Search tips
Search criteria

Results 1-21 (21)

Clipboard (0)

Select a Filter Below

Year of Publication
Document Types
1.  Timed sequential analysis of creatine kinase in the diagnosis of myocardial infarction in patients over 65 years of age. 
Journal of Clinical Pathology  1994;47(11):995-998.
AIM--To assess the value of timed sequential analysis of creatine kinase (CK) activity for the early diagnosis of acute myocardial infarction (AMI) in patients over 65 years of age. METHOD--Samples were collected on admission and eight to 12 hours later from 156 patients over 65 years of age. Routine cardiac enzyme activities were determined and serial electrocardiograms (ECGs) recorded. The predictive value of timed samples for CK activity, standard cardiac enzyme activities, and ECGs was compared with the final diagnosis on discharge. RESULTS--Forty one patients had a discharge diagnosis of AMI, 83 of angina pectoris, and the remaining 32 patients had other diagnoses. Electrocardiograms had a sensitivity of 55% and a specificity of 96%, giving a predictive value of 86% for a negative and 84% for a positive ECG. Standard cardiac enzymes had a predictive value of 99% for a negative result but only 68% for a positive result. The logarithm of the rate of change of CK activity had a predictive value of 97% for a negative result and 95% for a positive result. CONCLUSION--This study has shown that slope analysis of CK activity can be used for the early diagnosis of AMI in patients over 65 years of age, and that this was not affected by the presence of possible confounding diagnoses.
PMCID: PMC503059  PMID: 7829696
2.  Effect of Helicobacter pylori infection on intragastric urea and ammonium concentrations in patients with chronic renal failure. 
Journal of Clinical Pathology  1993;46(6):544-547.
AIM--To assess the value of measuring the gastric juice urea:ammonium ratio in detecting Helicobacter pylori infection in patients with chronic renal failure. METHODS--Twenty three (12 men) patients with established chronic renal failure and dyspepsia were studied. Gastric juice (2 ml) was aspirated during endoscopy to measure urea and ammonium. The upper gastrointestinal tract was routinely inspected and two antral biopsy specimens obtained. The 14C-urea breath test was conducted within 14 days of endoscopic examination to determine H pylori antibody response. RESULTS--The median (range) serum urea concentration in 11 patients with renal failure and H pylori infection was similar to that in 12 without H pylori infection. The median gastric juice urea concentration in subjects with infection was lower than that in the subjects without infection (p < 0.01). The median gastric juice ammonium concentration in subjects with the infection was higher compared with subjects without infection (p < 0.01). There was an overlap of the urea and ammonium concentrations in gastric juice from both H pylori positive and negative subjects. The urea:ammonium ratio was 0.16 (0.01-1.11) for subjects with H pylori compared with 1.63 (1.0-18.9) in subjects without infection (p < 0.001). CONCLUSION--The urea:ammonium ratio differentiated both groups, with the exception of one false negative result. The urea:ammonium ratio proved almost as effective in identifying the presence of H pylori infection in subjects with chronic renal failure as it had in subjects with normal renal function.
PMCID: PMC501292  PMID: 8331178
3.  Measurement of urea and ammonium concentrations in gastric juice. 
Journal of Clinical Pathology  1993;46(5):462-464.
AIM--To study the effect of known interference in the measurement of urea and ammonium concentrations in samples of gastric juice. METHODS--The effect of pH and ammonium concentration on the o-pthalaldehyde method, the diacetylmonoxime method, a Berthelot linked method and an enzymatic urease method for the measurement of urea in gastric juice was therefore conducted. An enzymatic method of the measurement of ammonium in gastric juice was also assessed. RESULTS--The o-pthalaldehyde and the enzymatic urease methods were unaffected by a low gastric juice pH, ammonium concentrations of 10 mmol/l, and had interassay coefficients of variation of 3.9-5.6% and 2.8-10.6%, respectively, over a urea concentration of 2.5 mmol/l-20 mmol/l. The Berthelot linked method resulted in low gastric juice urea concentrations. The enzymatic method of ammonium measurement also proved suitable when the effect of low gastric juice pH was controlled. CONCLUSION--Interference by low pH did not explain the differences in reports of gastric juice urea or ammonium concentrations.
