Biomedical subjects
Publications and source records attributed to H A Shepherd.
Ricin, one of the most potent toxins known, has a lethal dose range of 1-10 mg per kilogram (Crompton and Gall, 1980) when injected. There is no effective treatment. We report a case of sub-lethal poisoning by self-injection.
This double blind, double dummy study compares the rate of healing of erosive reflux oesophagitis, assessed endoscopically, with four and eight weeks treatment using omeprazole or cimetidine, and the effect of four and eight weeks treatment of reflux oesophagitis with omeprazole or cimetidine on reflux symptoms, microscopic healing, and in a subgroup of patients, oesophageal pH measurements. Omeprazole 40 mg once daily achieves (i) greater and more rapid symptom relief, (ii) more rapid and sustained endoscopic and histological healing, and (iii) greater reduction of oesophageal acid exposure than cimetidine 400 mg four times daily.
In a pilot study, 26 rheumatoid arthritic patients taking continuous, stable dosage regimens of nonsteroidal anti-inflammatory drugs and with developed gastric and duodenal lesions were administered sucralfate 1 g four times per day (14 patients) or cimetidine 400 mg twice daily (12 patients) in a single-blind regimen for six weeks. Eleven of the patients given sucralfate and eight of the patients taking cimetidine had improved lesion scores. The lesion score of 10 of the 14 patients taking sucralfate and four of the 12 patients taking cimetidine improved by 50 percent or better (not significant). The antrum and body of the gastric mucosa and the mucosa of the duodenum synthesized prostanoids and thromboxane A2, and there was no significant difference in the synthesis of individual prostanoids at entry to the trial in the groups assigned to sucralfate or cimetidine. After six weeks of administration of sucralfate, prostaglandin E2 (PGE2) synthesis by the antrum and body, but not the duodenum, was significantly greater than observed in the biopsy specimens at entry despite continuation of non-steroidal anti-inflammatory drug therapy. After six weeks of cimetidine treatment, no change in PGE2 synthesis was noted in any biopsy specimens when compared with the synthesis at entry. No change in the synthesis of PGF2 alpha, 6-oxo-PGF1 alpha, or thromboxane B2 was noted in gastric or duodenal biopsy specimens in any treatment group. Sucralfate and cimetidine administration resulted in improved gastroduodenal lesion scores in rheumatoid arthritic patients continuing with nonsteroidal anti-inflammatory drug therapy.
A total of 52 jaundiced elderly patients who had malignant obstruction of the distal common bile duct and who required palliative biliary decompression were randomized to receive either an endoscopically placed biliary endoprosthesis (10 French gauge) or conventional surgical bypass. Patients within the two treatment groups were well matched and 51 were followed until their death. Patients treated with endoprosthesis had a significantly shorter initial hospital stay than those treated surgically. In the long term, overall survival in the two groups was similar and jaundice was relieved in over 90 per cent of patients. Despite more re-admissions to hospital for those patients treated endoscopically, the total time spent in hospital still remained significantly shorter in this treatment group compared with those subjected to surgery. The endoscopically placed biliary endoprosthesis is a valuable alternative to conventional surgical bypass in the palliation of extrahepatic biliary obstruction.
After a two-year history of recurrent abdominal pain, an 84-year-old man presented with acute pancreatitis and obstructive jaundice. An endoscopic retrograde cholangiogram demonstrated two filling defects approximately 1.0 cm in diameter, in a dilated common bile duct. Endoscopic papillotomy was performed which resulted in a polypoid tumour delivering itself into the wound followed by a free flow of bile. In addition, a single 1.0 cm gallstone was removed from the common bile duct, above the tumour, using a Dormia basket. The patient recovered completely. Histological examination of biopsies of the tumour taken on three subsequent occasions showed it to consist only of inflammatory tissue (an inflammatory polyp) and later, regenerating bile duct mucosa. After six months this tumour had completely regressed.
The efficacy of a 5-day intensive intravenous regimen (IVR), used as treatment for severely active Crohn's disease in 49 patients, has been evaluated retrospectively. The value of such systemic therapy has not been reported before. Immediate remission was achieved in 38 (76%) patients with no significant difference between those with established disease and those seen for the first time. Patients with ileocolonic disease had the poorest response. There was no apparent change in the natural history of the Crohn's disease after IVR therapy. Nevertheless, this is a safe and effective method of achieving remission in most sick patients with severely active Crohn's disease.
