Neonatal pure red cell aplasia due to anti-M.
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Biomedical subjects
Publications and source records attributed to R F Hinchliffe.
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AIMS: To search for laboratory evidence of hereditary spherocytosis (HS) among apparently healthy children with the chance finding of an isolated increase in hyperchromic red cells (cells with intracellular haemoglobin concentration > 410 g/litre). METHODS: Blood and reticulocyte counts and Pink tests were performed on successive children found on routine counts to have > 4% hyperchromic red cells, and compared with age and mean cell haemoglobin concentration (MCHC) matched controls and children known to have HS. RESULTS: Thirty four patients with > 4% hyperchromic red cells had significantly higher absolute numbers of such cells (p < 0.0001) and higher reticulocyte counts (p < 0.01) than age matched controls, together with higher MCHC (p < 0.0001) and haemoglobin distribution width (p < 0.0001) values and lower mean cell volume (p < 0.02) values. Significant differences were also found among hyperchromic red blood cell, reticulocyte, and haemoglobin distribution width values when subjects were compared with MCHC matched controls. Pink test values were higher in children with increased hyperchromic red blood cells, but not significantly so. In patients with HS, most variables measured were significantly different both from those of children with > 4% hyperchromic cells and controls. Despite the differences found, few MCHC, HDW, reticulocyte, or Pink test values were outside of the normal limits, and only one child with increased hyperchromic cells had both a mild reticulocytosis and a slightly raised Pink test value. CONCLUSIONS: Subjects with an isolated increase in hyperchromic red blood cells have a profile of red blood cell changes similar to that of patients with HS, but to a lesser degree. They may carry a recessive form of the disease but lack the laboratory features of clinically manifest HS.
Reference ranges for the total and differential leucocyte counts were determined from venous blood collected at 2, 5 and 13 months of age from a cohort of 112 healthy children of north European ancestry. At 2, 5 and 13 months, the ranges for neutrophils were found to be 0.7-4.7, 1.1-5.6 and 1.0-7.6 x 109/l, and for lymphocytes 3.3-10.5, 3.4-11.3 and 3.5-10.4 x 109/l, respectively. The upper limits for monocytes at each age were 1.2, 1.2 and 0.91 x 109/l, and for eosinophils 0.84, 1.0 and 0.88 x 109/l, respectively. Mean counts for all cell types, except monocytes, increased between 2 and 5 months of age. There was little change in mean counts between 5 and 13 months. Statistically significant correlations existed between the numbers of each cell type at 2 months of age, and were still present at 13 months between monocytes and each of the granulocyte series and between basophils and all other cell types. By comparison with older data these findings indicate a lower reference limit for neutrophils at 2 months of age, and a narrower range for this cell type at both 2 and 5 months of age. Reference ranges for lymphocytes and eosinophils are wider than indicated by some previous studies.
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The study aimed to investigate local concerns about clinically important discrepancies between repeat HemoCue haemoglobin measurements from single drops of blood. Two biomedical scientists and two health visitors each obtained a series of paired haemoglobin values by fingerprick sampling from healthy volunteers. Seven of 20 paired values obtained by health visitors and three of 20 obtained by scientists from the first drop of blood forming at the puncture site differed by > or = 10 g/l; 11 of 20 paired values obtained by health visitors and one of 20 by the scientists from the fourth drop of blood differed by > or = 10 g/l. After collecting and mixing a number of drops in EDTA tubes before analysis, seven of 40 paired values differed by > 5 g/l, and none by > 10 g/l. Pooling drops of blood before analysis improves precision of HemoCue haemoglobin measurement and allows users to achieve results comparable to those obtained by experienced laboratory staff. Measurement of haemoglobin from single drops of skin puncture blood should be discontinued.
AIM: To investigate the efficacy and safety of daily low-dose colloidal bismuth subcitrate in reducing duodenal ulcer relapse. DESIGN: Double-blind, double-dummy group comparative clinical trial with random allocation. Healing Phase: colloidal bismuth subcitrate 240 mg twice daily vs ranitidine 150 mg twice daily for up to 12 weeks. Maintenance Phase: nightly, colloidal bismuth subcitrate 120 mg vs ranitidine 150 mg vs placebo for up to 12 months (high-risk patients received active treatment only). ASSESSMENT: clinical, endoscopy, random blood bismuth levels (and rapid urease test for Helicobacter pylori in a subgroup). PATIENTS: 194 with active duodenal ulcer. OUTCOME: Cumulative healing at 12 weeks was 93% on colloidal bismuth subcitrate (of 92 patients) and 97% on ranitidine (of 102 patients). Relapse at 1 year was significantly less on active treatment as follows: placebo (50 patients) 60%; ranitidine (71 patients) 21%; colloidal bismuth subcitrate (64 patients) 33%. This was independent of the results of the rapid urease test which was positive in 78%, 88% and 76% of the patients respectively. Treatment was well tolerated. The highest median blood bismuth level (mcg/L) was 25 in the healing phase and fluctuated between 6 and 10 in the maintenance phase. CONCLUSIONS: Colloidal bismuth subcitrate, 120 mg nightly, is effective in reducing duodenal ulcer relapse and is well tolerated.
