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Biomedical subjects

R A Erickson

Publications and source records attributed to R A Erickson.

At least 19 recordsLinked to original sources

Endoscopic ultrasound and fine needle aspiration for the evaluation of pancreatic masses.

HYPOTHESIS: Endoscopic ultrasound (EUS) and endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) are accurate for the preoperative staging of pancreatic ductal carcinoma. DESIGN: Retrospective medical record review. PATIENTS: A prospective registry of 98 patients having EUS-FNA for peripancreatic masses from April 1994 to April 1998 was analyzed. MAIN OUTCOME MEASURE: The accuracy of EUS-FNA for preoperative diagnosis and staging of peripancreatic neoplasms. RESULTS: Ninety-eight patients, aged 41 to 91 years (mean age, 67 years) with peripancreatic masses were evaluated by EUS-FNA. All patients had initial computed tomography scanning with a mass seen in 49 patients, "fullness" to the pancreas in 28 patients, and no mass seen in 21 patients. Evaluation with EUS-FNA revealed 22 benign lesions, 18 T2 masses, 37 T3 masses, 1 T4 mass, and 20 masses representing nonpancreatic tumors. Results of EUS-FNA of adjacent lymph nodes were positive in 27 patients. Twenty-seven patients had surgical resection or palliation permitting operative and pathologic staging. On comparison of EUS-FNA staging with surgical staging, 12 patients were the same stage, 14 patients were upstaged, and 1 patient was downstaged. The remaining patients who did not have surgery have been followed up for a mean of 15 months. Overall accuracy of EUS-FNA for differentiating benign from malignant masses was 96%. CONCLUSIONS: Endoscopic ultrasound-guided fine needle aspiration is a useful technique for the evaluation of pancreatic masses. It is highly accurate for differentiating between benign and malignant lesions and for predicting T stage, but is limited for predicting nodal status.

Adult

Domestic violence: legal, practice, and educational issues.

Domestic violence is a recognized and growing public health concern in the United States. Health care professionals have a duty to improve the identification of victims of domestic violence, intervene effectively, and advocate for better education to break the cycle of abuse.

Documentation

Endoscopic ultrasonography: a new diagnostic imaging modality.

Endoscopic ultrasonography uses high-frequency ultrasound to visualize the gut wall and the surrounding structures of the mediastinum, the abdomen and the pelvis. Echoendoscopes are available in two different designs. A radial scanning echoendoscope produces a 360 degree real-time view perpendicular to the shaft of the echoendoscope. A linear-array instrument produces a 100 degrees real-time view parallel to the shaft of the echoendoscope, permitting direct ultrasonographic guidance of fine needles exiting the biopsy channel. Endoscopic ultrasonography has been established as the preferred diagnostic tool for the evaluation of submucosal masses of the upper gastrointestinal tract and the rectosigmoid, for differentiating benign from pathologic thickened gastric folds and for locating pancreatic endocrine tumors. The widest application of endoscopic ultrasonography is in the diagnosis and staging of esophageal, gastric, rectal and pancreaticobiliary neoplasms. Endosonography is the most accurate modality available for determining the T and N stages of these tumors. The recent development of endoscopic ultrasound-guided fine-needle aspiration provides physicians with the ability to cytologically diagnose lesions visualized endosonographically and to confirm cancer staging with tissue.

Algorithms

Endoscopic ultrasound for peripancreatic masses.