PMCID: PMC501260  PMID: 8320328
4.  Use of multichannel discrete analyser to reduce unnecessary biochemical tests. 
Journal of Clinical Pathology  1993;46(5):459-461.
AIM--To investigate the waste of laboratory reagents which resulted from the process of ordering biochemistry profiles. METHODS--The frequency of measurement of 15 analytes was recorded during the six months before the introduction of a system of discretionary requesting and analysis of samples (high capacity multichannel discrete analyser), and also during the same six month period one year and two years after its introduction. RESULTS--The frequency of measurement of 10 of the 15 analytes decreased during the six month period one year after the change to discretionary testing. The remaining five analytes were measured up to 22% more frequently. There was an overall decrease in the measurement of biochemical tests by 31,359. This created an annual cost saving of 7124 pounds. In the second year five analytes still continued to be measured less frequently than originally but the remaining 10 analytes were measured more frequently. This resulted in an overall increase in the measurement of biochemical tests by 53,678 compared with the six month period before discretionary analysis. The pattern of requests was similar during both periods of discretionary requesting studied and as a result, a small annual cost saving of 1672 pounds was again made. CONCLUSION--Discretionary requesting and analysis of tests may eliminate the measurement of clinically unnecessary test which had previously resulted from the processes of ordering tests. These cost savings may be rapidly eroded by an increase in the laboratory workload.
PMCID: PMC501259  PMID: 8320327
5.  Ammonium metabolism and protection from urease mediated destruction in Helicobacter pylori infection. 
Journal of Clinical Pathology  1993;46(1):75-78.
AIM: To investigate further the intracellular ammonium metabolism of Helicobacter pylori and the mechanism of its urease mediated destruction. METHODS: The mechanism of the in vitro destruction of H pylori was investigated by incubating it in buffer solutions, at pH 6.0, containing isocitrate or alpha ketoglutarate in addition to urea concentrations which had previously been shown to destroy H pylori. RESULTS: The median (range) 5 minute survival of H pylori in 0.2 mol/l citrate buffer (pH 6.0) in the absence of urea was 88% (18-184%) and was similar to its survival in 0.2 mol/l isocitrate buffer in the absence of urea, median 88% (15-274%). In the presence of 50 mmol/l urea the survival of H pylori in the citrate buffer was reduced, 9.9% (0-146%), compared with its survival in isocitrate buffer with the same concentration of urea 37% (0-274%) (p < 0.01). A 72 hour preincubation of the organism with 10 mmol/l alpha ketoglutarate also increased the 5 minute survival of the organism in 0.2 mol/l citrate buffer containing 50 mmol/l urea to 36% (9-145%) compared with its survival in the same buffer but without preincubation with alpha ketoglutarate 0% (0-62%). CONCLUSION: The protection of H pylori from rapid destruction by the supply of compounds used in the intracellular metabolism of the ammonium shows that the urease mediated destruction of H pylori can be explained by intracellular depletion of alpha ketoglutarate as a result of over production of ammonium by uncontrolled urease activity.
PMCID: PMC501120  PMID: 8432895
6.  Suicidal destruction of Helicobacter pylori: metabolic consequence of intracellular accumulation of ammonia. 
Journal of Clinical Pathology  1991;44(5):380-384.
