Biomedical subjects

A Shenkin

Publications and source records attributed to A Shenkin.

At least 19 recordsLinked to original sources

PubMed1998

Patients' reactions to attempts to increase passive or active coping with surgery.

It is generally regarded as valuable for patients to exercise control over aspects of their medical treatment. Although psychological and other interventions are commonly used with the aim of increasing patients' ability or willingness to control events, it is not known whether patients experience these procedures in the way assumed. The present study compared responses to (i) a psychological intervention designed to increase patients' readiness to exercise control and cope actively and (ii) a comparable intervention intended to induce acceptance and passive coping. Hip or knee arthroplasty patients were visited preoperatively by a researcher who administered the active (N = 15) or passive (N = 15) intervention in a dialogue with the patient. Patients' verbal responses to the interventions were analyzed qualitatively to identify the range of reactions to each type of intervention. Patients readily accepted the passive message on the grounds of doctors' and nurses' authority and the value of the patients' emotional detachment from their surgery. Few responses to the active message indicated acceptance that patients have control over their care and its outcomes; instead, recipients typically interpreted it in terms of the need for obedience to medical and nursing authority. In conclusion, patients do not automatically accept messages intended to change ways of coping. In particular, the attempt to increase patients' readiness to take control over aspects of care can be perceived by patients in an opposite way to that intended. This and previous studies suggest that patient control over aspects of treatment is a professional and theoretical construction that often means little to patients.

Adaptation, Psychological↗

PubMed1998

Proximal renal tubular peptide catabolism, ammonia excretion and tubular injury in patients with proteinuria: before and after lisinopril.

1. Progression to renal failure may be linked to the degree of proteinuria through tubulo-interstitial mechanisms. However, there are no data in man on the kinetics of proximal renal tubular protein catabolism or markers of tubular injury before and after lisinopril. We developed a method to allow such studies, and found increased tubular catabolism of 99mTc-labelled aprotinin (Trasylol) in patients with nephrotic range proteinuria which was associated with increased ammonia excretion. 2. In this study, 10 patients with mild renal impairment (51Cr-EDTA clearance 63.7 +/- 8.3 ml.min-1.1.73 m-2) and heavy proteinuria (8.2 +/- 2.3 g/ 24 h) were given lisinopril (10-20 mg) for 6 weeks. Renal tubular catabolism of intravenous aprotinin was measured before and after lisinopril by renal imaging and urinary excretion of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Fresh timed urine collections were also analysed for ammonia excretion every fortnight from 6 weeks before treatment. Total urinary N-acetyl-beta-D-glucosaminidase and the more tubulo-specific N-acetyl-beta-D-glucosaminidase 'A2' isoenzyme were also measured. 3. After lisinopril proteinuria fell significantly as expected (from 9.5 +/- 1.6 to 4.5 +/- 1.0 g/24 h, P < 0.01). This was associated with a reduction in metabolism over 26 h (from 1.7 +/- 0.1 to 1.2 +/- 0.1% dose/h, P < 0.01) and in fractional degradation of aprotinin (from 0.08 +/- 0.02 to 0.04 +/- 0.007/h, P < 0.04). Ammonia excretion also fell significantly (from 1.2 +/- 0.1 to 0.6 +/- 0.1 mmol/h, P < 0.0001), as did both total urinary N-acetyl-beta-D-glucosaminidase (P < 0.0001) and the N-acetyl-beta-D-glucosaminidase 'A2' isoenzyme (P < 0.015). These observations after lisinopril treatment have not been described previously. There was no significant change in blood pressure nor in glomerular haemodynamics.

Acetylglucosaminidase↗

PubMed1998

Iron status in pregnant women: which measurements are valid?

Anaemia in pregnancy in developing countries continues to be a public health problem of significant proportion. At least 50% of the anaemia has been blamed on iron deficiency. In populations where chronic inflammation and iron deficiency anaemia coexist, the criteria to accurately define iron status are not always clear. Similarly, in pregnancy, with marked physiological changes, cut-off points for biochemical parameters need to be re-examined. In this study we examined the diagnostic accuracy of iron parameters including mean cellular volume (MCV), serum iron, transferrin, total iron binding capacity (TIBC) and its saturation, zinc protoporphyrin (ZPP), ferritin and serum transferrin receptor (TfR) for the assessment of iron status in a population of anaemic pregnant women in Malawi. Stained bone marrow aspirates were used as the standard for comparison. Results show that for the purpose of screening, serum ferritin is the best single indicator of storage iron provided a cut-off point of 30 microg/l is used. A number of other commonly used parameters of iron status were shown to have limited diagnostic accuracy. Logistic regression was used to obtain mathematical models for the prediction of bone marrow iron status using a combination of available parameters.

