Impact of renal functional impairment on serum tumor markers levels

The objective of this work was to study the impact of renal functional impairment on the circulating levels of alpha-fetoprotein [AFP], carcinoembryonic antigen [CEA], and cancer antigen 19-9 [CA-19-9]. Fifty-one subjects were enrolled in this study. They were divided into three groups. The first group consisted of 13 apparently healthy volunteers [five males and eight females] as a control group. The second group included 17 patients with end stage renal failure [ESRF] [eight males and nine females]. The third group comprised 21 patients [12 males and nine females] with ESRF maintained on hemodialysis [HD]. Tumor marker determinations were performed using enzyme-linked immunosorbent assay. Data management and analysis were performed using Statistical Analysis Systems. Data were summarized using means and standard deviations. Comparisons between groups were done using Kruskall-Wallis, nonparametric analysis of variance. To measure the strength of the association between two numeric variables, Pearson's correlation coefficient was computed. All p-values are two-sided. P-values <0.05 were considered significant. The results suggested that renal functional impairment should be added to the list of benign conditions associated with high serum CEA and CA-l9-9 levels. Before interpreting a tumor marker result in a patient with compromised renal function, it was showed that renal impairment might induce a misleading tumor marker elevation. The lack of significant correlation between elevated serum tumor marker values and serum creatinine and/or urea, and the observed normal serum AFP values raises many questions about the exact mechanisms responsible for increased some tumor markers levels in uremia. The recorded conflicting results of serum tumor markers in uremia indicated that the study of tumor marker kinetics in uremic patients deserves a more considerable attention

Role of the endothelial factors: Nitric oxide, substance P and endothelin, in mediating circulatory effects of halothane and isoflurane

Endothelial cells [ECs] contribute to the regulation of blood pressure and blood flow by releasing vasodilators such as nitric oxide [NO], substance P [SP], prostacyclin [PGI [2]] and adrenomedullin, as well as vasoconstrictors including endothelin [ET] and platelet-activating factor [PAF]. Several previous studies have discussed the relation between anaesthetics and the vascular endothelium in vitro only and demonstrated that volatile anaesthetics [halothane and isoflurane] can alter endothelium-dependant vasodilatation in vitro. In vivo studies are scarce in that field. This could be attributed to the radical nature of NO and its very short half-life and involvement of labor-intensive assay and handling of radioactive isotopes. Consequently, determination of the more stable end products of NO, nitrite and nitrate, was used as a measure for NO production. It is the aim of the current study to make use of this technique to ascertain whether NO, as well as SP and ET, is actually involved in the circulatory effects of isoflurane/halothane, in the clinical context. The study was conducted on 40 patients of [ASA classes I and II], scheduled for open abdominal and/or pelvic procedures of minimum 1 hour duration. Reduction of MBP more than 20% of the preoperative level was considered hypotension. Induction in both groups was done by IV fentanyl [2 micro g/ kg], sodium thiopentone [4-7mg/kg] followed by vecuronium [0.1mg/kg] for intubation and long acting muscle relaxation. Anaesthesia was maintaied using 100% oxygen and halothane 0.5-1%, or isoflurane 0.6-1-2%, in groups Land II respectively. Mechanical ventilation was adjusted to maintain normocapnia. Nitrous oxide was omitted and increments of fentanyl and vecuronium were titrated to the patients' needs. Monitoring of arterial blood pressure and heart rate was done every 5 minutes. Reversal was done using prostigmine [0.08mg/kg] and atropine sulphate [0.02mg/kg]. Venous blood samples were collected before induction, 15, 30 and 60 minutes after initiation of anaesthesia [T0, T1, T2, T3], at cessation of anesthesia and fifteen minutes later [T4 and T5]. Plasma endothelin concentration was determined by enzyme immunoassay technique. Plasma substance P was measured by radioimmunoassay. Determination of serum nitrite and nitrate was done by a colorimetric assay. We have succeeded in ascertaining the role of nitric oxide in isoflurane-induced hypotension, but not halothane. The hypotensive effect of isoflurane which is known to be basically related to peripheral vasodilator mechanism may be via its stimulatory effect on vasodilator mediator [NO]. The role of ET and SP could be related to the short-term changes, mediated by the endothelium, in vasomotor tone in response to alterations in shear stress, in face of the significant hypertension that follows cessation of isoflurane anaesthesia

Study of the interaction between insulin, insulin-like growth factor-1 [IGF-1] and sympathetic nervous system in patients with hepatorenal syndrome

The current study was conducted to understand the interactions between the sympathetic nervous system [SNS], insulin and IGF-1 in cirrhotic patients with renal impairment. This study included 42 patients with cirrhosis [14 cases without ascites, 16 with ascites and 12 with HRS] and 13 healthy subjects as a control group. Enzyme immunoassay technique was used for measurement of serum insulin, serum IGF-1 plasma noradrenaline and plasma neuropeptide Y [NPY]. The results suggested that low circulating IGF-1 might contribute to renal functional impairment in cirrhotic patients. Further studies are necessary to evaluate whether IGF-1 can become a useful therapeutic agent in patients with liver cirrhosis and HRS. Progressive impairment in systemic hemodynamics in cirrhotic patients might underlie a detective sympathetic response which deserves intensive research studies