The role of pH, citrate buffer, and urea were investigated in the suicidal destruction of Helicobacter pylori, with particular reference to the organism's urea and ammonia metabolism. The median five minute survival of H pylori in the presence of 50 mmol/l urea in 0.2 M citrate buffer at pH 6.0 was only 14%, compared with 53% in the same solution at pH 7.0. The median amount of ammonium released into the incubating solution over five minutes was lower at pH 6.0 (9 mumol) than at pH 7.0 (18 mumol) despite similar uptake of urea. The median five minute survival of H pylori in 0.2 M citrate buffer, pH 6.0, decreased from 89% to 14% when the urea concentration was increased from 1 mmol/l to 50 mmol/l. Likewise, the recovery in the incubating solution of ammonia resulting from the hydrolysis of urea fell from 27% to 3% when the initial urea concentration was increased from 1 mmol/l to 50 mmol/l. Survival of H pylori in the presence of 30 mmol/l urea at pH 6.0 was compared in 0.2 M citrate, acetate, and phosphate buffers. The median five minute survival was less in the citrate buffer, at 29%, than in either the acetate buffer 80% or the phosphate buffer 100%. The percentage recovery of ammonia was similar in the three buffers. These findings indicate that the suicidal destruction of the bacterium may be explained by intracellular accumulation of ammonia due to production in excess of the rate of excretion.
PMCID: PMC496867  PMID: 2045495
7.  Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations. 
Gut  1991;32(9):973-976.
Helicobacter pylori possesses unusually high urease activity that lowers the urea concentration and raises the ammonium concentration of the gastric juice in infected people. The value of measuring urea and ammonium concentrations in gastric juice obtained during upper gastrointestinal endoscopy as a means of diagnosing the presence and eradication of the infection was assessed. Twenty four subjects with the infection and 14 in whom it had been eradicated were examined. Their H pylori status was confirmed by antral biopsy and 14C urea breath test. The median (range) gastric juice urea concentration in infected subjects was 0.8 mmol/l (0.5-2.9 mmol/l), which was lower than that in the uninfected subjects (2.1 mmol/l (1.0-3.7 mmol/l)) (p less than 0.001). The median gastric juice ammonium concentration in infected subjects was 3.4 mmol/l (1.0-13.0 mmol/l), which was higher than that in the uninfected subjects (0.64 mmol/l (0.02-1.4 mmol/l)) (p less than 0.001). Though the two groups overlapped in respect of their urea and ammonium concentrations, they were completely different when the urea: ammonium ratios were calculated--the ratios ranged from 0.04-0.7 (median 0.26) and from 1.1-113 (median 3.4) in infected and uninfected subjects respectively (p less than 0.001). Treatment with H2 antagonists did not change the concentrations of urea and ammonium or their ratio in gastric juice. Measurement of the urea: ammonium ratio in aspirated gastric juice obtained during routine upper gastrointestinal endoscopy may provide a rapid method of detecting H pylori infection and of confirming its eradication.
PMCID: PMC1379031  PMID: 1916500
8.  Creatine kinase isoform electrophoresis for the early confirmation of myocardial infarction detected by timed sequential CK slope analysis. 
Postgraduate Medical Journal  1994;70(829):805-808.
Creatine kinase (CK)-MM and -MB isoforms were evaluated for the early diagnosis of myocardial infarction in patients aged over 65 years admitted to a district general hospital with acute chest pain. Samples were collected for standard cardiac enzymes, timed CK slope analysis, and CKMM and CKMB isoform analysis from 48 patients admitted with acute chest pain. CKMM and CKMB isoform analyses were conducted using a Helena Rep electrophoresis system under standard conditions supplied by the company. In addition to the results of the biochemical tests the discharge diagnosis of the patients were also recorded. CKMM isoform analysis resulted in three false-negative classifications of patients and one false-positive. The predictive value of this test was 100% for a positive result and 94% for a negative result. CKMB isoform analysis was less accurate and there were six false-negative results and five false-positive results. The predictive value of a positive result was 75% and 85% for a negative result. CK isoform analysis became unreliable when mean total CK levels in serum were 210 IU/l (+/- 171). CK isoform analysis may be of use in the investigation of patients whose samples have a total CK concentration greater than the reference range but was no better than timed CK slope analysis for the detection of myocardial infarction in patients aged more than 65 years.
PMCID: PMC2397833  PMID: 7824414
10.  Making the new deal for junior doctors happen. 
BMJ : British Medical Journal  1994;308(6943):1553-1555.
