Search

Objective: To test the hypothesis that minor chronic insults such as smoking, chronic bronchitis, and two persistent bacterial infections may be associated with increases in C reactive protein concentration within the normal range and that variations in the C reactive protein concentration in turn may be associated with levels of cardiovascular risk factors and chronic coronary heart disease., Design: Population based cross sectional study., Setting: General practices in Merton, Sutton, and Wandsworth., Subjects: A random sample of 388 men aged 50-69 years from general practice registers. 612 men were invited to attend and 413 attended, of whom 25 non-white men were excluded. The first 303 of the remaining 388 men had full risk factor profiles determined., Interventions: Measurements of serum C reactive protein concentrations by in house enzyme linked immunosorbent assay (ELISA); other determinations by standard methods. Coronary heart disease was sought by the Rose angina questionnaire and Minnesota coded electrocardiograms., Main Outcome Measures: Serum C reactive protein concentrations, cardiovascular risk factor levels, and the presence of coronary heart disease., Results: Increasing age, smoking, symptoms of chronic bronchitis, Helicobacter pylori and Chlamydia pneumoniae infections, and body mass index were all associated with raised concentrations of C reactive protein. C Reactive protein concentration was associated with raised serum fibrinogen, sialic acid, total cholesterol, triglyceride, glucose, and apolipoprotein B values. C Reactive protein concentration was negatively associated with high density lipoprotein cholesterol concentration. There was a weaker positive relation with low density lipoprotein cholesterol concentration and no relation with apolipoprotein A I value. C Reactive protein concentration was also strongly associated with coronary heart disease., Conclusion: The body's response to inflammation may play an important part in influencing the progression of atherosclerosis. The association of C reactive protein concentration with coronary heart disease needs testing in prospective studies.

Objective: To describe the current epidemiology of acute upper gastrointestinal haemorrhage., Design: Population based, unselected, multicentre, prospective survey., Setting: 74 hospitals receiving emergency admissions in four health regions in the United Kingdom., Subjects: 4185 cases of acute upper gastrointestinal haemorrhage in which patients were aged over 16 years identified over four months., Outcome Measures: Incidence and mortality., Results: The overall incidence of acute upper gastrointestinal haemorrhage in the United Kingdom is 103/100,000 adults per year. The incidence rises from 23 in those aged under 30 to 485 in those aged over 75. At all ages incidence in men was more than double that in women except in elderly patients. 14% of the haemorrhages occurred in inpatients already in hospital for some other reason. In 27% of cases (37% female, 19% male) patients were aged over 80. Overall mortality was 14% (11% in emergency admissions and 33% in haemorrhage in inpatients). In the emergency admissions, 65% of deaths in those aged under 80 were associated with malignancy or organ failure at presentation. Mortality for patients under 60 in the absence of malignancy or organ failure at presentation was 0.8%., Conclusions: The incidence of acute upper gastrointestinal haemorrhage is twice that previously reported in England and similar to that reported in Scotland. The incidence increases appreciably with age. Although the proportion of elderly patients continues to rise and mortality increases steeply with age, age standardised mortality is lower than in earlier studies. Deaths occurred almost exclusively in very old patients or those with severe comorbidity.

Objective: To investigate the current prevalence of Helicobacter pylori infection in childhood, the risk factors for infection, and the effect of infection on growth in preadolescent schoolchildren., Design: Population based sample of 7 year old schoolchildren followed up at age 11; data on risk factors for infection collected at age 7; presence of infection at age 11 determined by measurement of salivary IgG against H pylori by a newly developed enzyme linked immunosorbent assay (ELISA). Height was measured at 7 and 11 years of age., Subjects: 554 schoolchildren from Edinburgh., Results: 62 (11%) children had H pylori infection. Independent risk factors for infection were single parent families (adjusted odds ratio = 2.5; 95% confidence interval 1.1 to 5.7), the 10% most crowded homes (3.1; 1.3 to 7.2), and schools serving predominantly rented housing estates (2.5; 1.0 to 6.5). School catchment area was more important than parental social class or housing tenure. Growth in height between 7 and 11 was diminished in infected children by a mean of 1.1 cm (0.3 to 2.0 cm) over four years. This growth reduction was largely confined to girls (1.6 cm over four years), among whom it correlated with salivary IgG (P = 0.015)., Conclusion: Data from salivary assay to investigate the epidemiology of H pylori suggest that factors relating to the type of community in which the child lives may now be as important for acquisition of this infection as features of the family home. The greater reduction of growth among infected girls raises the possibility that H pylori infection may delay or diminish the pubertal growth spurt.

