Biomedical subjects
I W Dymock
Publications and source records attributed to I W Dymock.
Neuroleptic malignant syndrome: another medical cause of acute abdomen.
We present a patient with neuroleptic malignant syndrome and intestinal pseudo-obstruction misdiagnosed as being secondary to septicaemia. The management of the patient is discussed with emphasis on the role of creatine kinase and liver function tests.
Azapropazone induced hepatitis.
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A prospective randomized trial of vagotomy in chronic duodenal ulceration.
In a prospective, randomized trial, 76 patients with duodenal ulceration treated by truncal vagotomy and pyloroplasty were compared with 77 patients who underwent highly selective vagotomy. A total of 149 patients was followed up for from 1 to 4 years, the average follow-up period being 2.6 years. There was no operative mortality and no significant difference in postoperative morbidity between the two groups. The incidence of recurrent ulceration was greater after highly selective vagotomy, but this difference was not statistically significant. The clinical results were comparable in each group, and although the incidence of diarrhoea and dumping was greater after vagotomy and pyloroplasty, this difference was not statistically significant.
Leucocyte ascorbate levels and postoperative deep venous thrombosis.
Forty-four general surgical patients were included in a prospective, randomized double-blind controlled trial of ascorbic acid (500 mg b.d.) or placebo for 7 days before operation. This was to test the hypothesis that vitamin C may reduce the instance of deep venous thrombosis postoperatively. Venous blood samples were taken before entering the trial, just immediately before surgery, on the day of operation and on three further occasions at 3-day intervals postoperatively for leucocyte ascorbic acid concentration (LAC). Venous thrombosis was diagnosed using the 125I-fibrinogen test and the leg scans interpreted by Roberts' criteria. There was no significant difference in the incidence of DVT between the treatment and placebo groups. In those with DVT (n = 23) the mean LAC on the day of operation was not significantly different from that in those without DVT. However, on the sixth and ninth postoperative days LAC levels were significantly lower in the DVT group. These results suggest that the administration of ascorbic acid preoperatively does not reduce the incidence of DVT, but a striking decrease in the LAC levels in the DVT patients is in keeping with the hypothesis that the initial event in the pathogenesis of DVT is adherence of leucocytes to the venous endothelium.
Prophylaxis with deglycyrrhizinised liquorice in patients with healed gastric ulcer.
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Association of abnormal fibrin polymerisation with severe liver disease.
The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
Abnormal fibrin polymerization in liver disease.
Although there have been isolated reports of an acquired abnormal fibrinogen in patients with liver disease, its frequency and clinical significance is not known. In this study 121 consecutive patients with a wide spectrum of hepatic disorders were screened for abnormal fibrin polymerization. A simple colorimetric method using Reptilase was employed. Of 32 patients with proven cirrhosis, 16 (50%) showed abnormal fibrin polymerization. The incidence in decompensated alcoholic cirrhosis was particularly high. The abnormality was also detected in all patients with acute liver failure and seven of 15 with chronic active liver disease. Clinical improvement often correlated with its disappearance. Two patients with primary liver cell tumours demonstrated the abnormal polymerization. In patients with bleeding oesophageal varices the detection of abnormal fibrin polymerization was associated with a poor prognosis. None of the patients with surgical obstructive jaundice (26) or miscellaneous liver disorders (37) had abnormal fibrin polymerization. The occurrence of abnormal fibrin polymerization in liver disease is more frequent than previously suspected and usually signifies severe primary hepatocellular dysfunction. Evidence is presented to support the presence of a primary abnormality of fibrinogen as the cause of impaired fibrin monomer polymerization.
Simple clinical method of measuring gastric emptying of solid meals.
The radioisotope techniques used for the measurement of gastric emptying of solid meals in man require complex and expensive scintiscanners of cameras. We have evaluated a simple technique which uses a fixed scintillation detector and compared the results with those obtained from a gamma camera. The rates and patterns of gastric emptying recorded by the two methods correlated well in both healthy volunteers (mean r= 0.95) and patients with duodenal ulcer (mean r =0.89). The scintillation detector provides a reliable and inexpensive method for measurement of gastric emptying of solid meals.
Serial liver biopsies in blood donors with persistent HBs antigenaemia.
Initial liver biopsies from asymptomatic HBs antigen positive blood donors showed a range of histological abnormalities ranging from minor parenchymal lesions to cirrhosis. Twenty of these have now been followed up for periods of up to four years and during that time have had at least two liver biopsies. Throughout the period of study all the donors have remained carriers of HBs Ag, and there was no significant variation in the titers of antigen or the electron microscopic appearances of the serum in individual donors. The histological appearances of subsequent liver biopsies were not always the same as those seen initially, and while there appeared to be some improvement in three cases, there were nine in which the histological appearances were worse.
Factor VII as a marker of hepatocellular synthetic function in liver disease.
Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58% was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40%) than the "contrast" patients with surgical obstruction of the major bile ducts (93%). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic liver damage had mean activities similar to the contrast group. Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration. It is concluded that the prothrombin time using Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated.
