Low fecal elastase: potentially related to transient small bowel damage resulting from enteric pathogens

Fecal elastase is considered to be a highly sensitive and specific non-invasive exocrine pancreatic function test. However, enteropathy may theoretically cause decreased exocrine pancreatic enzyme secretion through alteration of enteric hormone release. Objective: The aim of this study was to evaluate the possible influence of transient small bowel damage on pancreatic elastase secretion. Methods: We studied 166 children (aged 4 months to 14 years, mean 2 years); 114 of these children had acute enteritis and 52 children were control subjects (with gastro-intestinal symptoms or extra-intestinal diseases). Feces were collected from each patient 3 days after the onset of diarrhea and then tested for fecal elastase, bacterial pathogens, Rotavirus, and Adenovirus. Liquid fecal samples were not considered eligible for elastase measurement. Pancreatic elastase was measured using an ELISA method (Sche.Bo.Tech, Germany). We classified the results, expressed in \u3bcg/g stool, as: severe pancreatic insufficiency (200 \u3bcg/g). Results: In the acute enteritis group we found severe levels in 14 (12%) children, moderate levels in 18 children (16%), and normal levels in 82 children (72%). In contrast, 52 of 52 (100%) control subjects demonstrated normal results. Statistical analysis (Wilcoxon rank test) demonstrated a significant difference between the enteritis and control groups (P < 0.01). Serial measurement of fecal elastase performed in 10 patients with enteritis showed a progressive increase of levels in 6 patients and an early decline with subsequent increases in the other 4 patients. Conclusions: Transient exocrine pancreatic insufficiency may be present in transient small bowel disease, caused by both bacterial and viral infections, possibly related to reduced enteric CCK secretion

Is the pancreas affected in patients with septic shock? A prospective study

Hyperamylasemia can be observed anecdotally during the course of severe sepsis or septic shock. This study aimed to investigate the possibility of pancreatic involvement in patients with septic shock using serum pancreatic enzyme determinations and imaging techniques in 21 consecutive patients with septic shock and 21 healthy subjects as controls. METHODS: The serum activity of pancreatic amylase and lipase was assayed initially in all subjects and 24 and 48 hours after the initial observation in the 21 patients with septic shock. All patients also underwent radiological examination to detect pancreatic abnormalities. RESULTS: The serum activity of pancreatic amylase was significantly higher in the 21 patients with septic shock than in the 21 control subjects during the study period, while the serum activity of lipase was similar to that of the control subjects. Amylase and lipase serum activity did not significantly changed throughout the study period in the 21 patients with septic shock. None of the patients with pancreatic hyperenzymemia had clinical signs or morphological alterations compatible with acute pancreatitis. CONCLUSION: The presence of pancreatic hyperenzymemia in septic shock patients is not a biochemical manifestation of acute pancreatic damage, and the management of these patients should be dependent on the clinical situation and not merely the biochemical result

Fecal Calprotectin Levels in Patients with Colonic Polyposis

Context: The usefulness of stool calprotectin determination in diagnosis of inflammatory disease of the colon has been reported; information about its usefulness for patients with polyposis are scarce, however. Objective: To evaluate the significance of stool calprotectin concentrations for patients affected by colonic polyposis. Patients: Sixty-three consecutive patients (35 males, 28 females, mean age 60.3 years, range 39-78 years) were enrolled: 26 patients (41.3%) with polyps, 17 patients (27.0%) with asymptomatic diverticular disease, and 20 subjects (31.7%) with normal endoscopic appearance of the colon. Results: Stool calprotectin concentrations were 17.4 ± 24.5 μg g-1 for patients with colonic polyposis, significantly higher than concentrations for patients with diverticulosis (7.1 ± 5.7 μg g -1; P = 0.026) or for patients with normal appearance of the colon (calprotectin 6.0 ± 5.8 μg g-1; P = 0.003). For patients with a single polyp, stool calprotectin concentrations were similar to those for patients with multiple polyps. Calprotectin fecal concentrations for patients with sessile polyps and those with flat polyps were not significantly different. Calprotectin concentrations were not significantly related to the size of the polyps. Conclusion: Our data show that colonic polyposis may cause an increase in stool calprotectin values and that these colonic lesions should be suspected when elevated stool calprotectin concentrations are found

