Case Presentation: A 47-year-old woman with psoriasis and psoriatic arthritis (on Enbrel) presented to our ER with a three-week history of abdominal pain, back pain, nausea, significant weight loss, and one week of severely painful groin and oral ulcers. Before admission, the patient had a recent negative CT abdomen and pelvis as well as had received a short course of amoxicillin without any improvement in symptoms. Upon presentation, she was afebrile with leukocytosis of 13 thousand/cubic mm, Hgb of 8 gm/dl, and elevated inflammatory markers. A repeat CT abdomen and pelvis revealed new development of periportal and retroperitoneal lymphadenopathy, multiple splenic lesions, and a nonocclusive splenic vein thrombus. This led to multiple diagnostics, and invasive procedures along with multiple subspecialist consultations given concern for infection, malignancy, or an autoimmune process. Endoscopic ultrasound-guided periportal lymph node biopsy yielded fibrofatty tissue with inflammation and necrosis. Later the patient underwent hepatic lymph node biopsy via ex-lap with similar pathology findings. During ex-lap, lymph node, and splenic lesions were clarified to be abscesses with oozing purulence. However, cultures from abscesses remained sterile leading to the diagnosis of aseptic abscess syndrome. Concomitantly, a thorough infectious workup was done to rule out bacterial infection and infections like mycobacterial, fungal, toxoplasmosis, HSV, q fever, and Bartonella. The patient was treated with antibiotics for a significant time. Punch biopsy of the groin ulcers revealed to be pyoderma gangrenosum. Both pyoderma gangrenosum and aseptic abscess syndrome can develop in association with IBD. The patient underwent a colonoscopy which did not reveal evidence of IBD. Antibiotics were discontinued and systemic steroid therapy was initiated. After this change, the patient had significant improvement in symptoms and was transitioned to oral prednisone upon discharge and later was transitioned to biologics in clinic follow-up.
Discussion: The presentation of skin lesions, intra-abdominal lymphadenopathy, and splenic abscesses as well as leukocytosis initially suggested an infectious etiology. After a detailed negative workup and failure to respond to antibiotics, a diagnosis of aseptic abscess syndrome was suspected. The patient had a long hospital stay and underwent extensive diagnostics and invasive procedures before the final diagnosis was made and appropriate treatment was started. This case highlights the importance of knowing the clinical presentation and associated diseases of this rare diagnosis and keeping this in the differential, especially in a patient with concern for deep-seated abscess and negative extensive and repeated investigation for pathogens.
Conclusions: We present a case of Aseptic abscess syndrome which is a rare diagnosis and remains a diagnosis of exclusion. Differential diagnosis of true infection cannot be overlooked either and careful exclusion of infection is mandatory. Even though often associated with autoimmune disorders like IBD or pyoderma gangrenosum like in our case, there can be isolated aseptic abscess as well. This disease can also relapse and treatment remains difficult and mostly based on case reports.