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At least 919 records · Page 51Linked to original sources
PubMed1999

Faecal elastase 1: a marker of exocrine pancreatic insufficiency in cystic fibrosis.

Pancreatic elastase 1 (E1), a digestive protease, is synthesized by the acinar cells of the pancreas. Using an enzyme-linked immunosorbent assay, we evaluated stool E1 levels in the following groups of patients. (a) Specimens submitted for occult blood examination from 20 adults, over 3 consecutive days, to assess the inter-day variability in E1 excretion. There were no symptoms suggestive of pancreatic insufficiency in this group. The mean E1 concentration over all samples was 457 micrograms E1/g stool (range 124-1683). The intra-assay variation was 6.4% (n = 14) and the inter-assay variation was 8.8% (n = 12). The mean intra-patient variation was 17%. (b) Cystic fibrosis (CF) patients. Eight patients had E1 levels in the reference range (> 200 micrograms E1/g stool). The remaining 25 patients had undetectable E1 levels. (c) A control group of children presenting with unexplained bronchiectasis and/or recurrent respiratory infections and no symptoms of pancreatic dysfunction. The mean E1 concentration in the group was 519 micrograms E1/g stool (range 139-1941). There was no significant difference in E1 concentrations between the two non-CF groups, nor between the pancreatic-sufficient CF patients when compared with both non-CF groups. There was a significant difference between the pancreatic-sufficient and -insufficient CF groups (P < 0.001) using the Mann Whitney U test. All fifteen CF patients who were delta F508 homozygotes had undetectable E1. It may be possible to relate CF genotype to the presence or absence of E1 and to the degree of pancreatic insufficiency. Measurement of faecal E1 in children with CF appears to differentiate them into a group of children with normal pancreatic function and a larger group with severe insufficiency.

Adolescent↗
PubMed1988

Lack of unique ciprofloxacin pharmacokinetic characteristics in patients with cystic fibrosis.

The single-dose pharmacokinetics of oral ciprofloxacin 750 mg were evaluated in six subjects with cystic fibrosis (CF subjects) and six age, sex and approximate weight-matched control subjects (controls). In addition, the effect of concurrently administered oral pancreatic enzyme replacement on the pharmacokinetics of ciprofloxacin was studied in 12 CF subjects. Ciprofloxacin t1/2, VSSF, CLF, and CLR in the matched CF subjects averaged 4.5 hours, 2.8 L/kg, 2.73 mL/min/kg and 5.7 mL/min/kg, respectively. Forty-two percent of the ciprofloxacin dose was excreted in the urine (0-48 hours) as the parent compound. No statistically significant differences in these ciprofloxacin pharmacokinetic parameter estimates were observed between CF and control subjects. In three CF subjects and two controls, the urinary excretion of ciprofloxacin and four of its metabolities were similar. In contrast, CF subjects demonstrated a prolonged tmax (2.3 versus 1.3 hours P less than .05) though ciprofloxacin Cmax was similar (4.7 versus 3.8 mg/L, NS). The concurrent administration of oral pancreatic enzyme replacement had no effect on the pharmacokinetics of ciprofloxacin. Apparent ciprofloxacin pharmacokinetic parameters in sputum were similar to those observed in serum. Sputum ciprofloxacin concentrations lagged behind serum concentrations but, on average, exceeded serum concentrations for 20 hours of the 24-hour sampling period. These sputum ciprofloxacin concentrations exceeded the reported MIC90 for Pseudomonas aeruginosa for approximately 15 hours. These data suggest an oral ciprofloxacin dose of 750 mg administered q8h to promote accumulation and maintenance of sputum drug concentrations well above pathogen MICs for the majority of a dosing interval in patients with CF.

Adolescent↗
PubMed1985

Pathophysiologic factors in recurrent acute pancreatitis.

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.

Acute Disease↗
PubMed1984

Pancreatic function testing in cystic fibrosis.

None of the currently available clinical techniques for measuring pancreatic function in patients with CF can be considered "ideal". The "direct" pancreatic stimulation test provides the most information and remains the only truly accurate test of exocrine function, particularly in those individuals with pancreatic sufficiency. The invasive, complex nature of the pancreatic stimulation tests precludes its use as a routine method of assessing pancreatic function in all patients and limits its value for monitoring function in those individuals who are expected to deteriorate with time. Many of the indirect tests of pancreatic function are of value for identifying CF patients with complete pancreatic insufficiency who may require therapy with pancreatic enzyme supplements and fat soluble vitamins. However, none of the currently available "indirect" tests of exocrine function are sensitive enough to evaluate or monitor CF patients with pancreatic sufficiency. Blood tests, capable of measuring pancreatic enzymes in the circulation, such as immunoreactive trypsinogen, may be of value for monitoring pancreatic function in patients with CF, but further longitudinal studies are necessary to fully evaluate this approach. More sophisticated "indirect" tests of exocrine pancreatic function are vitally needed to facilitate adequate assessment of this important digestive organ in patients with cystic fibrosis.

Cystic Fibrosis↗
PubMed1988

The effect of exocrine pancreatic function on chloramphenicol pharmacokinetics in patients with cystic fibrosis.

The effect of exocrine pancreatic function on the pharmacokinetics of the choramphenicol oral capsule (CAP-base), chloramphenicol palmitate oral liquid (CAP-P), and chloramphenicol succinate intravenous (CAP-S) formulations was evaluated in 10 patients, aged 16-30 yr, with cystic fibrosis. Pancreatic insufficiency was assessed in each patient by measuring the absorption of p-amino-benzoic acid after oral administration of N-benzoyl-L-tyrosyl-p-aminobenzoic acid which requires chymotrypsin to cleave p-aminobenzoic from the parent molecule. In a controlled cross-over design, the overall biodisposition of each formulation was assessed in each patient with or without concurrent administration of oral pancreatic enzymes. The relative amounts of active chloramphenicol available in systemic circulation was CAP-base greater than CAP-S greater than CAP-P. Pancreatic enzyme replacement had little effect on the biodisposition parameters for the CAP-base and CAP-S formulation, but significantly increased the peak concentration and bioavailability of the CAP-P formulation. Although pancreatic enzyme replacement improved the absorption characteristics of the CAP-P formulation, absorption remained prolonged and unreliable. Serum concentration-time profiles for either CAP-base or CAP-S consistently exceeded the MIC of important nonpseudomonal pathogens. This finding was not observed after CAP-P administration independent of pancreatic enzyme replacement. The results of this study support the continued clinical use of either CAP-base or CAP-S, but the cautious use of CAP-P formulations in CF patients with concurrent pancreatic insufficiency.

Administration, Oral↗