Relationship between laboratory parameters and intensive care unit stay post-liver transplantation: proposal of a model.

UNLABELLED: The aim of this study was to create a model that forecasted the stay in the intensive care unit in post-liver transplantation. METHODS: Twenty-three consecutive patients who underwent liver transplantation provided samples for serum sodium, serum creatinine, total bilirubin, cholesterol, aspartate and alanine aminotransferase, alkaline phosphatase (ALP), albumin, and platelet count for correlation together with age at transplantation in a Pearson correlation model with intensive care unit stay. Multivariate analysis used a regression model to evaluate the relationship between the dependent variable "intensive care unit stay" and the predictor variables that were correlated by a Pearson correlation test. To test the acceptability and strength of the model, analyses of variance was performed and a multiple correlation coefficient R was calculated for the model. RESULTS: Pearson correlation test showed a strong correlation between intensive care unit stay and creatinine (correlation coefficient = 0.34, P = .03), serum sodium (correlation coefficient = -0.42, P < .01), and total bilirubin (correlation coefficient = -0.29, P = .06). Other variables showed no significant correlation, namely correlation coefficients < 0.24 (P > .1). The final model to evaluate the relationship between the dependent variable "intensive care unit stay" and laboratory parameters included ALP, serum creatinine, serum sodium, and total bilirubin as well as a correction for age. CONCLUSIONS: The most significant parameters were total bilirubin, serum creatinine, and serum sodium. The proposal model significantly correlated with the variable "intensive care unit stay." Such data are particularly important since increased intensive care unit stay correlates with a significant reduction in 1-year survival rate.

[Helicobacter pylori and gastric carcinogenesis]. / Helycobacter pylori e carcinogenesi gastrica.

Gastric carcinogenesis is a multistep and multifactorial process beginning with chronic gastritis Helicobacter pylori (Hp) induced in most cases. There are some obstacles to an exclusive acceptance of the idea that the relation of Hp with the preneoplastic/neoplastic changes solely develops by means of the chronic gastritis with its atrophic evolution and achlorydria. Hp may be considered a trigger by means of alteration of cellular synetics without any direct influence on genetic alterations. Under the push of an intense proliferation, the expression of typical antigens of the organ is progressively lost, with acquisition of antigens from other organs. Cellular dedifferentiation displayed, with the progressive increase of immature elements that progress to the more or less total disappearance of differentiated gastric cells or differentiating ones, with the formation of metaplastic/dysplastic clones or even neoplastic ones. The bacteria, together with other environmental factors and individual genetic susceptibility, determine the final risk for the development of gastric cancer. Considering that 1-2% of the Hp positive subjects are estimated to develop gastric cancer and that Hp is considered the cause of 75% of gastric cancer, the eradication of the infection, not only in the initial phases but even in those with preneoplastic changes, involves an advantage for the prevention of gastric cancer. For the prevention among the general population testing Hp-positive subjects for serum antibodies against CagA protein might represent an effective way of identifying patients in whom Hp eradication is advisable also in term of gastric cancer prevention.