Periodic exchange of biliary stents.
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Biomedical subjects
Publications and source records attributed to W H Marsh.
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In patients with malignancy, jaundice may result from hepatic infiltration or metastatic lymph nodal compression along the bile duct. We attempted endoscopic stent placement on 31 consecutive patients with biliary obstruction from malignant adenopathy, with and without computerized tomographic (CT) scan evidence of hepatic parenchymal metastases. Endoscopic or combined endoscopic-percutaneous decompression was accomplished in 28 patients. Fifteen patients (53.6%) had CT evidence of concomitant metastatic disease to the liver. Thirteen patients had obstructing adenopathy only. Mean survival for patients with hepatic metastases after relief of extrahepatic obstruction was 117.4 days (range 9-386 days). Mean survival after biliary decompression in patients without hepatic involvement was significantly longer at 364.3 days (range 52-1098 days; p = 0.0087). Bilirubin levels fell in all patients in this group. No patient died from complications of obstruction or stent placement. Our data support the conclusion that patients with extrahepatic metastatic biliary obstruction without hepatic metastases have improved survival, compared with patients with both obstruction and hepatic involvement. In the absence of hepatic parenchymal involvement, endoscopic stent placement can safely and effectively palliate metastatic extrahepatic obstruction. Controlled trials are needed to assess the effect of such stenting on survival.
To evaluate the best method of palliation for obstructing nonresectable squamous cell carcinoma of the mid or distal esophagus, 27 patients were prospectively randomized to one of three treatment arms: (1) esophageal intubation with an Atkinson tube (AT, 10 patients), (2) esophageal intubation followed by radiation therapy (AT/RT, 8 patients), and (3) endoscopic laser therapy followed by irradiation (L/RT, 9 patients). Pretreatment characteristics were similar in the three groups. There was no procedure-related mortality. There were eight total complications related to the tube and none related to laser treatment (p = 0.02). Mean survival was 119 days in the AT group, 72 days in the AT/RT group, and 169 days in the L/RT arm (p = not significant). Quality of survival was most dependent on swallowing ability, and the swallowing score increased by 2.3 units in the AT group, 1.8 units in the AT/RT group, and 1.4 units in the L/RT group (p = not significant). Adding RT to laser therapy significantly increased time in treatment (mean, 38.7 days) when compared with the AT group (mean, 12.5 days) (p less than 0.001). However, only 1 patient required repeat laser ablation. It is concluded that AT and L/RT result in good palliation as measured by relief of dysphagia and survival time. However, morbidity of AT is significantly greater than that of L/RT. Laser and radiation therapy with a reduced total dosage of RT or with a change in fractionation schedule to limit treatment time is the preferred method of palliation.
Reports now document hepatitis D infection in diverse clinical settings in the United States, indicating that the infection is becoming more common. The demonstration of the first case of Delta hepatitis in South Carolina emphasizes the need for a high index of suspicion for infection by this virus in the evaluation of patients with hepatitis.
Two patients with similar symptoms referred for diagnosis and treatment of hepatic failure subsequently proved to have cardiomyopathy as the cause of their hepatic decompensation. Except for fatigue and edema, symptoms of congestive heart failure were absent and no history of dyspnea, orthopnea, or paroxysmal nocturnal dyspnea could be elicited. Hepatomegaly was present in both patients, but neck venous distension and hypotension were not apparent, and both patients were able to lie flat. The diagnosis of cardiomyopathy was made by echocardiogram showing global hypokinesis and low ejection fractions; right atrial pressures were markedly increased. Liver biopsies demonstrated centrilobular necrosis and congestion. Treatment for heart failure led to a prompt response in both patients with rapid return of all hepatic parameters toward normal. Paradoxically, our patients had striking evidence of hepatic failure and a notable absence of symptoms and signs of congestive heart failure. An awareness of this unique presentation may avoid prolonged evaluations in such critically ill patients.
Point mutation and activation of c-Ha-ras oncogene was studied at various stages of carcinogenesis in cell lines developed from MNU-treated human pancreas explants. DNAs from normal pancreas and nontumorigenic cell lines showed no transforming activity in NIH 3T3 cells whereas DNA from one of the tumorigenic cell lines transformed NIH 3T3 cells. In this cell line the point mutation was demonstrated to be at codon 12 of c-Ha-ras gene by the loss of an Msp I site. The mutation possibly affected the transcription of c-Ha-ras gene which in turn contributed to the transformation of these cells.
