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Hepatitis and Lipase Elevation in Human Monocytic Ehrlichiosis in a Critically Ill Patient FREE TO VIEW

Karim Nathan, MD; Abhishek Agarwal, MD; Deborah Park, MD; Abhinav Agrawal, MD
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Cooper University Hospital, Philadelphia, PA

Chest. 2015;148(4_MeetingAbstracts):254A. doi:10.1378/chest.2281660
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SESSION TITLE: Critical Care Student/Resident Case Report Posters I

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Transaminase elevation is a well-described feature of human monocytic ehrlichiosis (HME). This case illustrates that lipase elevation can also occur, especially in the setting of septic shock.

CASE PRESENTATION: A 57 year-old man was admitted to the intensive care unit in June for fever, nausea, vomiting, diarrhea, and lethargy. He lived in rural New Jersey and reported that several of his family members had recently been bitten by ticks. His blood pressure was initially 60/40 but increased to 106/58 after he received five litres of intravenous fluid. Physical exam was notable for dry mucous membranes, a benign abdomen, no palpable organomegaly, and no rash. Lab abnormalities included a lipase of 1772 U/L, an aspartate aminotransferase of 110 U/L, an alanine aminotransferase of 83 U/L, a total bilirubin of 1.4 mg/dL, a direct bilirubin of 0.9 mg/dL, and a creatinine of 1.78 mg/dL. He had a platelet count of 69,000 U/L and a bandemia of 37%. Computed tomography of the abdomen revealed hepatosplenomegaly and a normal pancreas. All rickettsial serologies were negative, as were anaplasma and babesia PCR. However, ehrlichia chafeensis PCR returned positive. He promptly improved with doxycycline.

DISCUSSION: Gastrointestinal involvement of HME includes hepatosplenomegaly, cholestasis, jaundice, nausea, vomiting, diarrhea and even acute abdomen.1 Liver injury occurs as organisms proliferate within hepatocytes and stimulate an immune response, resulting in hepatitis and transaminase elevation.1 This case is the first to report an elevation in lipase in association with severe HME. The patient had no clinical or radiographical evidence of pancreatitis, and so we are left to wander about the cause. R rickettsii has been known to cause pancreatic injury through vasculitis. However, vasculitis is not a feature of E chafeensis infection. Most likely, the elevation in lipase was the result of two mechanisms. Firstly, the pancreas is susceptible from inflammation in surrounding intra-abdominal organs, including the bililary tree and the liver.2 Secondly, septic shock often leads to lipase elevation, either through pancreatic hypoperfusion itself, or through splanchnic hypoperfusion resulting in mesenteric ischemia and leakage of intra-intestinal pancreatic enzymes through injured submucosa.3

CONCLUSIONS: HME has numerous gastrointestinal manifestations and can cause direct hepatic damage. Furthermore, it can feature lipase elevation, which can be seen in virtually any critical illness.

Reference #1: Zaidi SA, Singer C. Gastrointestinal and hepatic manifestations of tickborne diseases in the United States. Clin Infect Dis. 2002; 34(9):1206-12.

Reference #2: Lam VW, Pleass HC. Significant elevations of serum lipase not caused by pancreatitis: a systematic review. HPB (Oxford). 2015 Feb;17(2):99-112.

Reference #3: Denz C, Siegel L, Lehmann KJ, Dagorn JC, Fiedler F. Is hyperlipasemia in critically ill patients of clinical importance? An observational CT study. Intensive Care Med. 2007 Sep;33(9):1633-6.

DISCLOSURE: The following authors have nothing to disclose: Karim Nathan, Abhishek Agarwal, Deborah Park, Abhinav Agrawal

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