How can the new deal for juniors be implemented in today's overstretched health service? How do you get clinicians and management to work together? On the Wirral falling house officer morale and recruitment stimulated a new approach, action learning, which proved to be highly successful. Action learning is not a new approach in management terms, but it is rarely used in the health service. Guided by an experienced facilitator, a group of people learn management skills by exploring and resolving practical problems relevant to them. A group of general practitioners and consultants used action learning to teach themselves more about management and at the same time to make changes which addressed many of the junior doctors' difficulties and solved the hospital recruiting problem.
PMCID: PMC2540511  PMID: 8019316
11.  Harnessing of urease activity of Helicobacter pylori to induce self-destruction of the bacterium. 
Journal of Clinical Pathology  1991;44(2):157-159.
Eradication of Helicobacter pylori with currently available antibacterial agents is unsatisfactory due to the risk of side-effects and the emergence of resistance. The organism rapidly dies in vitro in the presence of urea at pH 6. When incubated in citrate buffer (pH 6) plus urea (10 mM) the five minute survival was 26% compared with 96% without urea and the survival progressively decreased with increasing urea concentrations, being only 9% in 50 mM urea. The bactericidal effect depended on pH as the organism survived in citrate buffer (pH 7) plus urea (50 mM). The death of the organism at pH 6 in the presence of urea was prevented by the addition of the competitive urease inhibitor hydroxyurea. These findings indicate that destruction of the organism is mediated by its exceptionally high urease activity. Harnessing this enzyme to induce self-destruction could provide a new approach to eradicating this common infection.
PMCID: PMC496980  PMID: 1864988
12.  Role of ammonia in the pathogenesis of the gastritis, hypergastrinaemia, and hyperpepsinogenaemia I caused by Helicobacter pylori infection. 
Gut  1992;33(12):1612-1616.
Studies were performed in patients with and without renal failure to investigate the role of bacterial ammonia production in the pathogenesis of the mucosal abnormalities caused by Helicobacter pylori. The high rate of H pylori ammonia production in uraemic patients should accentuate any ammonia induced effects. The median (range) gastric juice ammonium concentration in the H pylori positive patients with renal failure was 19 mmol/l (II-43) compared with 5 mmol/l (1-11) in the H pylori positive patients without renal failure (p < 0.005). In the H pylori negative patients the values were 3 mmol/l (0.5-11) and 0.7 mmol/l (0.1-1.4) respectively in the patients with and without renal failure (p < 0.01). Despite the much higher ammonia production in the H pylori positive uraemic patients, the nature and severity of their gastritis was the same as that in the H pylori positive non-uraemic patients. The median (range) fasting serum gastrin concentration was raised in the uraemic patients compared with the non-uraemic patients but was similar in the uraemic patients with (95 pmol/l (52-333)) or without (114 pmol/l (47-533)) H pylori infection. The median (range) serum pepsinogen I concentration was also high in the uraemic compared with the non-uraemic patients and was significantly higher in uraemic patients with H pylori (352 ng/ml, range 280-653) than in those without H pylori infection (165 ng/ml, range 86-337) (p < 0.01). These findings indicate that the gastritis and hypergastrinaemia associated with H pylori infection are not the result of mucosal damage induced by the organism's ammonia production.
PMCID: PMC1379570  PMID: 1487161
13.  Is Helicobacter pylori associated hypergastrinaemia due to the bacterium's urease activity or the antral gastritis? 
Gut  1991;32(11):1286-1290.