BACKGROUND: Pancreatic neoplasms can be difficult to diagnose and stage preoperatively. Accurate staging allows the surgeon to select which patients can benefit from resection versus palliative therapy. Endoscopic ultrasound (EUS) with endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) is a diagnostic modality that provides visualization of peripancreatic tumors and their relationship to the surrounding structures as well as enabling cytologic diagnosis of the tumor and adjacent lymphadenopathy. METHODS: To define the role of this technique, a retrospective study was performed on 20 patients in the past year with peripancreatic tumors. RESULTS: Twelve men and 8 women ranging in age from 28 to 84 years (mean 67) were included in the study. Each patient underwent computed tomography followed by EUS-FNA, and the results were compared with operative findings or clinical course. The EUS-FNA findings included 10 pancreatic ductal carcinomas (50%), 5 pancreatitis (25%), 2 spindle cell neoplasms (10%), 1 cholangiocarcinoma (5%), 1 cystadenoma (5%), and 1 metastatic breast carcinoma (5%). Overall, EUS-FNA led to a significant change in the management of 12 patients (60%) through either diagnosing benign pathology, upstaging of the carcinoma, or determination that the peripancreatic mass represented a metastatic lesion. Five patients underwent resection of their peripancreatic tumors, and 3 patients had palliative procedures. Operative findings corresponded with EUS-FNA in all 8 patients. The 5 patients diagnosed with pancreatitis continued to be followed up for the possibility of a false negative FNA, but to date none have developed malignancy. CONCLUSIONS: EUS-FNA is a useful tool for the imaging and staging of peripancreatic tumors and will aid in the proper preoperative selection of patients who will benefit from resectional therapy.

Adult

The clinical utility of endoscopic ultrasound-guided fine-needle aspiration in the diagnosis and staging of pancreatic carcinoma.

BACKGROUND: Endoscopic ultrasound (EUS) guided fine-needle aspiration (FNA) of pancreatic lesions is being increasingly used. Our aim was to determine the safety, accuracy, and clinical utility of EUS-guided FNA in both the diagnosis and staging of pancreatic cancer. METHODS: Forty-four patients (24 men/20 women) had EUS-guided FNA of pancreatic lesions (39 head/neck, 5 body, 3 tail) and/or associated lymph nodes. The mean age was 61 (range, 28 to 88 years). The indication for EUS-guided FNA was a pancreatic lesion seen initially on CT (39%), ERCP (43%), or EUS (18%). Follow-up data were collected on all patients for mean of 14.5 months (range 1 to 33 months). RESULTS: CT detected only 15 of 61 (25%) focal lesions seen by EUS, Adequate specimens were obtained by EUS-guided FNA in 44 of 47 (94%) pancreatic lesions and 14 of 14 (100%) associated lymph nodes (overall adequacy was 95%). Of the 46 lesions in which specimens were adequate and a final diagnosis was available (32 malignant, 14 benign), EUS-guided FNA had a sensitivity of 92%, specificity of 100%, and diagnostic accuracy of 95% for pancreatic lesions and 83%, 100%, and 88% for lymph nodes, respectively. Six percent of pancreatic cases had inadequate specimens and, if included, lowered the sensitivity to 83%, specificity to 80%, and diagnostic accuracy to 88% for pancreatic lesions. In 3 patients with enlarged celiac nodes on EUS, EUS-guided FNA was able to make a tissue diagnosis of metastasis, which changed the preoperative staging and precluded surgery. EUS in combination with EUS-guided FNA precluded surgery in 12 of 44 (27%) and may have precluded surgery in an additional 6 of 44 (14%). EUS-guided FNA avoided the need for further diagnostic tests, thus expediting therapy in a total of 25 (57%) patients and influenced clinical decisions in 30 of 44 (68%) patients. The estimated cost savings based on surgeries avoided was approximately $3300 per patient. There was only one complication (2%), a post-FNA fever. CONCLUSION: EUS-guided FNA of the pancreas appears to be a safe and effective method that increases both the diagnostic and staging capability of EUS in pancreatic cancer. The clinical impact of EUS-guided FNA includes avoiding surgery and additional imaging studies with a substantial cost savings.

Adult

Endoscopic ultrasound (EUS) and EUS-guided fine-needle aspiration of the left adrenal gland.

