Mesenteric Panniculitis Secondary to Epstein–Barr virus

Dear Editor, A 36-year-old homemaker presented with fever, right hypochondrial pain, and vomiting for 5 days. She was febrile and had tachycardia, but had normal blood pressure. The abdomen was soft, with right hypochondrial tenderness, with no hepatosplenomegaly or shifting dullness, and bowel sounds were normally heard. Hemoglobin was 12.7 g/dl, leukocyte count 1900/ml with 50% neutrophils, platelet count 11,000/μl, and C-reactive protein was high. Peripheral smear showed reduced platelet count with atypical lymphocytes. Blood biochemical tests were normal except for high transaminase levels (alanine transaminase 115 and aspartate transaminase 225). Chest X-ray showed mild right-sided pleural effusion. Ultrasonography of the abdomen was unremarkable except for mild pleural effusion bilaterally. Contrast-enhanced computed tomogram of the abdomen and chest showed bilateral mild pleural effusion more on the right side [Figure 1a and b], mild ascites [Figure 1c], and fat stranding adjacent to the second and third parts of the duodenum and the ascending colon sparing the cecum [Figure 1d and e] consistent with mesenteric panniculitis (MP). The rest of the abdominal structures were normal. Pleural fluid was exudative with lymphocytic pleocytosis. Pleural fluid acid–fast bacilli, Gram stain, malignant cytology, culture, and antinuclear antibody were negative. Her serum ferritin was 5800 ng/mL, serum lactate dehydrogenase 1050 IU/L, serum triglycerides 250 mg/dl, and serum fibrinogen 180 mg/dl.Figure 1: Contrast-enhanced computed tomogram of the abdomen and chest showing bilateral mild pleural effusion more on the right side (marked with arrows in (a and b), mild ascites (marked with arrows in (c)), and fat stranding adjacent to the second and third part of the duodenum and the ascending colon sparing the caecum (marked with arrows in (d)) and marked with arrowhead in (e) consistent with MPEtiological workup including dengue, Leptospira, Brucella, Q fever, HIV, hepatitis B, and hepatitis C serologies were negative. The test for malarial parasite was negative and blood cultures did not reveal any growth. Autoantibody profiles including antinuclear antibody, rheumatoid factor test, and c and P antineutrophil cytoplasmic antibodies were all negative. C3 and C4 levels were normal. Epstein–Barr virus (EBV) polymerase chain reaction was 5 log IU/mL (normal range 5 0–2.7 log IU/mL). She was diagnosed with MP secondary to EBV infection and secondary hemophagocytic lymphohistiocytosis (The modified 2009 HLH criteria). She was managed with ceftriaxone initially which was discontinued when the blood cultures were negative. She was afebrile and had a reduction in abdominal pain 3 days following admission. Her cytopenias, deranged liver function, and ferritin started to improve after 3 days. She was discharged after 7 days of admission and was asymptomatic at discharge. When followed up after 1 week, she was asymptomatic and her laboratories were normal. Follow-up CT 6 months after initial presentation showed complete resolution of MP. MP is an inflammatory disorder with unclear pathophysiology.[1] MP has been associated with abdominal surgery, pancreatitis, autoimmune diseases, and malignant infiltration of the mesentery.[2] Mesenteric abnormalities on imaging were previously described in infections caused by various organisms.[3] Mesenteric lymphadenopathy can be associated with viral infections such as HIV, EBV, Parvovirus, and chronic hepatitis B and C.[3] A case of acute Vibrio cholerae infection with computed tomography changes consistent with MP was previously reported.[4] We describe a patient with MP secondary to EBV infection which to our knowledge is the first such report. Physicians should be aware of such unusual presentations of EBV infection which have excellent outcomes with conservative therapy. Research quality and ethics statement The authors followed applicable EQUATOR Network (https://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.