Eradication of Helicobacter pylori is associated with a fall in serum gastrin but the way in which the infection raises the serum gastrin concentration is not clear. It may be related to the ammonia produced by the bacterium's urease stimulating gastrin release by the antral G cells. Alternatively, the antral gastritis induced by the infection may modify the regulation of gastrin release. We have examined serum gastrin in 10 patients before and 24 hours after starting triple anti-H pylori treatment consisting of tripotassium dicitrato bismuthate 120 mg four times daily, metronidazole 400 mg three times daily, and amoxycillin 500 mg three times daily. The urease activity, assessed by the 20 minute value of the 14C-urea breath test, fell from a median of 176 (range 116-504) kg% dose/mmol CO2 x 100 pretreatment to 5 (2-15) at 24 hours (p less than 0.005). The median antral gastritis score was 6 (4-6) pretreatment and fell to 3 (2-5) at 24 hours (p less than 0.02), and this was due to resolution of the polymorphonuclear component. Despite this complete suppression of bacterial urease activity and partial resolution of antral gastritis the median basal gastrin concentration remained unchanged, being 57 ng/l (45-77) pretreatment and 59 ng/l (45-80) at 24 hours and the median integrated gastrin response to a standardised meal was also unaltered, being 4265 ng/l/min (range 1975-8350) and 4272 ng/l/min (range 2075-6495) respectively. These findings do not support a causal association between H pylori urease activity and hypergastrinaemia and show rapid improvement of antral gastritis after starting anti-H pylori treatment.
PMCID: PMC1379153  PMID: 1752456
14.  Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. 
Gut  1991;32(8):866-870.
The mechanism of the hypergastrinaemia associated with Helicobacter pylori infection is unknown. It may be an effect of the ammonia produced by the bacterium near the antral epithelial surface. We have examined the effect on serum gastrin of inhibiting H pylori urease activity with acetohydroxamic acid in six duodenal ulcer patients. On day 1 the fasted patients received placebo tablets at 8 am, a peptide meal at 10 am, and a 14C urea breath test at 11.30 am. The next day 750 mg acetohydroxamic acid was administered orally in place of the placebo. The median (range) 30 minute breath test value (dose/mmol CO2 X kg body wt X 100) was 152 (111-335) on day 1, but only 22 (14-95) the next day (p less than 0.03). Further studies performed in one subject confirmed that acetohydroxamic acid lowered the ammonium concentration and raised the urea concentration in gastric juice. The inhibition of urease activity and ammonia production did not result in a fall in the basal gastrin concentration or in the median integrated gastrin response to the peptide meal, which was 78 ng/1.h (range 21-222) on day 1 and 79 ng/1.h (33-207) the next day. Ten days after acetohydroxamic acid, the urea breath test values were similar to those before treatment. This study shows that the raised gastrin concentration in patients with H pylori infection is not directly related to the organism's urease activity. It also shows that temporary suppression of H pylori urease activity does not clear the infection.
PMCID: PMC1378953  PMID: 1885067
15.  Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. 
Gut  1991;32(1):21-24.
It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylori infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmol/l (range 0.3-1.6) to 15.5 mmol/l (range 7.9-21.3) and this resulted in an increase in the ammonium concentration from 2.3 mmol/l (range 1.3-5.9) to 6.1 mmol/l (range 4.2-11.9) (p less than 0.01). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p less than 0.05). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0.4 mmol/l (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.
PMCID: PMC1379207  PMID: 1991633
16.  Helicobacter pylori does not release cysteamine into gastric juice. 
Journal of Clinical Pathology  1997;50(9):769-770.
AIM: To determine whether Helicobacter pylori releases cysteamine into gastric juice as cysteamine is known to be ulcerogenic. METHODS: Samples of fasting gastric juice were collected from 22 individuals (four women); 10 subjects were H pylori negative. The presence of infection was confirmed by examination and culture of gastric biopsies. Cysteamine in gastric juice was measured by reversed phase gradient high performance liquid chromatography with a detection limit of 10 mumol/l. RESULTS: Cysteamine was not detected in any of the gastric juice samples or in extracts of cultured H pylori. CONCLUSIONS: If H pylori produces cysteamine then the amounts produced are insignificant and are unlikely to explain the association between H pylori infection and the development of duodenal ulcer disease.
PMCID: PMC500175  PMID: 9389979
17.  Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration. 
Postgraduate Medical Journal  1990;66(776):479-482.