Anemia, Iron-Deficiency↗

PubMed1998

Trace element supplementation modulates pulmonary infection rates after major burns: a double-blind, placebo-controlled trial.

Infections remain the leading cause of death after major burns. Trace elements are involved in immunity and burn patients suffer acute trace element depletion after injury. In a previous nonrandomized study, trace element supplementation was associated with increased leukocyte counts and shortened hospital stays. This randomized, placebo-controlled trial studied clinical and immune effects of trace element supplements. Twenty patients, aged 40 +/- 16 y (mean +/- SD), burned on 48 +/- 17% of their body surfaces, were studied for 30 d after injury. They consumed either standard trace element intakes plus supplements (40.4 micromol Cu, 2.9 micromol Se, and 406 micromol Zn; group TE) or standard trace element intakes plus placebo (20 micromol Cu, 0.4 micromol Se, and 100 micromol Zn; group C) for 8 d. Demographic data were similar for both groups. Mean plasma copper and zinc concentrations were below normal until days 20 and 15, respectively (NS). Plasma selenium remained normal for group TE but decreased for group C (P < 0.05 on days 1 and 5). Total leukocyte counts tended to be higher in group TE because of higher neutrophil counts. Proliferation to mitogens was depressed compared with healthy control subjects (NS). The number of infections per patient was significantly (P < 0.05) lower in group TE (1.9 +/- 0.9) than in group C (3.1 +/- 1.1) because of fewer pulmonary infections. Early trace element supplementation appears beneficial after major burns; it was associated with a significant decrease in the number of bronchopneumonia infections and with a shorter hospital stay when data were normalized for burn size.

Adult↗

PubMed1998

Fibrinogen synthesis is elevated in fasting cancer patients with an acute phase response.

The unusual amino acid composition of acute phase proteins may be relevant to our understanding of the mechanism of tissue wasting in chronic inflammatory disease. During periods in which demand for amino acids outstrips dietary supply, skeletal muscle protein may be mobilized to meet this demand. An imbalance in the amino acid composition of these proteins may thus be detrimental to the body's nitrogen economy. To address this problem, we have measured the synthetic rate of fibrinogen (perhaps the major acute phase protein) and plasma amino acid profiles in a group of patients with adenocarcinoma of the pancreas and an ongoing inflammatory response (serum C-reactive protein >10 mg/L in the absence of any other obvious infective or inflammatory cause). These were also measured in a control group with no evidence of inflammation. Fibrinogen synthesis was measured after an overnight fast, using a flooding dose of 2H5-phenylalanine. The fractional rate of fibrinogen synthesis was significantly elevated in the cancer group compared with healthy controls [39.3 (20.0-49.9) and 21.9 (13.2-37.7) %/d, respectively; median (range), P < 0.05]. The absolute rate of fibrinogen synthesis was also elevated [84 (33-143) and 26 (15-43) mg/(kg.d), respectively; median (range), P < 0.01]. We calculated that, in cancer patients with anorexia-cachexia (i.e., documented ongoing weight loss in the absence of an obvious cause such as obstruction or malabsorption), aromatic amino acid supply (predominantly tryptophan) most limits fibrinogen synthesis from skeletal muscle reserves. Demand for the nonessential amino acids serine and glycine was elevated. Assuming that tryptophan is limiting, up to 2.6 g muscle protein ( approximately 12 g skeletal muscle tissue) may be wasted to synthesize 1 g fibrinogen. Interpretation of the observation that circulating free tryptophan concentrations were significantly reduced in the cancer patients will have to await flux measurements. The metabolic changes accompanying the inflammatory response suggest that down-regulation of this process may be beneficial.

Acute-Phase Reaction↗

PubMed1998

Effect of a chimeric antibody to tumor necrosis factor-alpha on cytokine and physiologic responses in patients with severe sepsis--a randomized, clinical trial.