BACKGROUND: We reported the application of endoscopic ultrasound (EUS) and EUS-guided fine-needle aspiration (FNA) in the local staging of lung cancer. Up to 16% of patients with lung cancer may have adrenal masses. The role of EUS in the characterization of the adrenal gland, as well as EUS-guided FNA of the adrenal gland, has not been described. METHODS: The adrenal gland was characterized by EUS in 30 of 31 (97%) patients. EUS-guided FNA of an adrenal was performed in one patient. Anatomic correlation and ex vivo images were obtained. RESULTS: The average dimension was 2.5 cm (range 1.4 to 3.5) x 0.8 cm (range 0.3 to 1.4) with two morphologic types: "seagull" and "elliptical." One patient with lung cancer and a left adrenal mass with a nondiagnostic CT-guided FNA underwent EUS-guided FNA, which established the diagnosis of metastatic adenocarcinoma. Surgery was avoided. CONCLUSIONS: The left adrenal can be imaged by EUS in almost all patients. EUS-guided FNA may be useful when applied to left adrenal metastatic tumors for tissue diagnosis.

Adenocarcinoma

A primer on linear array endosonographic anatomy.

Linear array endosonography, with its capacity to perform EUS-guided FNA and EUS-guided injections, as well as color mapping and Doppler ultrasonography, is becoming an important instrument for the endosonographer. Familiarity with linear array anatomy, as introduced here, is the critical foundation on which these diagnostic and therapeutic procedures can be performed safely and effectively.

Biopsy, Needle

Mechanism of colonic permeation of inulin: is rat colon more permeable than small intestine?

BACKGROUND/AIMS: Colonic epithelium is considered to be relatively tight. The colonic "pore" diameter is 6 A; therefore, colonic epithelium has generally been considered to be impermeable to hydrophilic probes with a cross-sectional diameter of > 6 A. This study examined whether rat colon is permeable to inulin, a large hydrophilic macromolecule having a molecular weight of 5000 g/mol and a cross-sectional diameter of 15 A (hydration diameter, 20 A). METHODS: The colonic permeation of inulin (10 mumol/L) in vivo was investigated by perfusion of rat colonic segments. RESULTS: There was significant colonic permeation of inulin, but tissue retention of inulin was low. The net colonic flux of inulin was strongly dependent on net water flux, showing a strong solvent drag effect. Addition of 16,16-dimethyl prostaglandin E2 decreased water flux with a corresponding decrease in inulin flux; this process seemed to be mediated by 5'-cyclic adenosine monophosphate because both the phosphodiesterase inhibitor aminophylline and dibutyryl adenosine 5'-cyclic adenosine monophosphate decreased water and inulin flux in a parallel manner. Chenodeoxycholic and taurocholic acids decreased net mucosal-to-serosal water flux but increased inulin flux. The net colonic permeation rate of inulin was higher than the small intestinal permeation rate. CONCLUSIONS: Rat colon is permeable to inulin. The higher net colonic permeability may be caused by differences in mucosal surface, permselectivity, solvent drag effect, and differences in net water fluxes of the colon and small intestine.

16,16-Dimethylprostaglandin E2

The role of endoscopic retrograde cholangiopancreatography in patients with laparoscopic cholecystectomies.

BACKGROUND & AIMS: The best clinical strategy for using endoscopic retrograde cholangiopancreatography (ERCP) with laparoscopic cholecystectomy is unknown. The aim of this study is to use decision analysis to assess four different approaches to using ERCP in patients undergoing laparoscopic cholecystectomy. METHODS: Decision trees were designed for four clinical strategies: (1) preoperative ERCP, with sphincterotomy for choledocholithiasis; (2) selective preoperative ERCP for patients at high risk for choledocholithiasis, choledocholithiasis found at surgery treated by postoperative ERCP; (3) no preoperative ERCP, choledocholithiasis detected intraoperatively treated by postoperative ERCP; and (4) no preoperative ERCP, choledocholithiasis detected intraoperatively treated with open common bile duct exploration. Using decision analysis with literature-derived data, the impact on outcome parameters was calculated. RESULTS: Postoperative ERCP resulted in the lowest cost, procedure numbers, and hospital and back-to-work days. With high preoperative likelihood of choledocholithiasis, selective preoperative ERCP was probably a clinically equivalent strategy. Sensitivity analysis supported these conclusions when the probabilities and utilities were varied over a wide range. The open operative approach to choledocholithiasis was only favored if ERCP had < 75% diagnostic and < 50% therapeutic success rates or lengthened hospitalization by > 7 days. CONCLUSIONS: This study suggests that performing ERCP after laparoscopic cholecystectomy minimizes costs and morbidity; however, when choledocholithiasis is likely, selective preoperative ERCP may be a clinically equivalent strategy.