We report a patient who developed persistent nephrogenic diabetes insipidus associated with renal tubular acidosis, renal resistance to parathyroid hormone, aminoaciduria and proximal tubule pattern proteinuria in the presence of a reduced glomerular filtration rate (19-24 ml/min). A review of the previous reports of persistent nephrogenic diabetes insipidus revealed that in all patients the glomerular filtration rate had been less than 60 ml/min at presentation. Chronic renal failure may therefore predispose to the development of persistent nephrogenic diabetes insipidus in patients receiving lithium.
PMCID: PMC2429604  PMID: 2170960
18.  On-call service: the role of chemical pathologists. 
Journal of Clinical Pathology  1989;42(12):1233-1236.
The workload of the chemical pathology advisory on-call service was investigated. Over three years 317 calls were recorded, giving a mean of nine calls a month. Seasonal variation in the number of calls was observed, with an increase in calls during December, January, and February. Requests for the arrangement of analysis accounted for 231 calls, while there were 98 requests for advice. Authorization of a request for analysis was the outcome of 156 calls. Advice with respect to investigation, treatment, or interpretation of results was offered during 173 calls. The acute medical and surgical wards, the accident and emergency department, renal unit and intensive care unit accounted for 198 of the calls. The two analyses most frequently requested, through the advisory on-call service, were serum digoxin and blood ethanol, with 51 and 33 requests, respectively. The "acute" wards and accident and emergency department had the greatest request rate, accounting for 35 of the requests for digoxin and 26 of the requests for blood ethanol. The acute care areas were responsible for the major part of the workload, and a clinical requirement for the services of chemical pathologists out of hours, was observed.
PMCID: PMC502044  PMID: 2613914
19.  Effect of calcium, magnesium and sodium ions on in vitro nucleation of human gall bladder bile. 
Gut  1989;30(5):665-670.
The effect of increasing the calcium, magnesium and sodium concentration in gall bladder bile samples from 21 patients with gall stones and nine controls on the in vitro rate of formation of cholesterol microcrystals and numbers of cholesterol microcrystals formed was examined. Addition of these cations to raise the mean maximum concentration of calcium ions to 19.8 mmol/l, of magnesium ions to 20 mmol/l and sodium ions to 998 mmol/l did not trigger nucleation in control bile samples or samples from patients with gall stones. Increasing the mean concentration of calcium ions to 8.6 mmol/l and of sodium to 320 mmol/l increased the numbers of cholesterol monohydrate crystals/0.1 mm3 counted by light polarisation phase contrast microscopy at the time of nucleation in samples from patients with gall stones from a median of 2 (range 1-10) in control portions to 18 (range 2-128) for calcium ions and 10 (range 2-141) for sodium ions (p less than 0.001). Calcium and magnesium ions were more effective than sodium ions, and calcium ions could increase crystal numbers at concentrations found in samples from patients with gall stones, median 4.6 mmol/l (range 2.7-16.9 mmol/l). The concentrations of calcium and magnesium present in bile may therefore influence the rate of development of gall stones.
PMCID: PMC1434218  PMID: 2731760
21.  Nutritional survey of patients in a general surgical ward: is there an effective predictor of malnutrition? 
Journal of Clinical Pathology  1987;40(7):803-807.
A survey of patients in a general surgical ward was undertaken to establish biochemical and anthropometric standards which could be used to detect malnourished patients in hospital. Results of biochemical and anthropometric tests of nutritional status were compared with assessment by a clinician and the quick nutritional index of Seltzer. Triceps skinfold thickness and serum albumin concentrations indicated that 29% and 35% of patients, respectively, were undernourished compared with 16% by clinical assessment and 17% by the quick nutritional index. Significant correlations (p less than 0.001) between serum albumin and transferrin concentrations and arm muscle area were found for men but not for women. Poor nutritional specificity and sensitivity of some anthropometric and biochemical tests may account for the difference in the level of undernutrition found by these tests and clinical assessment. This shows the importance of the choice of test in influencing the level of undernutrition detected.
PMCID: PMC1141102  PMID: 3624502

Results 1-21 (21)