Gall-bladder sensitivity to cholecystokinin (CCK) was determined by dynamic cholescintigraphy in 18 patients with radiolucent gall stones and 18 matched controls during an infusion of CCK in which the rate of infusion was increased. In 10 of the matched pairs the patient was more sensitive than the control, in one the control was more sensitive, and in seven no difference was detected (p = 0.012). It is concluded that patients with cholesterol gall stones have increased gall-bladder sensitivity to CCK, and that this may be important in the pathogenesis of this disease.

Sixteen patients with gall stones were treated with chenic acid (14-16 mg/kg/day) given at three different times in random order for one month each. Before treatment the mean (+/- SE of mean) cholesterol saturation index (SI) of fasting gall-bladder bile was 1.28 +/- 0.06. During bedtime administration of chenic acid the mean SI fell to 0.78 +/- 0.04, which was significantly lower than that obtained with administration in the morning (0.92 +/- 0.05) or with three divided doses at mealtimes (0.92 +/- 0.04). The bile remained supersaturated in seven patients when they received a single morning dose, in five patients when they received mealtime doses, but in only one patient when a single bedtime dose was given. There was no significant difference in side effects between the three different dose timings, or in the proportion of bile acids present in the bile as chenic acid. This enhanced effect obtained with bedtime administration may be due to the enterohepatic circulation of bile acids being maintained during overnight fasting.

Fifteen patients with gall stones who were taking chenodeoxycholic acid(CDCA) 15 mg/kg at bedtime participated in two separate experiments to investigate the effects of altering sterol intake on the cholesterol saturation index (SI) of fasting gall-bladder bile. In experiment I the 15 patients on an unrestricted diet had a SI of 0.87 +/- 0.04 (mean +/- SE of mean), which fell to 0.75 +/- 0.04 after one week in hospital on a diet of 100 mg cholesterol daily. In experiment II seven of the patients were given four different dietary regimens lasting one month each in random order as outpatients. On a diet of 600 mg of cholesterol daily the mean SI was 0.72 +/- 0.05, which fell to 0.67 +/- 0.05 when the patients were put on a 100 mg cholesterol diet. The addition of plant sterols (3 g daily) to both diets raised the mean SIs to 0.80 +/- 0.05 and 0.77 +/- 0.05 respectively. The percentage CDCA in bile was unaffected by alterations in the cholesterol and plant sterol intakes. We conclude that a low-cholesterol diet but not a high intake of plant sterols enhances the effect of CDCA in patients with gall stones.

Gall-bladder emptying in response to a standard meal was assessed in 34 patients with radiolucent gall stones and 34 matched controls. Percentage gall-bladder emptying, derived from volume measurements made on standardised oral cholecystography, was significantly higher at 15 minutes in the patients than the controls (mean +/- SE of mean 38.0 +/- 3.7% v 28.0 +/- 3.8%). This difference was maintained at 30 and 60 minutes. It is concluded that postprandial gall-bladder emptying is increased in patients with cholesterol gall stones, and that this may be the cause of the small bile-acid pool found in these patients.

