Prolonged Diarrhea, Protein Losing Enteropathy, and Intestinal Perforation: An Illustrative Case of HIV-Associated Kaposi Sarcoma
P Benjamin, N Brownlee, A Jain, K Alwood, S Dorman, A Agwu
diarrhea, enteropathy, hivaids, kaposi sarcoma
P Benjamin, N Brownlee, A Jain, K Alwood, S Dorman, A Agwu. Prolonged Diarrhea, Protein Losing Enteropathy, and Intestinal Perforation: An Illustrative Case of HIV-Associated Kaposi Sarcoma. The Internet Journal of Gastroenterology. 2006 Volume 5 Number 2.
A 24 year-old male with AIDS, chronic non-bloody diarrhea, abdominal pain, and anasarca, developed a jejunal perforation. This case highlights a constellation of rare findings associated with Kaposi's sarcoma – GI lesions in the absence of cutaneous lesions, protein losing enteropathy with anasarca, and intestinal perforation.
A 24 year old male with AIDS (CD4 count 4 cells/mm3, HIV viral load 29,500 copies/ml) presented with 2 months of non-bloody diarrhea, abdominal pain, fatigue, and subjective fevers. He was being treated presumptively for
Treatment with intravenous ganciclovir was initiated for CMV, and oral vancomycin was started pending results of repeat stool studies for
An emergent exploratory laparotomy for the presumed diagnosis of
There was thickening of the peritoneum and visceral walls, attributed to inflammation from peritonitis, but no other abnormal pathology was noted. The colon was grossly unremarkable, but due to the patient's sepsis, colitis on CT imaging, perforation, and concern for fulminant and refractory
There was no evidence of infectious colitis due to CMV,
Epidemic KS is the most common HIV-associated malignancy. Though classically limited to the skin, KS can be aggressive and can involve nearly every organ. Visceral KS rarely occurs in the absence of cutaneous lesions, but is frequently present once cutaneous KS is diagnosed. At autopsy, visceral KS has been recognized in 30-77% of patients with a history of cutaneous KS lesions1,2,3,4,5,6.
In HIV-associated KS, gastrointestinal lesions are typically asymptomatic, but can cause diarrhea, gastrointestinal bleeding, bowel obstruction, mesenteric cyst formation, protein-losing enteropathy, intussusception, and diverticulitis2,7. To our knowledge, there are only 3 prior case reports of intestinal perforation attributed solely to KS7,8,9, with the few other reported cases of KS-associated intestinal perforation complicated by CMV vasculitis10, mycobacteria and candida11. In our case, histopathology showed no other contributing factors, further emphasizing that isolated gastrointestinal KS can have catastrophic outcomes.
Protein-losing enteropathy (PLE) is frequently seen in AIDS, and can be caused by infections (e.g. cryptosporidium, giardia, CMV) or malignancy (e.g. lymphoma), or be idiopathic (e.g. HIV enteropathy) 12. PLE can result from mucosal erosion, increased permeability, or lymphatic obstruction -- all of which can occur in KS. In a series of 83 HIV patients evaluated for PLE by measure of fecal alpha-1 antitrypsin, 33% with normal serum albumin, and 70% with hypoalbuminemia were found to have PLE. Of the patients who underwent GI evaluation, the five percent that were identified to have KS had the highest degree of protein loss. KS is an unusual, but important cause of PLE in HIV patients13,14,15.
In our patient, chronic diarrhea, profound hypoalbuminemia and anasarca were a result of KS-associated PLE, in the setting of a large tumor burden in the intestines and mesentery, and in the absence of significant hepatic or renal disease. This case illustrates that even in the absence of cutaneous findings, KS can cause PLE and visceral perforation resulting in significant morbidity.
Allison Agwu, M.D. Department of Infectious Diseases 1830 Monument Street Rm 402 Baltimore, Maryland 21287 Phone: 410-614-3917 Fax: 410-614-8488 Email: firstname.lastname@example.org