal lesion within the pancreatic neck compatible with insulinoma. This was further evaluated with EUS FNA which confirmed the diagnosis of insulinoma on pathology. Her chromogranin A was 46.5 ng/mL. She is scheduled for surgical removal of the lesion. Conclusion: Pregnancy leads to an increased insulin resistance through hormonal changes with increased expression of placental growth hormone, human placental lactogen and the placental variant of corticotrophin-releasing hormone (via ACTH and cortisol production), TNF-alpha and leptin. These changes that increase the insulin resistance act as a protective mechanism against the detrimental effects of an insulinoma. Pregnancy most likely also delayed the diagnosis of the insulinoma in this patient. Further research is warranted to evaluate the effects of an insulinoma on the mother and fetus. References: 1) Lowy AJ, Chisholm DJ. Insulinoma masked by pregnancy. Intern Med J. 2001 Mar;31(2):128-9. doi: 10.1046/j.1445-5994.2001.00017.x. PMID: 11480477.