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The Bayer H1 automated blood counter was used to assess the MCHC values of 40 nonanaemic patients with HbC trait, 21 with HbD trait, 23 with HbE trait and 69 with HbS trait. These were compared with values from controls with a normal Hb phenotype. Values were significantly higher in those with HbC, D and S traits and approached significance in those with HbE trait. In 45%, of subjects with HbC trait the MCHC value was > or = 35 g/dl. Such values may prove a useful marker for this abnormality. In a further 12 patients with HbC, D, E or S traits and coexisting iron deficiency anaemia, MCHC values were usually higher and the percentage of hypochromic cells (red cells with CHC <28 g/dl, directly measured by the H1) usually lower than values derived from controls with a normal Hb phenotype and iron deficiency anaemia of similar degree. In individuals with HbC, D, E or S traits, the MCHC and proportion of hypochromic cells are less sensitive indicators of iron lack than in subjects with a normal Hb phenotype.
Values for MCV, MCH, MCHC and red cell distribution width (RDW) derived from subjects with HbC and HbE traits using a Technicon H*1 automated blood count analyser were compared. Significantly higher MCH, MCHC and RDW values were found in those with HbC trait. By use of a simple discriminant function (MCHC2 x RDW/1000), 19/20 subjects with HbC trait gave a value > or = 16.3, and 20/21 subjects with HbE trait gave a value < or = 16.2. The function described may be of value as an adjunct to electrophoresis in intralaboratory quality control.
To determine whether skin puncture blood can be used reliably for CD4 lymphocyte counts, the numbers of the major subsets of lymphocytes were assessed in paired venous and skin puncture blood samples from 22 children and 10 adults. Paired values were highly correlated, with skin puncture values being about 7% higher than venous values for each cell type. Differences were of borderline statistical significance for total lymphocytes and for each subset except CD3+ CD8+ T lymphocytes. Nevertheless, the magnitude of the differences was small and unlikely to be of clinical importance, and it seems that skin puncture samples may be preferable for CD4 counts in children or adults with difficult venous access.
A study was carried out to determine the frequency of combined iron deficiency and beta-thalassaemia trait in a cohort of British Asian children to see whether the trait protects iron status. Of 470 consecutive children with red cell microcytosis, 77 had beta-thalassaemia trait and 26 (34%) of these also had evidence of iron deficiency. It was most common and profound in children under five years of age where the prevalence was 16 in 33 (48.5%). This suggests that iron deficiency is no less common in Asian children with beta-thalassaemia trait than in those without. It should not be presumed that the trait protects iron status or that the two are in any way mutually exclusive, at least in the early years.
AIMS: To evaluate the reliability of fluorescence in situ hybridisation (FISH) in the retrospective cytogenetic assessment of old bone marrow smears stored for periods of up to 20 years. METHODS: A series of bone marrow smears either Romanowsky stained, or frozen and unstained, and aged from one month to 20 years were hybridised with biotin labelled probes specific for the centromeric regions of human chromosomes X, 6, and 18. Sites of hybridisation were detected with fluoresceinated avidin. One hundred to 400 cells from each preparation were examined and the number of signals observed was recorded. RESULTS: All smears exhibited signals in most cells examined. In cytogenetically normal cases, an average 67.6% of cells (range 36%-90%) demonstrated the appropriate number of X centromere signals. In those samples known to contain extra chromosomes X, 6, or 18 the presence of cells with the abnormal copy number was clearly detected in each case. CONCLUSION: When applied in the way described, FISH can give consistent and accurate results with a variety of archival bone marrow smears, including aged prestained material. This will permit retrospective assessment of specific cytogenetic abnormalities in patients with leukaemia using their initial diagnostic slides even where these are several years old.
