Quicksilver cholecystitis.
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Cholecystitis↗
Biomedical subjects
Stefan Urbanski
Publications and source records attributed to Stefan Urbanski.
Stromelysin-2 (matrix metalloproteinase 10) is inducible in lymphoma cells and accelerates the growth of lymphoid tumors in vivo.
Matrix metalloproteinase (MMP) 10 (stromelysin-2) is known to degrade various components of the extracellular matrix; however, the signals that regulate its expression and its role in lymphoma growth remain unknown. In the present work, we report the up-regulated expression of MMP10 in T lymphoma cells following contact with endothelial cells. The induction of MMP10 was found to be dependent on the specific interaction between LFA-1 and ICAM-1, which play a central role in regulating the expression of genes involved in the rate-limiting steps of lymphoma development. MMP10, but not MMP3 (stromelysin-1), was also up-regulated in human B lymphoma cells following exposure to IL-4, IL-6, and IL-13, but not to IL-1. To gain further insight into the role of MMP10 in lymphoma development, we generated lymphoma cell lines constitutively expressing high levels of MMP10 and studied these cells for their ability to form thymic lymphoma in vivo. Mice injected with lymphoma cells constitutively expressing MMP10 developed thymic lymphoma more rapidly than those injected with control lymphoma cells. These results provide the first in vivo evidence that overexpression of MMP10 promotes tumor development, and indicate that MMP10 induction is an important pathway activated not only upon ICAM-1/LFA-1-mediated intercellular contact, but also following activation of tumor cells with inflammatory cytokines.
Animals↗
Isolated visceral small artery fibromuscular hyperplasia-induced ischemic colitis mimicking inflammatory bowel disease.
A unique case of fibromuscular hyperplasia (FMH) of the visceral vasculature is presented. A 31-yr-old patient presented with a chronic colitis initially diagnosed as ulcerative colitis 1 yr earlier. On presentation, the endoscopic appearance showed deep linear ulcerations and cobblestoning and was more consistent with Crohn's disease. Biopsies of the area, however, suggested an ischemic etiology. The patient failed to respond to local 5ASA and prednisone therapy and progression of the disease led to a left hemicolectomy. A diagnosis of a small vessel fibromuscular arteriopathy was made on the resected specimen. This is the first case presentation of FMH mimicking inflammatory bowel disease. The lack of any systemic involvement of FMH with isolated small vessel disease has never been reported and serves as an index case of which clinicians should be aware. The literature is reviewed and the possible implications are discussed.
Adult↗
Primary amyloidosis presenting as small bowel encapsulation.
Amyloidosis is a pathological process which encompasses a spectrum of diseases that result from extracellular deposition of pathological fibrillar proteins. Clinical presentations vary depending on the organs involved. There is no documented case of amyloidosis presenting as small bowel encapsulation. A previously healthy 62-year-old man developed a small bowel obstruction in 1997. At surgery, a peculiar membrane encasing his entire small bowel was discovered. This appeared to have no vascularity and was removed without difficulty, exposing a grossly normal bowel. Histopathology revealed thick bands of collagen overlying the peritoneal surface, which was congo red positive and showed apple green birefringence. The findings were consistent with encapsulating peritonitis due to amyloidosis. There was no history or symptoms of any chronic inflammatory condition and he became symptom-free postoperatively. An abdominal fat pad biopsy failed to demonstrate amyloidosis. Endoscopic duodenal biopsies revealed classical primary amyloidosis. Quantitative immunoglobulins, lactate dehydrogenase, C3, C4 and beta-2 microglobulin were normal. Protein electrophoresis identified monoclonal paraprotein, immunoglobulin G lambda 3.7 g/L. Bone marrow biopsy and aspirate revealed only a mild plasmacytosis (5% to 10%). Echocardiogram and skeletal survey were normal. He had mild proteinuria. Complete blood count, C-reactive protein, calcium, albumin and total protein were normal. No specific therapy was instituted. In January of 1998 the patient remained asymptomatic with no gastrointestinal, cardiovascular or constitutional symptoms. He had developed nephrotic range proteinuria (3.95 g/24 h), microalbuminuria, hypoalbuminemia and a renal biopsy consistent with renal amyloidosis. In 1999 there was an increase in the monoclonal paraprotein (6.2 g/L). The remaining investigations were normal except for an echocardiogram which showed left ventricular hypertrophy but a normal ejection fraction and no diastolic dysfunction. He went on to have high-dose chemotherapy and an autologous stem cell transplant in September, 2000. He has subsequently developed renal insufficiency. To our knowledge this is the first reported case of primary amyloidosis presenting as small bowel obstruction from encapsulating peritonitis.
Amyloidosis↗
Reversible sclerosing cholangitis secondary to cryptosporidiosis in a renal transplant patient.
Cryptosporidium parvum is a well-known cause of chronic diarrhea. In human immunodeficiency virus (HIV)-infected patients as well as in other immunocompromised patients it has also been shown to cause sclerosing cholangitis. We report a case of reversible C. parvum-induced sclerosing cholangitis in a renal transplant patient. This 40-year-old female received a renal transplant 9 years prior to presentation. She had no history of liver disease and was doing well on tacrolimus, prednisone, and azathioprine. She developed diarrhea and was found to have C. parvum present in the stool. Shortly after, she developed clinical, biochemical, radiologic, and histologic features of SC. After accidental reduction in her immunesuppression secondary to starting her on rifampin to treat her itching, she cleared C. parvum from her stool and had a marked improvement in her diarrhea, jaundice, and general health. Her liver enzymes normalized and magnetic resonance cholangiography showed complete resolution of biliary abnormalities. To our knowledge, this is the first case of C. parvum-induced sclerosing cholangitis in a renal transplant patient and one of a few in non-HIV patients. It is also the first to document resolution of sclerosing cholangitis after eradication of C. parvum in a non-HIV patient.
Adult↗