Biliary fistulas have in the past been managed by a variety of methods, including surgical correction or endoscopic sphincterotomy. From 1984 to 1989, we used endoscopic indwelling biliary stents in seven consecutive patients with and without sphincterotomy and have attained fistula closure in all patients studied. The etiologies of the fistulous tracts varied, as did the type and number of stents used. The duration of time between stent placement and observed closure of the fistulous tracts ranged from 3 days to 5 months. Of note, all patients had a dramatic reduction of drainage within the first week. From our study we conclude that surgical correction of biliary fistulas is not required, that sphincterotomy is not mandatory for stent placement or fistula management in patients without distal obstruction, and that a single, small caliber stent alone may be effective.
Pancreatitis secondary to organophosphate insecticide toxicity is extremely rare. The few previously reported cases have resulted from oral ingestion of these agents. We present the first reported case of acute pancreatitis occurring after cutaneous exposure to an organophosphate insecticide. Symptoms of pancreatitis persisted for 6 months, followed by total resolution. The proposed mechanisms of pancreatic injury caused by organophosphate compounds are discussed.
In a randomized, double-blind trial, sucralfate therapy, 1 g four times daily, was compared with placebo in 143 symptomatic patients to assess the treatment of gastrointestinal symptoms and gastric mucosal damage associated with nonsteroidal anti-inflammatory drugs (NSAIDs). All patients followed a fixed regimen of NSAIDs, were assigned to one of two groups based on the presence or absence of gastric erosions at baseline endoscopy, and were then assigned randomly to receive sucralfate or placebo for four weeks. Patients were then followed for up to six months while receiving open-label sucralfate 1 g twice daily to up to 1 g four times daily. After four weeks of double-blind therapy, patients taking either nonsalicylate NSAIDs or long half-life NSAIDs and who were treated with sucralfate experienced a significant reduction in both peptic symptom frequency and intensity (p less than 0.03) as compared with patients receiving placebo. Sucralfate-treated patients with baseline endoscopic lesions showed a significant reduction in lesion scores (p less than 0.005) at four weeks as compared with baseline, whereas no improvement was observed in gastric mucosal lesions of patients given placebo. Long-term sucralfate therapy resulted in continued improvement in gastrointestinal symptoms and gastric lesion scores in patients receiving all types of NSAIDs. The results indicate that sucralfate used in conjunction with NSAIDs may allow patients to continue therapy by relieving gastrointestinal symptoms and mucosal damage associated with NSAID therapy.
For identification of hamster acinar cells, murine monoclonal antibodies to dispersed adult hamster acinar cells were developed. One of these, Ham-Acl, with strong affinity for a membrane-associated adult acinar cell antigen, was purified by HPLC, isotyped as IgG1 and used for the characterization of a species-specific, immunoprecipitable post-differentiation antigen on adult acinar cells. This antigen of 98 kDa was identified on paraffin sections of adult hamster acinar cells by an indirect immunofluorescence technique. It was undetectable in fetal hamster pancreas, but was present on 2-week-old and older hamster acinar cells.
c-Ki-ras-2 sequences were visualized in paraffin-embedded sections from normal fetal and adult human pancreases, a chemically induced transplantable human pancreas carcinoma (PT-1) and three carcinomas of pancreas by in situ hybridization technique. A biotinylated 1-kilobase-pair (kb) EcoRI fragment of pHiHi3 DNA was used as probe and the oncogene was visualized as one or two large grains of reaction products produced by streptavidin-peroxidase complex and diaminobenzidine tetrachloride in more than 9% of normal pancreas nuclei. Its amplification in the chemically induced cell line was detected as one or more large grains in 72% of the nuclei and numerous cytoplasmic grains. The detection of oncogene in normal pancreases and its amplification in PT-1 cells was validated by Southern analysis of EcoRI digests of genomic DNA extracted from normal pancreases and PT-1 cell line. The oncogene was also demonstrated to be equally amplified in two adenocarcinomas and one undifferentiated carcinoma of human pancreas by in situ hybridization.