OBJECTIVES: Tumor necrosis factor (TNF)-alpha appears central to the pathogenesis of severe sepsis, but aspects of the cytokine cascade and the link to physiologic responses are poorly defined. We hypothesized that a monoclonal antibody to TNF-alpha given early in the course of severe sepsis would modify the pattern of systemic cytokine release and, as a consequence, resuscitation fluid requirements, net proteolysis, and hypermetabolism would be reduced. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Critical Care Unit and University Department of Surgery in a single tertiary care center. PATIENTS: Fifty-six patients (from 92 eligible patients) with severe sepsis. Twenty-eight patients were randomized to treatment, and were comparable with the placebo group for age, gender, race, Acute Physiology and Chronic Health Evaluation II score, and site and type of infection. INTERVENTIONS: A 300-mg single dose of cA2 (a chimeric neutralizing antibody to TNF-alpha) was given intravenously within 12 hrs of the onset of severe sepsis. Standard surgical and intensive care therapy was otherwise delivered. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of TNF-alpha, interleukin (IL)-1beta IL-6, IL-8, IL-10, soluble 75-kilodalton TNF-alpha receptor (sTNFR-75), and IL-1beta receptor antagonist (IL-1ra) were measured by sandwich enzyme-linked immunosorbent assay before cA2 infusion, 8 hrs later, and then daily for a minimum of 4 days. Sequential changes in total body protein, body water spaces, and resting energy expenditure over 21 days were measured, as soon as patients achieved hemodynamic stability, by in vivo neutron activation analysis, tritium and bromide dilution, and indirect calorimetry, respectively. Twenty-one patients died, ten having received cA2. Suppression of measurable TNF-alpha was observed at 8 hrs with subsequent rebound by 24 hrs after cA2 treatment. The concentrations of other cytokines were high, were not reduced by intervention, and decreased logarithmically over 5 days. Both groups reached hemodynamic stability at similar times (57.5 +/- 11.8 hrs in controls vs. 58.6 +/- 9.2 hrs in the cA2 group) and following similar volumes of infused fluids (29.1 +/- 3.4 L vs. 28.9 +/- 4.4 L). No differences in net proteolysis, resolution of body water expansion, or alteration in resting energy expenditure were demonstrated. CONCLUSION: A single dose of cA2 did not alter the overall pattern of cytokine activation or the profound derangements in physiologic function that accompany severe sepsis.

Adult↗

PubMed1998

Proteinuria and renal tubular damage: urinary N-acetyl-beta-D-glucosaminidase and isoenzymes in dissimilar renal disease.

Markers of renal tubular injury are difficult to interpret in patients with proteinura. The 24-hour urinary N-acetyl-beta-D-glucosaminidase (NAG) concentration was measured in 167 patients with dissimilar renal disease, function, and proteinuria. NAG isoenzymes were also separated in 69 patients, using a modified fast protein liquid chromatography technique. The 'A2' isoenzyme predominated at all levels of renal function and in all diagnostic groups. Urinary NAG and proteinuria were well correlated at all levels of renal function, as was NAG 'A2' isoenzyme. Proteinuria and urinary NAG were similarly correlated in patients with different glomerulonephritides, hypertensive nephrosclerosis, and chronic pyelonephritis, but not in those with diabetic nephropathy.

Acetylglucosaminidase↗

PubMed1998

Tubular peptide hypermetabolism and urinary ammonia in chronic renal failure in man: a maladaptive response?

Excessive renal tubular peptide uptake and degradation reflecting hypercatabolism may be a maladaptive response in chronic renal failure (CRF). It may also offer an explanation for the increased ammoniagenesis, per surviving nephron, observed in CRF but as yet unexplained. Neither has been explored in man. We have shown in patients with normal renal function and heavy (>5.0 g/24 h) proteinuria that tubular catabolism of a technetium-labelled peptide marker, aprotinin, and urinary ammonia were increased compared to others with less proteinuria. We now measure tubular kinetics of aprotinin and urinary ammonia in 16 CRF patients with variable proteinuria. Metabolism and turnover of aprotinin and ammonia excretion were increased, corrected for glomerular filtration rate, to levels found in patients with normal function and heavy proteinuria.

Acids↗

PubMed1998

Dietary treatment of hypercholesterolaemia: lack of relationship between individual response and genetic variation at the lipase loci. The Fluvastatin Genotyping Group.