Fecal calprotectin levels in patients with colonic polyposis

Context: The usefulness of stool calprotectin determination in diagnosis of inflammatory disease of the colon has been reported; information about its usefulness for patients with polyposis are scarce, however. Objective: To evaluate the significance of stool calprotectin concentrations for patients affected by colonic polyposis. Patients: Sixty-three consecutive patients (35 males, 28 females, mean age 60.3 years, range 39-78 years) were enrolled: 26 patients (41.3%) with polyps, 17 patients (27.0%) with asymptomatic diverticular disease, and 20 subjects (31.7%) with normal endoscopic appearance of the colon. Results: Stool calprotectin concentrations were 17.4 \ub1 24.5 \u3bcg g-1 for patients with colonic polyposis, significantly higher than concentrations for patients with diverticulosis (7.1 \ub1 5.7 \u3bcg g -1; P = 0.026) or for patients with normal appearance of the colon (calprotectin 6.0 \ub1 5.8 \u3bcg g-1; P = 0.003). For patients with a single polyp, stool calprotectin concentrations were similar to those for patients with multiple polyps. Calprotectin fecal concentrations for patients with sessile polyps and those with flat polyps were not significantly different. Calprotectin concentrations were not significantly related to the size of the polyps. Conclusion: Our data show that colonic polyposis may cause an increase in stool calprotectin values and that these colonic lesions should be suspected when elevated stool calprotectin concentrations are found

Serum N-terminal pro-brain natriuretic peptide is a sensitive marker of myocardial dysfunction in AL amyloidosis

Background - Brain natriuretic peptide (BNP) is a marker of ventricular dysfunction and can be used to assess prognosis in heart failure and after myocardial infarction. Heart involvement is the most important prognostic factor and causes death in almost all patients with light-chain amyloidosis (AL). We investigated the prognostic value of NT-proBNP and its utility in monitoring amyloid heart dysfunction. Methods and Results - NT-proBNP was quantified at diagnosis in 152 consecutive patients seen at the coordinating center of the Italian Amyloidosis Study Group (Pavia) from 1999 throughout 2001. Heart involvement was estimated on the basis of clinical signs, electrocardiography, and echocardiography. NT-proBNP concentrations differed in patients with (n=90, 59%) and without (n=62, 41%) heart involvement (median: 507.8 pmol/L versus 22.1 pmol/L, P= 10-7). The best cutoff for heart involvement was at 152 pmol/L (sensitivity: 93.33%, specificity: 90.16%, accuracy: 92.05%) and distinguished two groups with different survival (P<0.001). The Cox multivariate model including NT-proBNP was better than models including echocardiographic and clinical signs of heart involvement. NT-proBNP appeared to be more sensitive than conventional echocardiographic parameters in detecting clinical improvement or worsening of amyloid cardiomyopathy during follow-up. Conclusions - NT-proBNP appeared to be the most sensitive index of myocardial dysfunction and the most powerful prognostic determinant in AL amyloidosis. It adds prognostic information for newly diagnosed patients and can be useful in designing therapeutic strategies and monitoring response. NT-proBNP is a sensitive marker of heart toxicity caused by amyloidogenic light chains

Assessing heteroplasmic load in Leber's hereditary optic neuropathy mutation 3460G->A/MT-ND1 with a real-time PCR quantitative approach

