Hepatic capillariasis in Maine presenting as a hepatic mass.

We report the first case of hepatic capillariasis in Maine. The patient was a 54-year-old male carpenter who presented with a subacute history of severe abdominal pain, fevers, and weight loss. Initial diagnostic studies suggested a hepatic mass associated with para-aortic lymphadenopathy. The patient underwent open laparotomy for resection of the mass. He was found to have an eosinophilic granuloma in the liver; further evaluation revealed degenerating Capillaria hepatica. The exact route of infection in this case is unknown but is most likely due to accidental ingestion of soil contaminated with mature capillaria eggs. This patient had a low parasite burden and did not exhibit significant peripheral eosinophilia. After treatment with thiabendazole, he recovered uneventfully.

Sepsis and the kidney.

Acute renal failure (ARF) secondary to sepsis is a highly prevalent diagnosis in the ICU setting and continues to be associated with a high rate of morbidity and mortality. The pathophysiology of sepsis-induced acute renal failure involves ischemic or toxic injury to the renal tubular epithelia, resulting in necrosis or apoptosis, and clinically is characterized as acute tubular necrosis. The management of sepsis-induced ARF includes both conventional intermittent hemodialysis and continuous renal replacement therapies. Experimental therapies to improve outcomes in sepsis-associated ARF include the provision of plasmapheresis and adsorption therapies, and the recent development and deployment of a renal tubule assist device.

Impaired monocyte cytokine production in critically ill patients with acute renal failure.

BACKGROUND: Plasma levels of pro- and anti-inflammatory cytokines are predictive of mortality in patients with acute renal failure (ARF). Anti-inflammatory strategies are postulated to be beneficial in treatment. However, there are few studies simultaneously examining monocyte cytokine production and plasma cytokine levels in patients with ARF. METHODS: Study populations consisted of 20 critically ill patients with ARF, 19 critically ill patients without ARF (CRIT ILL), 28 healthy subjects (HS), 19 patients with chronic kidney disease (CKD), and 15 patients with end-stage renal disease (ESRD). Monocyte intracellular content of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interleukin-8, and tumor necrosis factor-alpha (TNF-alpha) was determined by flow cytometry in whole blood. Plasma interleukin 6 and TNF-alpha concentrations were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: At baseline, there were no differences in intracellular monocyte cytokine levels between groups. After lipopolysaccaride stimulation, monocyte production of IL-1beta, TNF-alpha, and IL-6 in ARF patients was reduced by 41%, 84%, and 45%, respectively, compared to healthy subjects (P < 0.01 in each case), and similarly reduced compared to CKD and ESRD patients, and were similar to CRIT ILL patients. Plasma IL-6 levels were significantly higher in ARF patients than healthy subjects, CKD, and ESRD patients (all P < 0.001). CONCLUSION: Critically ill patients with acute renal failure have impaired monocyte cytokine production and elevated plasma cytokine levels in a pattern that closely resembles critically ill patients without ARF, and that is dissimilar to CKD and ESRD patients.

Oxidative stress is increased in critically ill patients with acute renal failure.

Patients with acute renal failure (ARF) experience a high mortality rate. Dysregulated inflammation and altered metabolism may increase oxidative stress in ARF patients. Thirty-eight patients who met the Program to Improve Care in Acute Renal Disease (PICARD) Study inclusion criteria underwent plasma protein oxidation and plasma cytokine measurements. For comparison, similar measurements were also performed in 21 critically ill patients without ARF, 28 patients with ESRD, and 49 healthy subjects. Plasma protein thiol oxidation was measured by spectrophotometry. Plasma protein carbonyl content and cytokine concentrations were measured by ELISA. Plasma protein thiol oxidation and carbonyl content were markedly different in ARF patients compared with healthy subjects, ESRD patients, and critically ill patients (P < 0.001 in all cases). There were significant but less marked differences in plasma protein oxidation between ESRD patients and critically ill patients compared with healthy subjects. Plasma protein thiol oxidation in ARF patients improved with dialysis (P < 0.001); however, there was significant plasma oxidant reaccumulation during the interdialytic period (P < 0.001) not due to rebound equilibration of compartmentalized solutes. Plasma proinflammatory cytokine levels were significantly higher (P < 0.05) in ARF patients and critically ill patients than in healthy subjects. Plasma protein oxidation is markedly increased in ARF patients compared with healthy subjects, ESRD patients, and critically ill patients. Increased oxidative stress may be an important target for nutritional and pharmacologic therapy in ARF patients.