The individual benefits of dietary therapy for hyperlipidaemia are known to be unpredictable. Variants at the lipoprotein lipase gene have been shown to associate with atherogenic lipoprotein phenotypes and the delayed clearance of triglyceride-rich lipoproteins. Together with variants of the closely homologous hepatic lipase gene, these may influence the extent of amelioration of plasma lipoprotein concentrations seen in dyslipidaemic patients treated with a low saturates/low cholesterol diet. We correlated the lipid changes seen following an 8-week diet in 83 subjects with primary hypercholesterolaemia (fasting plasma cholesterol > 6.5 mmol/L) with alleles of three restriction polymorphisms (LPL-Hind III and Pvu II; HL-Msp I). Although dietary changes produced a significant improvement in fasting lipids [total cholesterol falling by 5.2% (range -27.9% to +24.3%) and low-density lipoprotein cholesterol reduced by 6.0% (-30.5% to +29.3%)], no significant difference in response between different genotypes could be detected.

Adult↗

PubMed1998

Oral sodium bicarbonate reduces proximal renal tubular peptide catabolism, ammoniogenesis, and tubular damage in renal patients.

Oral sodium bicarbonate (NaHCO3) is widely used to treat acidosis in patients with renal failure. However, no data are available in man on the effects on proximal renal tubular protein catabolism or markers of tubular injury. We have developed methods to allow such studies, and both increased tubular catabolism of 99mTc-labelled aprotinin (Apr*), as well as tubular damage were found in association with increased ammonia (NH3) excretion in patients with nephrotic range proteinuria. We now examine the effects of reducing renal ammoniogenesis, without altering proteinuria, using oral NaHCO3 in 11 patients with mild/moderate renal impairment and proteinuria. Renal tubular catabolism of Apr* was measured before and after NaHCO3 by renal imaging (Kidney uptake, K% of dose) and urinary excretion of free 99mTcO4- (metabolism, Met% of dose/h) over 26 h. Fractional degradation (Frac) was calculated from Met/K (/h). Fresh urine was also analyzed for NH3 excretion every fortnight from 6/52 before treatment. Total urinary N-acetyl-beta-D-glucose-aminidase (NAG) and the more tubulo-specific NAG "A2" were measured. 51CrEDTA clearance and 99mTc-MAG 3 TER were also assessed. After NaHCO3 Met over 26 h was significantly reduced (from 1.3 +/- 0.2% of dose/h to 0.9 +/- 0.1% dose/hr, p < 0.005), as was Frac of Apr* (from 0.06 +/- .006/h to 0.04 +/- 0.005/hr, p < 0.003). NH3 excretion also fell significantly (from 0.9 +/- 0.2 mmol/h to 0.2 +/- 0.05 mmol/h, p < 0.007), as did both total urinary NAG (from 169 mumol/24 h, 74-642 mumol/24 h to 79 mumol/ 24 h, 37-393 mumol/24 h, p < 0.01), and the NAG 'A2' isoenzyme (from 81.5 mumol/24 h, 20-472 mumol/24 h to 35.0 mumol/24 h, 6-388 mumol/24 h, p < 0.001). Proteinuria remained unaltered, and there was no change in blood pressure nor in glomerular haemodynamics. Oral NaHCO3 may thus pro-tect the proximal renal tubule and help delay renal disease progression.

Acetylglucosaminidase↗

PubMed1997

Micronutrients and outcome.

Micronutrient deficiency not only causes symptoms of severe deficiency, but may also cause more subtle effects on tissue function, including immune deficiency and oxidative damage. The duration of a deficiency state, which is necessary before such effects are clinically significant, is not known. Most biochemical tests are relatively insensitive in detecting changes in micronutrient status, although they do provide a crude index. Many tests are nonspecific, being affected by the acute phase response as well as by nutritional status. Cellular tests are more sensitive and specific than tests in plasma. When interpreted carefully in association with the knowledge of the patient's clinical condition and nutritional intake, laboratory tests can be helpful in diagnosing deficiency states or conditions of excess provision, and in monitoring progress. Well conducted clinical trials of micronutrients in nutritional support are beginning to appear in the literature. Further studies are urgently required that relate outcome to levels of provision and biochemical indices of nutrient status.

Antioxidants↗

PubMed1997

Impact of disease on markers of macronutrient status.

