Liver transplantation in Australia: the Queensland experience.
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Biomedical subjects
Publications and source records attributed to P Kerlin.
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The indirect, noninvasive technique of breath hydrogen (H2) analysis was evaluated in 45 patients suspected of having bacterial overgrowth of the small intestine. Bacterial overgrowth, defined as a jejunal culture yielding at least 10(5) organisms/ml, was present in 27 patients. After dietary preparation and a 12-h fast, subjects received in random order and on separate days 50 g of glucose or 50 g of rice flour in the form of two pancakes. Normal values were established in 20 healthy controls. Twelve of 27 patients with proven bacterial overgrowth had an elevated (greater than 15 ppm) fasting breath H2 level on at least 1 test day. Fifteen of 18 patients with negative cultures had low fasting breath H2 levels. Based on values in controls, a positive breath test was defined as an increase in breath H2 of greater than or equal to 12 ppm after glucose or greater than or equal to 14 ppm after rice flour. A 2-h glucose breath H2 test had a sensitivity of 93% and a specificity of 78% in the diagnosis of overgrowth. The predictive value of a positive test was 86% and that of a negative test was 88%. The combination of both a high fasting breath H2 level and a diagnostic rise of breath H2 after glucose was present in 41% of patients with overgrowth and in none of the patients without overgrowth. Extending the test to 4 h did not increase sensitivity, but decreased specificity. Rice flour was a less satisfactory substrate in predicting the presence of bacterial overgrowth. In conclusion, a high fasting breath H2 level after dietary preparation suggests bacterial overgrowth but lacks sensitivity. The finding of a rise in breath H2 of at least 12 ppm within 2 h of a 50-g glucose challenge is a simple screen for bacterial overgrowth. The combined criteria of a high fasting breath H2 level and a significant rise after glucose are specific for bacterial overgrowth.
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High esophageal stricture associated with a circumferential "inlet patch" of heterotopic gastric mucosa is reported in 2 patients. Biopsy specimens taken from the strictures demonstrated inflamed or ulcerated gastric fundal-type mucosa in both cases. Dilatation of the strictures followed by treatment with histamine H2-antagonists produced almost complete resolution of dysphagia in both patients.
During the four year period 1983-87 transjugular liver biopsy was performed on 67 patients (M43, F24) aged 17-79 yr (mean 45.6 yr). Standard percutaneous biopsy was contraindicated by coagulation disorders (95%) often with ascites (17%). Biopsies were taken using a specially modified Ross trans-septal needle passed into hepatic veins under fluoroscopic guidance. Hepatic tissue samples were obtained from the initial biopsy in 62 (93%) patients. In 30 consecutive transjugular biopsies a mean area of 38.2 mm2 per section (0.9-100 mm2) was available for histology compared with an area of 15.9 mm2 (9.3-48.8 mm2) in 50 consecutive percutaneous biopsies. Improved techniques of sample washing, sieving and fixation optimised separation of hepatic tissue from blood clot and fibrin. Four patients experienced significant complications but no deaths occurred. Individual diagnoses were changed in 17 patients as a result of biopsy findings. This study confirms the efficacy and relative safety of the transjugular approach in obtaining liver biopsies from patients with contraindications to standard percutaneous techniques.
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A 65-year-old male developed a rapidly progressive disease characterized by severe hemolysis, with spur cells (acanthocytes) and liver disease. Autopsy findings were consistent with a diagnosis of idiopathic hemochromatosis. Investigation of the patient's family uncovered four out of five first degree relatives with significantly raised serum ferritin levels. A sister had biopsy proven hemochromatosis. Spur cell anemia is a recognized, though rare, complication of alcoholic liver disease and indeed the patient had a regular alcohol intake of up to 50 g daily. Although the alcohol intake could have contributed to the formation of spur cells, the possible association with hemochromatosis should be considered. A diagnosis of hemochromatosis has important implications for family members.