Cholangiopancreatography, Endoscopic Retrograde

Endoscopic ultrasound-guided fine needle aspiration of pancreatic carcinoma.

Endoscopic ultrasound (EUS) is reported to be the single best modality for visualizing small pancreatic carcinomas. Whereas tissue diagnosis by fine needle aspiration (FNA) can be performed with computed tomography (CT) or transabdominal ultrasound guidance, the diagnostic accuracy is limited by the ability of these modalities to visualize the lesion. Real time EUS-guided fine needle aspiration has recently been reported as a new diagnostic modality. The application of EUS-guided FNA in the diagnosis of small pancreatic carcinoma has not been reported. We present a case in which transduodenal EUS-guided FNA was successful in establishing a definitive tissue diagnosis of pancreatic carcinoma in a 1.6-cm lesion in the head of the pancreas. This case along with a review of the literature highlights the great potential of this new modality in the diagnosis of pancreatic carcinoma.

Adenocarcinoma

Effect of difluoromethylornithine (DFMO) on NSAID-induced intestinal injury in rats.

Combination therapy with difluoromethylornithine (DFMO) and a nonsteroidal antiinflammatory drug (NSAID) has been proposed for the chemoprevention of colonic neoplasia. The purpose of this study was to examine whether DFMO would affect NSAID-mediated intestinal injury. Male Sprague-Dawley rats were gavaged with 20 mg/kg of indomethacin, after seven days of exposure to drinking water with or without 2% DFMO. The rats were killed 24 or 48 hr later, and the small intestine removed for macroscopic and microscopic quantitation of intestinal injury by computerized image analysis. Seven days of DFMO alone had no effect on overall mucosal thickness, but did increase the depth of proximal intestinal crypts. Forty-eight hours after indomethacin, DFMO treatment decreased the number of indomethacin-induced ulcers and percent of the surface area ulcerated. However, DFMO also decreased the mucosal thickness, villus height, and crypt depth in indomethacin-treated rats. Thus although DFMO decreases macroscopic intestinal ulceration by indomethacin, the reduction in villus and crypt height suggests that it also impairs the mucosa's ability to recover from microscopic indomethacin-induced damage. This study shows DFMO does impact NSAID-mediated intestinal injury and therefore human trials with combinations of DFMO and NSAIDs should include monitoring for small intestinal injury.

Animals

16,16-Dimethyl prostaglandin E2 reduces bile acid-mediated intestinal vascular injury in rats.

To examine the effects of prostaglandin on bile acid-mediated intestinal vascular injury, male rats were given 50 mg/kg of fluorescein isothiocyanate (FITC)-stained dextran 70 or 25 mg/kg of Evans Blue intravenously. Before intestinal injury with 45-minute perfusion of 5 mmol/L chenodeoxycholic acid, rats received 16,16-dimethyl prostaglandin E2 (5 micrograms/kg intravenously or 0.5 micrograms/mL or in the perfusate for 15 minutes or vehicle). FITC-dextran clearance from the blood to the intestinal lumen and tissue Evans Blue content were used as measures of intestinal vascular injury. Morphological mucosal injury was assessed by transmission electron microscopy and quantitative histological analysis. Chenodeoxycholic acid perfusion caused villous denudation and shortening of and ultrastructural damage to villous venules. Functional vascular injury was evidenced by a 10-fold increase in the rate of FITC-dextran blood-to-lumen clearance and a 3-4-fold increase in tissue Evans Blue content. Pretreatment with either intravenous or intraluminal 16,16-dimethyl prostaglandin E2 reduced FITC-dextran clearance by 70%-80% and tissue Evans Blue content by 50%. However, only luminal prostaglandin reduced superficial mucosal morphological injury, possibly because of differences in the local concentrations of 16,16-dimethyl prostaglandin E2 or chenodeoxycholic acid or because of superficial mucosal protection and injury being, at least in part, independent of mucosal microvascular injury and protection.