It is apparent that illness, particularly acute illness, affects most tests which are used to assess macronutrient status. In acutely-ill patients, the best tests in terms of specificity for nutritional status are in vivo neutron-activation analysis for body composition and N balance as an assessment of recent intake. Changes in plasma protein concentration must be interpreted with great care, and this is best done in conjunction with changes in the acute-phase-protein response. Measurement of plasma IGF-1 may be helpful in the presence of an acute-phase response, but this requires further validation. In many such patients, the most important part of the assessment continues to be the clinical and dietary history, together with a careful physical examination. However, the need for accurate measurement remains, so that nutritional status and its progress can be accurately quantified. This was best expressed many years ago by William Thompson, Lord Kelvin, when he stated '... when you can measure what you are speaking about and express it in numbers you know something about it... when you cannot express it in numbers your knowledge is of a meagre and unsatisfactory kind; it may be the beginning of knowledge, but you have scarcely, in your thoughts, advanced to the stage of science...'.

Acute Disease↗

PubMed1996

Origin and significance of urinary N-acetyl-beta, D-glucosaminidase (NAG) in renal patients with proteinuria.

In patients with proteinuria, indices of tubular damage are unreliable since filtered plasma enzymes could contribute to tubular enzymuria. Previous work has suggested the existence of various forms of the 'A' isoenzyme of N-acetyl-beta, D-glucosaminidase (NAG), one of which could be kidney specific and thus a useful marker of renal tubular damage. By using fast protein liquid chromatography, two forms of the 'A' isoenzyme, 'A1' and 'A2' were separated in human urine, plasma and kidney tissue. The isoenzyme profile in pathological urine resembled that seen in kidney tissue, the 'A2' isoenzyme predominating. The ratio A2/A1 in the urine of renal patients was significantly greater than in the plasma of renal patients, end-stage renal failure patients and healthy volunteers. There was no difference in the plasma ratios of the three groups studied. The clearances of total NAG, 'A1' and 'A2' isoenzymes were all greater than that of the lower molecular weight protein transferrin. This indicates that the origin of urinary NAG in patients with proteinuria is from the kidney itself. Thus, analysis of urinary NAG and its isoenzymes may be of benefit as an early predictor of renal tubular damage and may also be useful as a non-invasive indicator of disease progression.

Acetylglucosaminidase↗

PubMed1996

International Federation of Clinical Chemistry. Laboratory assessment of protein-energy status.

Laboratory and non-laboratory methods for assessing protein-energy nutritional status are reviewed. These are classified into methods for assessing adequacy of recent nutritional intake, methods for assessing whole body status, and tests which assist in the interpretation of these assessments. Each measurement is critically discussed in terms of the rationale for its use, the method of analysis, reference values, technical interference and limitations of methods, the effects of nutritional status and of other factors on the results, its overall usefulness in nutritional assessment, and its value relative to other methods. Non-laboratory tests such as dietary assessment, indirect calorimetry, functional tests and the many methods available for assessment of body composition, including anthropometry, bioelectrical impedance and isotope and imaging techniques, are compared with the clinical chemistry tests in common use, such as nitrogen balance, plasma protein measurements and urinary markers of muscle metabolism. This review provides comprehensive and practical advice on the use and limitations of these tests in the assessment of protein-energy nutritional status of a group, or of an individual patient.

Calorimetry↗

PubMed1996

RT-PCR detection of cytokine transcripts in a series of cultured human meningiomas.

The expression of cytokine transcripts has been investigated in a series of cultured human meningiomas using reverse transcriptase linked polymerase chain reaction (RT-PCR), which allowed simultaneous analysis of a range of cytokines. The main histological subgroups of meningioma were investigated; these included transitional, fibroblastic, and syncytial as well as atypical meningiomas. Meningiomas from each of the different histological subgroups were subjected to a standard tissue culture regime. Total RNA was extracted from representative cultures and reverse-transcribed to yield cDNA. PCR was performed using oligonucleotide primers designed to detect interleukin (IL)-1 alpha/beta to IL-8, transforming growth factor (TGF)beta 1-3, tumour necrosis factor (TNF)alpha/beta, and interferon (IFN)gamma. Transcripts for IL-3, IL-6, IL-8, and TGF beta 3 were detected in all cultures. Transcripts for the three isomers of TGF beta were expressed in the transitional and fibroblastic meningioma cells. TGF beta 2 and TGF beta 3 transcripts were expressed in the syncytial and TGF beta 1 and TGF beta 3 in the atypical meningioma cells. IL-1 beta transcripts were expressed in fibroblastic and atypical cultures and TNF beta transcripts were expressed in syncytial and transitional cultures only. Transcripts for IL-1 alpha, IL-2, IL-4, IL-5, IL-7, TNF alpha, or IFN gamma were not detected in any of the meningioma cultures. This investigation using cells cultured from a small number of tumours from each of the classic histological subtypes suggests that there is a distinct pattern of cytokine mRNA expression linked with histological classification.