Emergency arteriography was carried out on 35 patients with acute gastrointestinal bleeding, in 31 of them within two hours of active bleeding (a haematemisis; a diagnostic change in central venous pressure, pulse rate, or blood pressure; or gastric aspiration of fresh blood). A definite site of bleeding was identified in 27 patients (77%)-this being a small-intestinal vascular abnormality in three--and a probable site in three. Confirmation of the bleeding site was obtained in 20 out of 23 patients treated surgically. An intra-arterial vasoconstrictor infusion was given as a temporary measure before surgery in seven patients, only one of whom showed active bleeding at operation. An intra-arterial vasoconstrictor infusion was tried as definitive treatment in an additional 10 patients, but in four out of seven with a chronic ulcer bleeding recurred after 5-68 hours and was therefore treated surgically. We recommend the diagnostic use of arteriography in patients with reliable evidence of active bleeding if its site cannot be determined by endoscopy. We do not recommend its therapeutic use in those with a chronic ulcer, except to facilitate resuscitation before surgery; further studies are needed to define its role in those with an acute lesion.

The postprandial concentrations of free and conjugated bile acids were measured in total content and micellar phase of jejunal aspirates from nine patients with steatorrhoea due to the stagnant loop syndrome and from 11 normal controls. Aspirates from the stagnant loop syndrome patients, but not from the normal controls, had a high concentration of free (unconjugated) bile acids. There was a reciprocal decrease in the concentration of conjugated bile acids, but total bile acid concentration in the whole aspirate remained normal. Total bile acid concentration in the micellar phase of intestinal content was reduced, indicating precipitation of bile acids. These findings suggest that precipitation of unconjugated bile acids, rather than passive absorption, leads to a reduced postprandial concentration of bile acids in the micellar phase of jejunal content, and are consistent with the hypothesis that fat malabsorption in the stagnant loop syndrome results from decreased micellar dispersion of lipolytic products.

Acid-base balance has been studied in 21 patients with acute upper gastrointestinal bleeding. A low plasma bicarbonate concentration was found in nine patients, accompanied in each case by a base deficit of more than 3 mEq/litre, indicating a metabolic acidosis. Three patients had a low blood pH. Hyperlactataemia appeared to be a major cause of the acidosis. This was not accompanied by a raised blood pyruvate concentration. The hyperlactataemia could not be accounted for on the basis of hyperventilation, intravenous infusion of dextrose, or arterial hypoxaemia. Before blood transfusion it was most pronounced in patients who were clinically shocked, suggesting that it may have resulted from poor tissue perfusion and anaerobic glycolysis. Blood transfusion resulted in a rise in lactate concentration in seven patients who were not clinically shocked, and failed to reverse a severe uncompensated acidosis in a patient who was clinically shocked. These effects of blood transfusion are probably due to the fact that red blood cells in stored bank blood, with added acid-citrate-dextrose solution, metabolize the dextrose anaerobically to lactic acid. Monitoring of acid-base balance is recommended in patients with acute gastrointestinal bleeding who are clinically shocked. A metabolic acidosis can then be corrected with intravenous sodium bicarbonate.

The rate of absorption of gas from a pneumothorax was studied in 12 patients breathing air and in 10 patients breathing air and a high concentration of oxygen alternately. The mean rate of absorption while breathing air was the same in both groups of patients. In the second group the rate consistently increased during periods of oxygen therapy and decreased again on breathing air. The mean rate of absorption increased fourfold during periods of oxygen therapy. This increase was most pronounced in patients with a large pneumothorax.

A retrospective survey of 472 consecutive hospital admissions for acute upper gastrointestinal bleeding showed that patients with a large initial bleed are more likely to bleed again than those with a small initial bleed. The incidence of recurrent haemorrhage is also related to the interval since the last bleeding episode, so that patients showing no clinical evidence of haemorrhage for 48 hours are unlikely to bleed again in the near future. Patients admitted after a haematemesis have a higher incidence of recurrent haemorrhage than those admitted after melaena only. Aetiology has been confirmed as an additional important factor, the incidence being highest in those with oesophageal varices or a chronic gastric ulcer. Contrary to widespread belief, age does not appear to affect the incidence of recurrent haemorrhage, nor do other constitutional factors such as sex or the ABO blood group.