To quantify the amount of the 3460G\u2192A/ND1 point mutation responsible for Leber's hereditary optic neuropathy, we developed a quantitative real-time polymerase chain reaction method based on the SYBR Green assay and a new approach using the TaqMan assay. Both methods were based on the amplification refractory mutation system, comparing the heteroplasmic load quantified by restriction fragment length polymorphism in 15 Leber's hereditary optic neuropathy family members, with the results obtained using quantitative real-time polymerase chain reaction methods. The comparative evaluation of mitochondrial DNA (mtDNA) heteroplasmy from blood samples showed significant correlation between restriction fragment length polymorphism. analysis, real-time SYBR Green assay, and TaqMan assay. We validated the last method by measuring experimental samples composed by a known proportion of cloned plasmids containing either the wild-type or mutant sequence, giving a correlation coefficient of 0.999 (P < 0.0001). The real-time amplification refractory mutation system polymerase chain reaction by Taq-man assay provides a rapid, reliable, sensitive, reproducible, and one-step quantitative method to detect heteroplasmic mutant mtDNA. This method allows the quantitation of a broad range of mutational load (up to 100%, down to 0.01%) on the basis of in vitro calibration, thus rendering the TaqMan assay suitable for the diagnostic analysis of heteroplasmic load in mtDNA-related disorders. Copyrigh

Variability of NT-proBNP and Its Relationship with Inflammatory Status in Patients with Stable Essential Hypertension: A 2-Year Follow-Up Study

The variability of NT-proBNP levels has been studied in heart failure, yet no data exist on these changes over time in hypertensive patients. Furthermore, studies on the relationship between natriuretic peptides and inflammatory status are limited.220 clinically and functionally asymptomatic stable patients (age 59 ± 13, 120 male) out of 252 patients with essential hypertension were followed up, and NT-proBNP was measured at baseline, 12 and 24 months. No differences in NT-proBNP were found with respect to the basal stage in the hypertrophic group, but significant changes were found in non-hypertrophic subjects. The reproducibility of NT-proBNP measurements was better in patients with hypertrophy than in the non-hypertrophic group for the three intervals (stage I-basal; stage II-stage I; stage II-basal) with a reference change value of 34%, 35% and 41%, respectively, in the hypertrophic group. A more elevated coefficient of correlation was obtained in the hypertrophic group than in patients without hypertrophy: basal versus stage I (r = 0.79, p < 0.0001 and r = 0.59, p < 0.0001) and stage I versus stage II (r = 0.86, p < 0.0001 and r = 0.56, p < 0.0001). Finally, levels of NT-proBNP significantly correlated with sTNF-R1 (p < 0.0001) and IL-6 (p < 0.01) during follow-up. A multivariate linear regression analysis showed that sTNF-R1 is an independent factor of NT-proBNP.This work shows that there is good stability in NT-proBNP levels in a follow-up study of asymptomatic patients with stable hypertension and left ventricular hypertrophy. As a consequence, assessment of NT-proBNP concentrations may be a useful tool for monitoring the follow-up of hypertensive patients with hypertrophy. Measured variations in peptide levels, exceeding 35% in a 12-month follow-up and 41% in a 24-month follow-up, may indicate an increase in cardiovascular risk, and therefore implies adjustment in the medical treatment. In addition, this study shows a link between neurohormonal and inflammatory activation in these patients

Determination of neurochemicals in biological fluids by using an automated high-performance liquid chromatographic system with a coulometric array detector

The chromatographic separation of 33 neurochemicals was achieved by using a combined gradient of organic modifier, pH and counter-ion. A secondary separation of unresolved analytes was obtained by using electrochemical detection with a coulometric array of sixteen electrodes. The stability of the analytes was studied and data on analytical performance are reported in addition to a list of neurochemicals detected in a normal plasma sample

Valutazione delle catecolamine plasmatiche: influenza di fattori ambientali e delle procedure di campionamento

Ruolo di fattori inerenti le procedure di campinamento o l'individuo nelle variazioni dei lievvi di catecolamine plasmatiche, come studio del sistema nervoso simpatic