16,16-Dimethylprostaglandin E2

Chronic omeprazole treatment increases duodenal susceptibility to ethanol injury in rats.

To test whether omeprazole would increase the susceptibility of the duodenum to damage, 200 to 250-g male Sprague-Dawley rats were given 10 mg/kg of omeprazole (Losec) by gavage every morning for 29 days. Control rats were given gavage buffer alone. After fasting overnight, half the rats received 10 mg/kg indomethacin intraperitoneally; then all rats were given 2 ml of 50% ethanol by gavage. Three hours later the rats were killed and the stomach and duodenum removed and histologic injury to the duodenal mucosal was quantitated. In omeprazole pretreated rats, gavage with ethanol resulted in a significant twofold worsening of duodenal injury. Pretreatment with indomethacin to decrease endogenous prostaglandin production resulted in more severe ethanol-induced duodenal injury in both groups; however, there were no longer statistically significant differences between the omeprazole and control groups. Measurement of duodenal mucosal synthesis of prostaglandin E2 showed no difference between the omeprazole and control groups. Thus chronic administration of omeprazole appears to increase the susceptibility of the duodenal mucosa to ethanol injury in rats. The mechanism of this effect is as yet unknown but does not appear to be prostaglandin-mediated.

Animals

The effect of portal hypertension on indomethacin-induced small intestinal ulceration in the rat.

The purpose of this study was to determine whether portal hypertension potentiates intestinal ulceration induced by indomethacin. Portal hypertension was produced in male Sprague-Dawley rats by two-staged ligation of the portal vein. Sham-operated rats were used as controls. The rats were given 20 mg/kg of indomethacin intragastrically, 7 and 14 days, respectively, after complete portal vein ligation. Forty-eight and 72 h after indomethacin, portal pressures were measured and the whole small intestine removed for quantitative measurement of the percent of the mucosa ulcerated by computerized image analysis. There were no differences in the area of ulceration between the portal hypertensive and sham-operated rats at either 7 or 14 days, despite the presence of significant portal hypertension. Portal hypertension does not appear to potentiate small intestinal ulceration induced by indomethacin in rats.

Animals

Is the small intestinal epithelium truly "tight" to inulin permeation?

In this study, we evaluated the "leakiness" of intestinal epithelium through examination of small intestinal absorption of inulin in vivo by perfusing rat jejunum with 10 microM inulin. In physiological conditions, we found significant absorption of inulin at a rate of 44.6 nmol.100 cm-1.h-1 or absorption of 14.7%.100 cm-1.h-1 of the amount perfused. Increasing water flux by changing the luminal osmolarity resulted in linear (y = 31.1 + 2.4x, r = 0.97) increase in absorption of inulin, indicating a significant convective component of inulin absorption. There was large permeation of inulin at net water secretion and at zero net water fluxes (31.1 nmol.100 cm-1.h-1), indicating significant absorption of inulin by diffusive movement as well. The small intestinal tissue retention of inulin occurred rapidly within the first 15 min of perfusion, and the total tissue retention remained unchanged thereafter at approximately 10.8 nmol/100 cm. 16,16-Dimethylprostaglandin E2 decreased water flux, whereas cyclooxygenase inhibitors, indomethacin and acetylsalicylate, increased water flux. Inulin absorption closely paralleled changes in water flux induced by these agents. Taurocholate also caused parallel decrease in water and inulin absorption. Varying the resistance of unstirred water layer with changing luminal flow rate, the addition of mucolytic agent acetylcysteine, or alterations of luminal pH did not affect water or inulin absorption. We conclude that inulin permeates the small intestinal epithelium in significant amounts under normal physiological conditions, presumably through the paracellular pathways utilizing aqueous channels.

16,16-Dimethylprostaglandin E2

Cimetidine reduces bile acid-mediated small intestinal mucosal injury in rats in vivo.