Cytokines↗

PubMed1995

Effect of ibuprofen on the acute-phase response and protein metabolism in patients with cancer and weight loss.

The aim of this study was to determine whether administration of the non-steroidal anti-inflammatory agent ibuprofen might attenuate the acute-phase response in patients with colonic cancer. Cytokines and acute-phase proteins were measured before administration of ibuprofen and again 3 days later, when protein synthesis was measured using 15N-glycine. In patients with cancer, ibuprofen caused a significant reduction in the plasma concentration of all five acute-phase proteins studied. Although interleukin 6 levels were raised, they did not change following administration of ibuprofen. Unlike the situation in patients with cancer who did not receive ibuprofen, whole-body protein kinetics were similar to those of control subjects in patients with cancer who received ibuprofen. Whether or not ibuprofen had been administered, non-export hepatic protein synthesis rates were significantly lower in patients with than in those without cancer. These results suggest that short-term administration of ibuprofen can attenuate accelerated whole-body protein kinetics and the acute-phase response in patients with advanced cancer.

Acute-Phase Proteins↗

PubMed1995

The effect of nutritional status on the cytokine and acute phase protein responses to elective surgery.

Weight loss and impaired nutritional status are associated with increased complications following surgery. This study aimed to assess the effect of nutritional status on the magnitude of the acute phase protein response, and determine if this is associated with changes in the magnitude of the related cytokine responses. Nineteen patients (10 wellnourished, 9 malnourished on the basis of body composition) undergoing major abdominal surgery were studied by frequent blood sampling in the early postoperative period. There was a significant reduction in the plasma C-reactive protein response in the malnourished group, but no difference between the groups in the responses of alpha 1-antitrypsin, alpha 1-acid glycoprotein, or in the trace elements iron or zinc, which reflect induction of ferritin and metallothionein. There was an early increase in IL-6, soluble receptors of TNF, and in IL-1 receptor antagonist in both groups, but no detectable increase in plasma IL-1 or TNF. There was no difference between the wellnourished and malnourished group for any of these markers of activation of the cytokine network. Weight loss is therefore associated with a reduction in aspects of the acute phase response, but this is due to impaired effectiveness rather than reduced magnitude of the cytokine response.

Acute-Phase Proteins↗

PubMed1995

The relationship between pancreatic enzyme release and activation and the acute-phase protein response in patients with acute pancreatitis.

It has been suggested that the severity of an attack of acute pancreatitis is related to the presence of intraglandular trypsinogen activation and that disease severity is also reflected by the degree of the acute-phase protein response. In this study we examine the relationships among amylase release, the degree of trypsinogen and prophospholipase A2 activation [as measured by urinary trypsinogen activation peptide (TAP) and prophospholipase A2 activation peptide (PLAP) concentrations], and the serum concentrations of the acute phase-protein C-reactive protein (CRP) and the principal mediator of the acute-phase protein response, interleukin-6 (IL-6). Twenty-four patients (14 mild and 10 severe attacks) were studied. Peak serum amylase concentrations were seen within 12 h and peak urinary TAP/creatinine (Cr) and PLAP/Cr ratios between 12 and 24 h after the onset of symptoms, preceding those of IL-6 and CRP. The integrated TAP/Cr and PLAP/Cr responses were significantly greater in those with severe disease [95% confidence internal (CI) = 106-259.6 pmol/mmol/h, p < 0.0008; and 95.1% CI = 462.2-3887 pmol/mmol/h, p < 0.003, respectively]. The integrated amylase response was not significantly greater in those with severe disease (95.6% CI = -415 to 832 IU/L/h, p < 0.14). There was a strong correlation among the integrated IL-6, TAP/Cr (r = 0.63, p < 0.01), and PLAP/Cr (r = 0.64, p < 0.01) responses but a poor correlation with the integrated amylase response (r = 0.19, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