Granulomatous gastritis, iron deficiency, vitamin B12 malabsorption and immunoglobulin deficiency.
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e Antigen-antibody system as indicator of liver damage in patients with hepatitis-B antigen.
The clinical relevance of the e antigen-antibody system was investigated in 61 people persistently positive for hepatitis-B surface antigen, including 22 healthy carriers. The e antigen was not detectable in any of the healthy carriers, whereas it was found in 15 out of 28 patients with chronic aggressive hepatitis and two out of 11 with chronic persistent hepatitis. Its presence therefore indicates chronic liver disease but its absence does not exclude it. It may prove to be a particularly useful prognostic aid in chronic persistent hepatitis, since one of the two patients in whom it was found later developed aggressive hepatitis. In contrast, e antibody is of little diagnostic help, for, though it was found mostly in healthy carriers (18;82%), it was also detectable in 9 (23%) of the patients with chronic hepatitis. In 13 (76%) of the patients positive for e antigen Dane particles were seen on electron microscopy, but these were also present in 5 (19%) of the patients positive for e antibody. These findings are consistent with other evidence suggesting that e antigen is not a surface component of the Dane particle, but rather an independent soluble protein manufactured by the host in response to infection with the hepatitis-B virus.
Use of factor-VII-rich prothrombin complex concentrate in liver disease.
A prothrombin complex concentrate rich in factor VII has been used in the management of the clotting defect in thirteen patients with liver disease. Adequate correction of coagulation was achieved immediately after infusion in all cases. Within 4 hours there was some deterioration and by 24 hours the results approximated to pre-fusion values. Liver biopsies were performed without haemorrhagic complication in the immediate post-infusion period. There was no evidence of induced intravascular coagulation. Since other prothrombin complex concentrates have proved disappointing, both in their failure to correct the clotting defect and in their production of disseminated intravascular coagulation, this factor-VII-rich concentrate may be the treatment of choice in patients with liver disease who require temporary correction of their coagulation defect.
Proceedings: Leucocytotoxicity in malignant and non-malignant colonic diseases.
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Coagulation studies as a prognostic index in acute liver failure.
A coagulation screen has been performed on 12 patients with acute liver failure. Six died and six recovered. All six fatal cases developed a haemorrhagic state with haemostatic failure. An attempt has been made to delineate the various mechanisms for the production of the coagulation defect. The significance of the different haematological parameters in assessing prognosis has been assessed. The study emphasizes the importance of the synthetic ability of the liver in determining survival prospects. A good correlation between the factor-VII level, which is a guide to liver synthesis, and recovery has been shown. The value of a specific factor-VII assay in acute liver failure appears considerable. Where this assay cannot be performed the clot opacity fibrinogen technique provides a reasonable guide to the prognosis. The presence or absence of DIC was not a determinant factor in survival in this series.
Cell-mediated immunity to hepatitis B surface antigen in blood donors with persistent antigenaemia.
Cellular immunity to the hepatitis B surface antigen (HBsAg) and a liver-specific lipoprotein was studied, using the leucocyte migration test, in 38 asymptomatic blood donors found to have HBsAg in the serum. Sensitization to HBsAg was found in 26% and was related to the presence of liver damage, being detected in 47% of those with elevated serum aspartate aminotransferase but in only 13% with normal enzyme levels. The frequency of sensitization to this antigen in those with chronic persistent or chronic aggressive hepatitis on biopsy was also higher than in those with unrelated or minimal changes. The findings using the liver-specific lipoprotein as antigen were similar and there was a correlation between the results obtained with this and the hapatitis B surface antigen. This study supports the hypothesis that a T-lymphocyte response to hepatitis B virus antigen can initiate an autoimmune reaction to antigens such as liver-specific lipoprotein on the hepatocyte surface, and that this reaction may be of importance in the production of chronic liver damage. In the absence of the T-cell response, the autoimmune reaction cannot occur and the virus is able to establish a harmless symbiotic union with the host.
Electron microscopy of serum of healthy hepatitis B antigen carriers.
The sera of 36 blood donors who are established HBsAg carriers were examined with the electron microscope. The findings were correlated with the histological and electronoptic appearances of the liver and the titre and subtype of the antigen. Antigen-antibody complexes could not be detected. Dane particles constituted 2 percent or more of the total particle count in five of the 36 sera, including three sera from five carriers with chronic aggressive hepatitis and two sera from 11 carriers with chronic persistent hepatitis. In sera from carriers with normal histology or the minimal histological lesion of focal parenchymal necrosis they were detected very infrequently or not at all. Three biopsies revealed intranuclear inclusions when examined electronoptically and the corresponding sera all contained greater than 2 percent Dane particles. Where greater than 2 percent Dane particles were seen the antigen titre tended to be high. The predominant subtype was ad. There was no correlation between the number of Dane particles and the antigen subtype nor between subtype and histology.