Serial reticulocyte counts on a patient with an unstable haemoglobin haemolytic anaemia whose red cells contained Heinz bodies were obtained by two automated methods. One false low and several false high counts were obtained with standard threshold settings; each was accompanied by activation of the appropriate alarm. With the FACScan a bimodal red cell distribution was found, corresponding to the proportions of Heinz body positive and negative cells. This case illustrates the fact that Heinz bodies can interfere with automated reticulocyte counting methods, and to a degree that could be clinically important.
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We tested the hypothesis that the gastric H+/K+ adenosine triphosphatase inhibitor, omeprazole, because of its different mode of action and pronounced inhibitory effect on gastric acid secretion, may be more effective in peptic ulcer that is refractory to histamine H2 receptor antagonist treatment than continuing the same therapy. Altogether 107 patients (duodenal ulcer, n = 88; prepyloric ulcer, n = 14; gastric ulcer, n = 3; mixed sites, n = 2) with refractory peptic ulcer - that is ulcer unhealed after at least two months' treatment with cimetidine 0.8 g or 1 g daily or with ranitidine 0.3 g daily - were randomly allocated to receive either omeprazole 40 mg daily (n = 54) or to continue treatment with the same H2 receptor antagonist and at the same dose (n = 53) for up to eight weeks. The patients in the two treatment groups were well matched demographically. Healing by 'intent to treat' analysis was as follows: at four weeks, omeprazole 46 of 54 (85%), H2 receptor antagonist 18 of 53 (34%) (p less than 0.0001); and at eight weeks, 52 of 54 (96%) and 30 of 53 (57%) respectively (p less than 0.0001). One patient was lost to follow up but of the 22 patients whose ulcers were shown to be unhealed at endoscopy after receiving continued H2 receptor antagonist treatment, 21 healed in four to eight weeks when changed to omeprazole. Daytime epigastric pain cleared at four weeks in 43 of 47 (91%) patients on omeprazole and in 32 of 46 (70%) on H2 receptor antagonists (p=0.01) and relief of all dyspeptic symptoms occurred in 39 of 47 (83%) and 23 of 45 (51%) (p=0.0009) patients respectively. Adverse events occurred in 11 of 54 (20%) patients on omeprazole and in 12 of 35 (34%) on cimetidine but in none on ranitidine. The events were mild and none required treatment withdrawal. The commonest event in patients on omeprazole was loose stools or diarrhoea (n=5). Omeprazole was significantly better than continued H2 receptor antagonist treatment for the short term management of refractory peptic ulcer as judged by healing rate and pain relief, and it was safe.
Enprostil is a synthetic prostaglandin E2 analogue with gastric antisecretory and mucosal protective properties. We compared the effects of enprostil and ranitidine on the healing of gastric ulcers and the subsequent relapse rates over 6 months. Patients (N = 156) were recruited for a double-blind study from 12 centers in Europe; 71 were randomly assigned to oral treatment with 35 micrograms enprostil twice daily and 85 to 150 mg ranitidine twice daily for up to 8 weeks. Both groups were of similar demography; their healing rates were also similar. Cumulative intent-to-treat healing rates were at 4 weeks enprostil 48%, ranitidine 41%: at 6 weeks enprostil 65%, ranitidine 68%; and at 8 weeks enprostil 72%, ranitidine 80%. Of those patients who met all protocol criteria and completed treatment, and were endoscoped at the prescribed times, healing rates were at 4 weeks enprostil 55%, ranitidine 54%, at 6 weeks enprostil 75%, ranitidine 84%; and at 8 weeks enprostil 80%, ranitidine 90%. Relief of pain was rapid and similar in both groups. The incidence of adverse events was low and similar in the two groups. The treatment-free relapse rate at 6 months was enprostil 64%, ranitidine 49%; the median times to relapse were 169 and 203 days, respectively. Enprostil and ranitidine appear to be equally effective in healing gastric ulcers.
Forty five patients with refractory oesophagitis, defined as persisting erosive changes or ulceration despite a minimum of three months' treatment with cimetidine 3.2 g daily or ranitidine 0.9 g daily, were treated in an open trial with omeprazole 40 mg daily for up to eight weeks. Endoscopically defined healing was observed in 73% of patients after four weeks' treatment and in 91% after eight weeks' treatment. Symptoms were completely relieved in 60% of patients, improved in 34%, unchanged in 4%, and worsened in 2%. After healing patients returned to maintenance treatment with cimetidine 1.6-3.2 g daily, depending on the severity of their illness before treatment with omeprazole. By six months and 12 months only 55% and 33% of patients respectively were still in remission. This study suggests that when erosive oesophagitis is refractory to treatment with high dose cimetidine or ranitidine, treatment with omeprazole 40 mg daily for up to eight weeks is effective in inducing healing and relieving symptoms.