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Orthotopic liver transplantation began in Brisbane in January 1985. During the first two years of the programme an assessment committee evaluated 55 patients (38 adults, 17 children). Patients were either accepted for transplantation, rejected as unsuitable or deferred for elective reassessment. All of the 10 adults who were rejected for transplantation because they had "too advanced" disease died within four months of assessment. Six children who were accepted for transplantation died before a suitable donor liver could be found. In the first two years, 21 orthotopic liver transplantations were performed on 18 patients (adults, 13 patients; children, five patients). Fifteen of 21 grafts were procured from within Queensland. Twelve (67%) patients are alive at three to 23 months and all have been discharged from hospital. Deaths in adults were due to sepsis (three patients), aspiration pneumonitis (one patient), rejection and hepatic artery thrombosis (one patient) and the recurrence of a hepatocellular carcinoma five months after discharge from hospital (one patient). Two patients underwent a second transplantation procedure because of chronic rejection at four months and at 11 months, respectively, after the initial operation. One patient received a second transplant for primary graft failure at four days after the operation. A scoring system which considered the presence of pre-operative patient factors, such as coma, ascites, malnutrition and previous abdominal surgery, partly predicted the operative blood loss and patient survival. In conclusion, orthotopic liver transplantation is being performed in Australia with survival rates that are comparable with those of established overseas units.
Yersinia enterocolitica was isolated from the feces of 29 patients over a three-year period following the introduction of a selective culture medium. Y. enterocolitica was the third most common enteric pathogen after Campylobacter jejuni and Salmonella in this series of 3795 specimens from a predominantly adult population. The isolation rate of Y. enterocolitica was 0.9% and this represented 15.8% of positive cultures. The usual symptoms of Yersinia infection were diarrhea (93%) and abdominal pain (72%), often associated with tenderness in the right iliac fossa and fever. Fourteen patients required admission to hospital and four came to surgery for possible appendicitis. Acute terminal ileitis and mesenteric lymphadenitis were noted in each case. Two patients who were HLA-B27 positive had a reactive arthritis as their dominant complaint. In conclusion, Y. enterocolitica has emerged as a common cause of diarrhea in adults. It is an important cause of symptoms resembling those of acute appendicitis and is occasionally complicated by reactive arthritis.
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The function of an autotransplanted jejunal graft used to reconstruct the pharyngoesophagus was evaluated in 12 patients, 2-40 mo after surgery. On clinical assessment most patients swallowed liquids and solids with minimal difficulty, although several described a need for liquids to "flush" solids to the stomach. Radiologic studies demonstrated a delay in orogastric transit in some patients above the lower anastomosis. The mechanism was apparent on motility studies: swallows generally failed to induce contractions in the graft, although the esophagus below exhibited stripping peristaltic waves. Regular contractile activity, characteristic of phase III of the intestinal migrating motor complex, was identified in 11 grafts. There was no temporal association between migrating motor complexes in the graft and those recorded at the jejunal donor site. Instillation of nutrients into the gastric antrum induced a typical "fed" pattern of contractions in the intact jejunum but not in the extrinsically denervated graft. In conclusion, the graft provides a useful, though generally passive conduit. The graft maintains its intrinsic motor repertoire, which is asynchronous with that of the donor site. The findings also support the hypothesis that extrinsic nerves are required to induce a "fed" pattern of intestinal motility.
A retrospective necropsy survey of 13 patients who had received endoscopic injection sclerotherapy was carried out to study tissue changes induced and to determine the causes of death. These results were compared with autopsy findings in nine patients with portal hypertension, comparable for age, sex, and nature and severity of underlying liver disease, who had not received sclerotherapy. Although all treated patients had variceal thrombosis with an associated vasculitis, residual varices were usually present, probably reflecting the brief duration of treatment (median, 12 days). The major complications of sclerotherapy resulted from necrosis, with resultant mucosal ulceration and abscess formation. These features were not present in the control group. Complications contributing to death were hemorrhage in three patients, and in one sepsis with deep necrosis and periesophageal abscess formation.