Pancreaticopleural fistula is an uncommon complication of chronic pancreatitis or pancreatic trauma. Clinical features include pleural effusion and resulting pulmonary symptoms. Abdominal pain and other clinical manifestations of pancreatitis may be minimal or absent. As in this case, computed tomography and endoscopic retrograde cholangiopancreatography may provide complementary diagnostic information in the evaluation of this condition. A discussion of the pathophysiology, diagnosis, and management of pancreaticopleural fistula is presented.
Peroral colonic lavage solutions are widely used to prepare patients for colonoscopy. The effects of peroral colonic lavage on cardiac rhythm have not been evaluated previously. Using continuous electrocardiographic monitoring, the authors evaluated cardiac rhythm in 22 patients undergoing 24 colonoscopic examinations. Monitored periods included a control phase, the period of preparation with the lavage solution, and the period of colonoscopy. In 12 of 24 evaluations, patients demonstrated an increase in ventricular ectopy during the preparation phase compared to the control period (p = 0.01). Two patients demonstrated ventricular tachycardia, four patients manifested complex ventricular ectopy without ventricular tachycardia, and six patients demonstrated an increase in simple premature ventricular contractions. The authors conclude that peroral colonic lavage is associated with increased ventricular ectopy.
Gastrointestinal telangiectasias cause hemorrhage in patients with chronic renal failure. Therapies using vasoconstrictors, endoscopic application of heat, and surgery have had limited efficacy. Because several reports have suggested that estrogen or estrogen-progesterone therapy may control mucosal bleeding from telangiectasias in patients with hereditary hemorrhagic telangiectasia, we treated seven patients with chronic renal failure and bleeding gastrointestinal telangiectasias with systemic estrogen or estrogen-progesterone in an uncontrolled trial. Bleeding ceased in all patients. Blood transfusion requirements decreased from a mean of 1.2 U/month before treatment to 0.21 U/month after treatment. No significant side effects were noted. Results of this trial indicate the need for controlled investigations of this type of hormonal therapy.
A patient with a clinical history of pulmonary tuberculosis presented with obstructive jaundice. Compression of the extrahepatic bile ducts was caused by calcified lymph nodes secondary to tuberculous adenitis of the porta hepatis. The role of radiologic methods in the diagnosis and management of this unusual complication is discussed.
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It has been possible to maintain adult human pancreas in organ culture in a chemically defined medium. Under these conditions, all cell types demonstrated at least a limited ability to proliferate. This in vitro model was employed to study the effects of three nitroso compounds, DMNA, MNU, and BHP, on adult human pancreas. The major effects of three nitroso compounds, DMNA, MNU, and BHP, on adult human pancreas. The major effects of these compounds in cytotoxicity, proliferation, and oncogenicity was evaluated morphologically. DMNA and MNU were both carcinogenic but with varying rapidity of induction. MNU produced greater necrosis but gave more rapid induction. BHP produced cytotoxicity sufficient to prevent any rating of its oncogenic potential. Morphologically malignant tissue were tested for growth potential in nude mice. All nude mice developed multiple subcutaneous tumor nodules within eight weeks after inoculation. The tumor nodules ranged morphologically from undifferentiated scirrhous carcinoma to well-differentiated papillary adenocarcinoma.
Portions of adult human pancreas from 20 donors were organ-cultured in a chemically defined medium in the absence or presence of DMNA for up to 12 weeks. In the absence of DMNA, necrosis of some acini occurred during the first week, while some clusters of well-preserved acini were maintained for up to 3 weeks. Proliferation of the epithelial linings of main and smaller ducts and ductules was noted during the first 2 weeks of culture. Ductal epitheliums thereafter showed some degeneration but remained viable during the 12 weeks of culture. In contrast to controls, the DMNA-treated explants showed better preservation of both acinar and ductal cells. DMNA induced both ductal hyperplasia and atypia of the epithelial linings of main ducts, smaller ducts, and ductules within 6 weeks, and carcinoma by the tenth week of culture. At the end of the first week cells devoid of zymogen within the acinar complex proliferated and progressively replaced necrotic cells. During the ninth and tenth weeks, foci of atypical cells developed among these cells. Cells derived from 10-week-old DMNA-treated explants produced multiple nodules of carcinoma when injected subcutaneously into nude mice.