Inappropriate use of non-siliconized citrate tubes for clotting tests.
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Biomedical subjects
Publications and source records attributed to W Hughes.
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Red cell folate specimens were added to the Quality Assurance Program (QAP) of the Royal College of Pathologists of Australasia in 1986. The interlaboratory variation in the results of these red cell folate surveys has been persistently unsatisfactory. This study reports an investigation into the factors contributing to the wide variation of results reported in QAP surveys. Survey results were studied, replies to a questionnaire regarding methods sent to all participants were assessed and some new experimental studies were performed. Factors contributing to the poor QAP results include variation in dilution and diluent, calculation errors, failure to freeze the hemolysate prior to assay and to follow the kit manufactorer's instructions, stability of dithiothreitol, and variations in kit methods, especially in the release of bound folate by "boil" and "no-boil" methods. Photodecomposition and the form and concentration of ascorbate may also be significant. Adequate preparation of the hemolysate sample should ensure release of all protein-bound red cell folate with the reduction of all folates to a single form. Kit manufactures, users and the QAP committee can all contribute in all attempt to rectify current sources of error.
It has been shown previously that it is difficult for a general practitioner to predict anal vs. colorectal sources of bleeding in patients presenting with rectal bleeding. The aim of the present study was to determine whether there are any aspects of such a patient's history or clinical features that strongly indicate bleeding from a colorectal cancer or polyp. One hundred forty-five consecutive patients, aged 40 years and older, who had complained of rectal bleeding to a general practitioner, were referred to a specialist for full colonic investigation. Among 15 symptoms and clinical features examined, few had any statistically significant association with the source of bleeding. There was an elevated probability of colorectal cancer (21 percent) in patients who had seen blood mixed with feces. Most bowel symptoms and clinical features are not helpful in deciding whether to proceed with full colorectal assessment in patients aged 40 and older who have rectal bleeding of recent onset.
A second Australian family is reported with Hemoglobin North Shore (beta 134 Val----Glu), an unstable hemoglobin, causing no clinical symptoms. All affected family members showed only mild reticulocytosis and microcytosis on the blood film, despite the strongly positive isopropanol test for Hb (hemoglobin) stability and numerous red cell inclusions. Hb North Shore constituted 31-38% of the total hemoglobin and migrated on the anodal side of Hb A at pH 8.9. The association of a mildly raised Hb A2 level and thalassemic phenotype with Hb North Shore previously reported, is confirmed in this study.
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All patients with the acquired immunodeficiency syndrome and a first episode of Pneumocystis carinii pneumonia seen at the San Francisco General Hospital between November 1984 and April 1985 were evaluated for oral treatment with dapsone (100 mg/d) plus trimethoprim (20 mg/kg body weight X d). All 15 patients who met the entry criteria improved clinically and radiographically within 3 to 10 days after starting treatment. Repeat pulmonary function tests and gallium lung scans after 3 weeks of therapy also showed improvement. Although side effects occurred in 14 patients, in only 2 were they severe enough to require stopping therapy. Both of these patients had worsening skin rash, and dapsone-trimethoprim therapy was stopped after 10 days. When compared with trimethoprim-sulfamethoxazole or pentamidine used to treat P. carinii pneumonia in similar patients, oral dapsone-trimethoprim is at least as effective, seems to be better tolerated, and may have a lower frequency of serious side effects.
The Royal College of Pathologists of Australasia introduced a comprehensive national external quality assurance programme (QAP) in hematology in 1979. This now provides regular monthly trials of full blood counting, supplemented by 3-monthly sets of samples for a large variety of other tests for "state of the art" studies, together with case slides for diagnosis for 294 participants. In addition educational supplements are provided, based on one or other aspect of each major quarterly trial. The frequency and variety of tests and analysis of participants' results conform to suggested standards for similar national schemes elsewhere in the world. There is evidence that the programme has helped raise the standards of hematopathology in Australasia and has identified areas which require improvement. It is envisaged that the scheme will satisfy the requirements of state legislation designed to accredit pathology laboratories. Future development should include a refinement of objective methods of scoring performance, especially in areas such as morphology where participants' results cannot readily be expressed numerically.
