Citrobacter freundii infection after acute necrotizing pancreatitis in a patient with a pancreatic pseudocyst: a case report

<p>Abstract</p> <p>Introduction</p> <p>Infections are the most frequent and severe complications of acute necrotizing pancreatitis with a mortality rate of up to 80 percent. Although experimental and clinical studies suggest that the microbiologic source of pancreatic infection could be enteric, information in this regard is controversial.</p> <p>Case presentation</p> <p>We describe a <it>Citrobacter freundii </it>isolation by endoscopy ultrasound fine needle aspiration in a 80-year-old Caucasian man with pancreatic pseudocyst after acute necrotizing pancreatitis.</p> <p>Conclusion</p> <p>Our case report confirms that this organism can be recovered in patients with a pancreatic pseudocyst. On-site cytology feedback was crucial to the successful outcome of this case as immediate interpretation of the fine needle aspiration sample directed the appropriate cultures and, ultimately, the curative therapy. To the best of our knowledge, this is the first reported case of isolated pancreatic <it>C. freundii </it>diagnosed by endoscopy ultrasound fine needle aspiration.</p

Microscopic polyangiitis complicated by the development of prostate cancer and utamide-induced hepatitis

We report a case of a 65-year-old man with microscopic polyangiitis who developed prostate cancer and gastric adenocarcinoma after prolonged oral use of cyclophosphamide. Acute hepatitis with jaundice and marked increase in aminotranferases occurred after 6 months of flutamide treatment for metastatic prostate carcinoma. It is suggested that patients with vasculitis or other autoimmune disorders should avoid prolonged use of cyclophosphamide and other cytotoxic drugs in order to minimize long-term adverse effects, of which the risk of cancer is by far the most important. In patients on flutamide treatment, careful monitoring of flutamide administration with repeated liver function tests should be undertaken, and the drug must be immediately discontinued in patients with abnormal results to avoid progression of liver injury

Disseminated tuberculosis complicating anti-TNF-alpha treatment

An unusually large number of cases of tuberculosis, often of miliary or disseminated form, have been reported in patients receiving infliximab therapy for rheumatoid arthritis or Crohn’s disease. We describe a patient with rheumatoid arthritis who was treated with infliximab and became systemically ill with Mycobacterium tuberculosis-disseminated infection. Patients who are candidates for treatment with turnout necrosis factor-alfa inhibitors should be evaluated for the presence of latent or active M. tuberculosis infection

Myofibroblasts and the progression of crescentic glomerulonephritis

Background. The cellular and humoral factors involved in the pathogenesis of glomerulosclerosis and renal fibrosis following a crescentic glomerulonephritis have not been fully elucidated. Myofibroblasts and transforming growth factor-beta (TGF-beta) have been implicated in the development of experimental and clinical renal fibrosis. We have attempted to identify these mediators in crescentic glomerulonephritis and determine their role in the progression of the disease. Patients and methods, We studied retrospectively 21 patients With crescentic and necrotizing glomerulonephritis (CNG) with emphasis on the renal expression (detected by immunohistochemistry) of myofibroblasts (alpha-smooth muscle actin(+) cells), TGF-beta and collagen (III and TV) as well as their relationship with the clinical outcome of these patients. In situ hybridization histochemistry was applied to determine the site of synthesis of TGF-beta 1 and collagen III. All the patients Were I-reared by immunosuppression and followed up for a median pet-led of 14 months. Results, Myofibroblasts and TGF-beta were detected in the crescents as well as in the periglomerular and tubulointerstitial areas in CNG biopsies. TGF-beta 1 was also detected within renal tubular cells. The percentage of glomeruli with fibrotic and fibrocellular crescents was positively correlated with the severity of Bowman’s capsule disruption (r=0.631, P&lt;0.01) and with the intensity of myofibroblast expression in the interstitium (r=0.504, P&lt;0.05). Strong interstitial immunostain for myofibroblasts and TGF-beta was also noted in association with interstitial fibrosis. In situ hybridization revealed the site of synthesis of TGF-beta 1 to be the renal tubular cells of patients with CNG. By contrast, the site of synthesis of collagen III appeared to be confined to interstitial cells surrounding vessels, tubules and the glomeruli in a distribution identical to that of myofibroblasts. There was a significant positive correlation between the number of interstitial alpha-SMA(+) cells and both interstitial TGF-beta (r=0,591, P&lt;0.01) and interstitial collagen IV (r=0.588, P&lt;0.01). In addition. the number of interstitial alpha-SMA(+) cells and the extent of immunostain for collagen IV were positively correlated with the final serum creatinine (r=0.517, P&lt;0.05 and r=0.612, P&lt;0.01 respectively) and partially predicted functional outcome (R-2=26,7% and 37.5% respectively) as well as the response to treatment. An association was observed between periglomerular myofibroblasts and the generation of fibrotic and fibrocellular crescents. Conclusion. These observations suggest a causal link. between myofibroblasts and fibrotic crescent formation. Mie also believe that interstitial myofibroblasts are actively involved in the pathogenesis of interstitial fibrosis in CNG