Over a 3-year period, arteriovenous malformations (angiodysplasia) were identified at upper gastrointestinal endoscopy in 41 patients. The lesions were multiple in one-third of patients and were predominantly situated in the proximal stomach. We considered angiodysplasia to be the cause of upper gastrointestinal bleeding in 11 (27%) patients and of anemia in nine (22%) patients. In these two groups other mucosal lesions were not seen at upper gastrointestinal endoscopy and there had been prior undiagnosed episodes of overt or occult bleeding in almost half. In 21 (51%) patients the lesions were judged to be incidental findings. Other medical conditions noted were the presence of an aortic systolic murmur (24%) and renal impairment (12%). Only three patients had mucocutaneous telangiectasia (two had Osler-Rendu-Weber syndrome, and one had scleroderma with CRST syndrome). Specific treatment in 14 symptomatic patients included endoscopic electrocoagulation or injection sclerotherapy. In eight patients with adequate post-treatment surveillance, endoscopy demonstrated obliteration of the vascular lesions.
To determine the clinical utility of routine determination of serum isoamylase (pancreatic/salivary) and/or lipase activity, sera were tested from 109 consecutive patients with elevated total serum amylase. Without knowledge of the isoamylase and lipase results, an assessment was made of the confidence with which the attending medical staff had made or excluded a diagnosis of acute pancreatitis. The attending staff had considered acute pancreatitis to be probable in 78, possible in 12 and unlikely in 19 patients. The confidence of the clinical diagnosis of acute pancreatitis was directly related to the degree of elevation of the serum total amylase: (mean IU/l +/- s.e.m.) probable pancreatitis 1807 +/- 313, possible pancreatitis 680 +/- 74, pancreatitis unlikely 493 +/- 50. Pancreatic isoamylase was elevated in 97% of patients with probable pancreatitis, 92% with possible pancreatitis and 68% in whom pancreatitis had been considered unlikely. Lipase elevations generally parallelled these results. Although gall-stones were usually sought among patients with probable pancreatitis, they were rarely sought in patients in the other categories. In conclusion, amylase isoenzyme or lipase determinations add little information in cases of clinically suspected acute pancreatitis with marked hyperamylasemia. The tests may have a role in the evaluation of patients with clinically unexplained hyperamylasemia by defining more precisely the origin of the amylase.
The columnar lined (Barrett's) esophagus is an acquired condition resulting from chronic gastroesophageal reflux. The clinical spectrum of 50 consecutive cases of endoscopically consistent, histologically proven Barrett's esophagus was reviewed. The mean age of patients was 65.9 +/- 12.4 (SD) years with only four patients younger than 50 years. The predominant presenting symptoms were dysphagia, heartburn, and regurgitation. At endoscopy, the columnar lined segment extended over 6.5 +/- 3.0 cm of the lower esophagus. Specialised columnar (intestinal) epithelium was the most frequent histological type identified. Radiologic or endoscopic evidence of a hiatal hernia was present in the majority. Complications were present at endoscopy in 38 (76%) patients. Reflux esophagitis (56%) was present at the area of the squamo-columnar junction. Stricture formation (38%) and ulceration (36%) were located either at the squamo-columnar junction or more distally within the columnar epithelium. Two patients (4%) had adenocarcinoma arising in a segment of Barrett's esophagus at presentation. Treatment included physical measures, dilatation, and cimetidine. Bougienage in 20 patients was successful in alleviating dysphagia but multiple treatment sessions were often necessary. Although esophagitis readily resolved with cimetidine therapy, ulceration was generally resistant to medical therapy. Indeed, by two months, healing was achieved in only five of 12 patients. Endoscopic surveillance of 12 patients who received cimetidine (1 g/day) for at least 12 months showed no regression of the metaplastic mucosa.
A patient is described with micronodular cirrhosis, partial (heterozygous, MZ) deficiency of alpha-1-antitrypsin (AAT) and hepatocellular carcinoma. The patient did not drink alcohol and all serological markers of infection with hepatitis B virus were absent. Death was due to intra-peritoneal bleeding from a multifocal liver tumour. Histology revealed multiple intracytoplasmic AAT globules in hepatocytes at the periphery of the cirrhotic nodules. Copper granules, present in the same non-neoplastic liver cells may have resulted from minor cholestasis. Within the neoplastic hepatocytes AAT globules were sparse and copper deposits co-existed with the globular variant of Mallory bodies. The case is presented in support of the postulated association of partial deficiency of AAT, chronic liver disease and hepatic neoplasia.