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Antral gastrin concentratin (AGC) was measured in forceps biopsy specimens of prepyloric mucosa obtained at endoscopy in 65 patients with various kinds of gastric ulcer and in 31 nonulcer control patients. AGC in 32 patients with a lesser curvature gastric ulcer, 10.0 +/- 2.0 (mean +/- 1 SE) ng gastrin/mg tissue was significantly less (P < 0.01) than AGC in 31 nonulcer control patients, 14.4 +/- 1.4. AGC was similar to the control values in 23 patients with a pyloric channel ulcer, 15.2 +/- 1.7; 5 patients with a greater curvature ulcer, 15.0 +/- 4.8; and 3 patients with both duodenal and gastric ulcers, 15.8 +/- 0.7. AGC was significantly greater (P < 0.01) than the control values in 3 patients with a vagotomy and pyloroplasty and a gastric ulcer, 29.8 +/- 5.0. In contrast with most lesser curvature gastric ulcer patients who had low AGC, 3 gastric ulcer patients had antral gastrin values which were about three times the mean AGC of the controls. Two of these patients had fasting serum gastrin values which were more than twice the mean control fasting serum gastrin. Meal-stimulated integraed gastrin responses in these 3 patients ranged from three to nine times the mean control response. These findings suggest that a high AGC may account for a few instances of increased serum gastrin concentrations in gastric ulcer patients.
Because little has been known regarding the dialyzability of lidocaine, we studied the clearance of this drug by hemodialysis. The dialysance of lidocaine was found to range between 10.6 to 21.3 ml/min. Lidocaine-urea extraction ratio averaged 11%. Because of the low therapeutic and even toxic plasma levels, the amount of drug removed by dialysis is negligible. Therefore, dose adjustment is unnecessary during dialysis, and dialysis appears to be of little help in the treatment of lidocaine toxicity.
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The effect of the gastric alkaline tide on serum-ionized calcium levels was determined in human subjects. Gastric acid seretion was stimulated by a standard steak meal, human synthetic gastrin, and betazole hydrochloride. Ionized calcium levels fell to a similar extent after each stimulus. The mean decrease in calcium ion concentration in all experiments was 5.4% of the basal concentration. The fall in serum calcium ion concentration was highly correlated with the rise in serum pH. We speculate that increased formation of calcium bicarbonate complex in the serum as well as increased binding of ionized calcium by serum protein accounts for the surprisingly large effect of the alkaline tide on serumionized calcium levels.
Basal lower esophageal sphincter (LES) pressure was measured in 6 patients with the Zollinger-Ellison syndrome (ZES) and hypergastrinemia, and in 6 patients with duodenal ulcer and normogastrinemia. Basal LES pressure in ZES patients, 17.0 +/- 3.7 (mean +/- SE) mm Hg was similar to basal LES pressure in duodenal ulcer patients, 18.3 +/- 3.5 mm Hg (P greater than 0.10). LES pressure and serum gastrin concentration were not related in the ZES patients, r = 0.03, or in the duodenal ulcer patients, r = 0.20. Intravenous infusion of calcium gluconate in ZES patients produced a marked rise in serum gastrin concentration, delta = 1580 +/- 1110 pg per ml (P less than 0.001), and a moderate but significant rise in LES pressure, delta = 5.9 +/- 0.9 mm Hg (P less than 0.05). In duodenal ulcer patients calcium infusion produced only slight rises in gastrin concentration, delta = 10 +/- 12 pg per ml, and LES pressure, delta = 2.1 +/- 0.5 mm Hg, which were not significant (P greater than 0.10). This study suggests that basal LES pressure is not regulated by blood gastrin levels in the ZES. We interpret the calcium infusion study to show that the LES pressure in patients with ZES may respond to acute changes in endogenous gastrin levels.
An unusual case of portal hypertension in an asymptomatic 33-year-old man is presented. The findings of splenomgealy, esophageal and gastric varices, a patent umbilical vein with associated venous hum, and three normal liver biopsies qualify him for the diagnosis of Cruveilhier-Baumgarten disease. Possible etiologic explanations of his portal hypertension are discussed.