The aetiology of primary sclerosing cholangitis is unknown, but it is closely associated with ulcerative colitis. Serum anticolon antibodies, crossreacting with portal tracts, have been reported in patients with ulcerative colitis but no studies have been carried out in primary sclerosing cholangitis. The frequency of serum anticolon antibodies and portal tract antibodies have been measured in 24 patients with primary sclerosing cholangitis and ulcerative colitis; 15 patients with primary sclerosing cholangitis without ulcerative colitis; 77 patients without primary sclerosing cholangitis: 25 patients with Crohn's colitis; 10 patients with primary biliary cirrhosis; 22 patients with extrahepatic biliary obstruction and 20 normal controls. Serum anticolon and portal tract antibodies were detected using immunoperoxidase techniques on normal colon and obstructed human liver. Tissue typing was undertaken using a standard microcytotoxicity technique. The frequency of anticolon antibodies was markedly increased in primary sclerosing cholangitis patients with ulcerative colitis (62.5%) compared with patients with ulcerative colitis (17%) and Crohn's colitis (16%) (chi 2 = 17.9; p less than 0.001). The antibodies were almost entirely of IgG and IgA classes in all groups. Anticolon antibodies were not found in sera from any other group. Sera from eight of 15 patients with primary sclerosing cholangitis, ulcerative colitis and anticolon antibody reacted with portal tracts of human obstructed liver. This reaction was also seen in four of nine patients with ulcerative colitis and primary sclerosing cholangitis and in three of 15 patients with primary sclerosing cholangitis alone. Portal tract antibody was of IgG class and was not present in sera from any other groups. Unlike anticolon antibody, there was a close relationship between HLA-B8 phenotype and the portal tract antibody (p<0.02; chi 2 = 6.04). Absorption studies confirmed that the anticolon antibody is distinct from portal tract antibody.
Primary sclerosing cholangitis was diagnosed radiologically in 16 of 681 patients (2.2%) with chronic ulcerative colitis in a follow up study at the gastroenterology unit in Oxford. On the basis of established histological criteria, the liver biopsy was considered diagnostic in only half of the cases. The histological findings in these cases were therefore reassessed to determine whether the accuracy of biopsy diagnosis could be improved. The most common specific histological feature was periductal concentric fibrosis of small interlobular bile ducts, even in the absence of inflammation. Other common features were bile ductular proliferation associated with diminution or absence of interlobular bile ducts. Degeneration of bile duct epithelium and diffuse infiltration of portal tracts by mononuclear cells and polymorphonuclear leucocytes were accompanying features. Piecemeal necrosis without rosette formation was found in about half the biopsies. When all these features were considered together a biopsy diagnosis of primary sclerosing cholangitis was established in 14 of 16 cases.
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Immune complexes of human intrinsic factor were prepared by mixing gastric juice saturated with vitamin B12, and sera from patients with pernicious anaemia that had a high proportion of binding (Type II) antibody. The complexes were isolated by sodium sulphate precipitation followed by Sephadex G-150 gel filtration. Acid conditions dissociated the immune complexes and allowed separation of specific antibody and purified antigen bound to vitamin B12 by Sephadex G-200 gel filtration. Specific antibody was covalently attached to Protein A Sepharose CL-4B by coupling with water soluble carbodiimide which allowed intrinsic factor-B12 complex to be purified directly from gastric juice. The intrinsic factor obtained after iodination, ran as a single band on SDS-polyacrylamide gel electrophoresis and was biologically active.
A clinical syndrome is described in 22 patients who present with epigastric pain alone or with hematemesis which is associated with a precedent history of recurrent early morning retching or postprandial retching. The characteristic endoscopic finding is a knuckle of inflamed and sometimes bleeding gastric mucosa which repeatedly prolapses into the esophageal lumen during retching. Other upper gastrointestinal lesions are not found. Retching is thought to cause the forceful prolapse and subsequent traumatization of gastric mucosa. The episodes of vigorous retching and resultant gastric trauma are now considered to be the cause of the abdominal pain and hematemesis, and it is proposed that this combination of clinical features illustrates a distinct syndrome which we have called prolapse gastropathy. This condition is a significant cause of hematemesis and abdominal pain in a group of nonalcoholic patients who demonstrate an unusual sensitivity to gag and retch.
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Three cases of upper gastrointestinal vasculitis presenting as acute abdominal emergencies highlight an uncommon but often fatal presentation of systemic vasculitis. Although abdominal symptoms are common in such diseases, there may be a doubt during assessment of the patient as to whether the gastrointestinal tract is the prime target organ. Radiology is often negative during the acute illness. Endoscopy was important in documenting early and more advanced bleeding lesions of polyarteritis nodosa (PAN) and Henoch-Schoenlein disease, both conditions in which upper gastrointestinal lesions are rare. The gastric and duodenal vasculitic lesions demonstrated by endoscopy in such a clinical setting were confirmed histologically. Endoscopic assessment and early aggressive medical therapy contributed significantly towards the overall successful outcome. Gastroduodenoscopy has not been used either routinely or as an emergency investigation for the assessment of patients with vasculitis who present with acute abdominal pain. Involvement of the stomach and duodenum by vasculitis is therefore poorly appreciated, but remains a serious complication of vasculitic disease when the gastrointestinal tract is the prime target organ, and the information gained by endoscopy in a difficult clinical situation might alter the overall outcome of the disease.
Six hundred and eighty-one patients with ulcerative colitis who attend the outpatient clinic in Oxford have been screened for the presence of persistently abnormal liver function tests. Of the 21 patients (3.0 per cent) found with abnormal liver function 17 (2.4 per cent) were shown by cholangiography to have primary sclerosing cholangitis. The liver biopsies from those patients demonstrated a wide range of histological features and were diagnostic of primary sclerosing cholangitis in only 50 per cent of the patients. When persistently abnormal liver function tests are demonstrated in patients with ulcerative colitis it is likely that primary sclerosing cholangitis will be present (81 per cent of patients in this study), and in order to make a reliable diagnosis it is necessary to perform cholangiography in addition to liver biopsy. A close association with primary sclerosing cholangitis and histocompatibility antigens HLA B8 and DR3 is also reported.
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