Whether cimetidine has protective effects on the gastrointestinal mucosa independent of its ability to reduce gastric acid secretion is still controversial. To study this, rats had small intestinal mucosal injury induced in vivo by perfusion with 5 mM chenodeoxycholic acid. Control rats were compared to rats receiving either intraperitoneal or intravenous pretreatment with 50 mg/kg cimetidine or intraluminal pretreatment with 0.5 mM cimetidine. Mucosal injury was assessed by measuring villus tip epithelial cell denudation by computerized quantitative morphology. Intraperitoneal cimetidine reduced the average denudation/villus (micrometers) caused by 45-min perfusion with chenodeoxycholic acid: control = 39.1 +/- 7.7 (SEM), intraperitoneal cimetidine = 20.8 +/- 3.5 (P less than 0.05). Additionally, both intraluminal and intravenous cimetidine reduced villus denudation caused from 30 min perfusion with chenodeoxycholic acid: control = 62.5 +/- 5.8, intravenous cimetidine = 42.6 +/- 4.7 (P less than 0.05), intraluminal cimetidine = 44.6 +/- 7.2 (P less than 0.05). The observation that reduced mucosal injury is observed in an in vivo model that is independent of gastric acid supports the conclusion that cimetidine indeed has acid-independent protective properties.

Animals

Effect of portal hypertension on in vivo bile acid-mediated small intestinal mucosal injury in the rat.

This study's purpose was to determine whether portal hypertension adversely affects small intestinal mucosal injury. Portal hypertension was produced in male Sprague-Dawley rats by two-stage ligation of the portal vein. Sham-operated rats were used as controls. Two weeks later, intestinal injury was produced by in vivo perfusion with 5 mM chenodeoxycholic acid for 30 min. Intestinal injury was assessed by quantitative morphometry and by measuring intestinal water and mannitol absorption. Portal hypertension resulted in more injury in the distal perfused intestine as manifested by increased villus tip denudation [portal hypertensive 52.5 +/- 9.6 (SEM) vs controls 28.1 +/- 5.7 microns, P = 0.05). Additionally there was a significant decrease in the unperfused duodenal villus height in portal hypertensive rats (portal hypertensive 755 +/- 22 vs controls 848 +/- 28 microns, P less than 0.02). Portal hypertension had no significant effect on the increase in mannitol absorption or water secretion caused by chenodeoxycholic acid perfusion. This study suggests that portal hypertension alters small intestinal mucosa and increases susceptibility to injury.

Absorption

16,16-Dimethyl prostaglandin E2 induces villus contraction in rats without affecting intestinal restitution.

In a previous study we found that 16,16-dimethyl prostaglandin E2 protects the small intestine against chenodeoxycholic acid injury in the rat. One possible explanation for prostaglandin's protective action may be that prostaglandin-induced villus contraction accelerates mucosal restitution. This hypothesis was tested in rats by perfusing intestinal segments in vivo in a single-pass fashion with 0.125-0.5 micrograms/L of 16,16-dimethyl prostaglandin E2. These studies showed a dose-dependent, reversible contraction of intestinal villi and crypts. To test the effect of this contraction on mucosal restitution, standardized intestinal injury was produced in indomethacin-pretreated rats perfused in vivo with 5 mmol/L chenodeoxycholic acid. The rats were then perfused with bile acid-free buffer containing either 0.5 microgram/mL of 16,16-dimethyl prostaglandin E2 or vehicle. This study showed that despite decreasing villus height after bile acid injury, 16,16-dimethyl prostaglandin E2 did not significantly affect the rate of morphologic (assessed by villus denudation) or functional (assessed by mannitol and water absorption) restitution of the injured intestinal mucosa. Thus, although 16,16-dimethyl prostaglandin E2 causes villus contraction, this effect does not result in more rapid restitution of the injured intestinal mucosa and is not a likely mechanism for prostaglandin-mediated protection of the intestinal mucosa.

16,16-Dimethylprostaglandin E2