Triple therapy for Helicobacter pylori in nonulcer dyspepsia.
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Biomedical subjects
Publications and source records attributed to H A Carpenter.
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H. pylori is a potent urease producer, a characteristic that has been exploited in the development of the [14C]- and [13C]urea breath tests. The prevalence of H. pylori infection also is known to increase with advancing age; however, the individual patient's age has not routinely been considered when interpreting urea breath test results. The aim of this study was to validate a short, age-adjusted [14C]urea breath test for use in diagnosing H. pylori infections. Forty-one subjects (28 volunteers, 13 patients) underwent esophagogastroduodenoscopy with biopsies. Subjects were defined as being H. pylori-positive if histology or culture was positive. In addition, all subjects completed a 120-min [14C]urea breath test. A logistic regression analysis adjusting for age was used to estimate the probability of H. pylori positivity as a function of the 14C values generated. Sixteen subjects were H. pylori-positive, and 25 were H. pylori-negative. The 14C values generated between 15 and 80 min were found to be equally predictive in identifying H. pylori-positive subjects. Advancing age was associated with a higher probability of H. pylori-positivity. By taking advantage of the statistical probabilities, older patients could be accurately diagnosed with H. pylori at lower 14C values. We found that [14C]urea breath test to be both a sensitive and specific test that can be abbreviated to a 30-min examination (total test time). Moreover, our mathematical model indicates that a patient's age should be considered in order to optimize interpretation of the [14C]urea breath test, although further observations are needed to confirm this model.
Endorectal ultrasonography is a valuable imaging method for examination of the rectum and perirectal tissues. We assessed 50 patients with known rectal carcinoma prospectively by using a 7.0-MHz endorectal transducer to determine the depth of invasion of the rectal wall by tumor and the presence of lymphadenopathy. Tumors were staged by using the Astler-Coller modification of the Dukes staging system, and the results were compared with histologic staging of the surgical specimen. Ultrasonography had an accuracy of 80%, a sensitivity of 92%, and a specificity of 76% for detection of invasion of the perirectal fat. Ultrasonography was sensitive in the detection of perirectal lymphadenopathy but was not specific in distinguishing benign from malignant nodes.
Based on a clinicopathologic study of 34 patients with biopsy-confirmed diffuse pulmonary hemorrhage (DPH), we present an approach to the differential diagnosis of DPH with attention to histologic features such as capillaritis and the importance of laboratory tests such as anticytoplasmic autoantibodies (ACPA). The following DPH syndromes were encountered: antibasement membrane antibody (ABMA) disease (four cases); idiopathic pulmonary hemorrhage (four cases); Wegener's granulomatosis (WG) (five cases); probable WG (six cases); systemic necrotizing vasculitis otherwise unclassified (three cases); systemic lupus erythematosus (two cases); rheumatoid arthritis (one case); seronegative juvenile rheumatoid arthritis (one case); IgA nephropathy (one case); idiopathic glomerulonephritis (two cases--one with and one without immune complexes); and unclassified pulmonary-renal syndromes (five cases). Capillaritis was found in lung biopsy samples from 30 of the 34 patients (88%) and included patients with every type of DPH syndrome. Serologic testing for ACPA was useful in the diagnosis of WG. Identification of ABMA in the serum, kidney, or lung was the defining feature for the diagnosis of ABMA-mediated disease. Subclassification of the cases could not be done solely on histologic grounds except for cases of WG that showed granulomatous inflammation, foci of necrosis, or vasculitis. Classification of the remaining cases required correlation with (a) clinical and laboratory data; (b) biopsy samples from other sites such as the kidney, nasal sinuses, or skin; and (c) results of immunofluorescence or electron microscopy of kidney or lung biopsy samples.
We have studied the histopathologic correlates of a significantly decreased urinary amylase excretion rate (UAER) to determine its reliability in predicting the presence of cellular rejection within pancreas allografts drained via a duodenocystostomy. Significant hypoamylasuria in pancreas allograft recipients was defined as a diminution of greater than 50% in UAER sustained for greater than 36 hr and not associated with a decrease in serum amylase activity. We observed 18 such episodes of hypoamylasuria in 13 of 18 patients receiving pancreas allografts. Pancreaticoduodenal material was obtained during 11 of these episodes, one attempt failed, and for the remaining 6 episodes we obtained 3 renal allograft biopsy specimens. Histopathologic examination of the 14 specimens revealed cellular rejection in 9 (64%), fibrosis in 2 (14%), enzymatic necrosis in 1 (7%), cytomegaloviral pancreatitis in 1 (7%), and no abnormal features in 1 (7%). During these 14 episodes, a genetically identical renal allograft was present for 11 and showed signs of dysfunction in 9; however, the pancreatic histologic features suggested rejection in only 7 of the 9. Thus even the combination of hypoamylasuria and renal dysfunction in recipients of genetically identical organs was not fully reliable in predicting pancreas allograft rejection. In addition, the interval between organ implantation and onset of hypoamylasuria did not predict the histologic diagnosis. As with other solid-organ allografts, biopsy is a useful adjuvant for determining patient management in the presence of organ dysfunction.
In 18 consecutive pancreaticoduodenal allograft recipients (15 combined kidney/pancreas and 3 pancreas only after a prior successful kidney transplantation) operated on between December 1987 and February 1989, we studied the soluble interleukin 2 receptor (SIL-2R) level over time. All pancreaticoduodenal allografts were transplanted with exocrine drainage via a duodenocystostomy that allowed for cystoscopically directed needle biopsies of the pancreas. Of these 18 recipients, at 6 weeks after transplantation, 6 had had no rejection episodes or cytomegalovirus disease (control group), an acute allograft rejection had developed in 7, CMV disease developed in 4, and both rejection and CMV disease developed in 1 by 12 days after transplantation. SIL-2R level increased in all patients during immunosuppressive induction therapy (preoperative mean +/- SE, 1637 +/- 284 U/mL; maximum, 4367 +/- 687 U/mL). After induction therapy, the mean was 2768 +/- 432 U/mL. In all 6 recipients in the control group, SIL-2R level continued to decrease. However, SIL-2R level was significantly higher compared with controls, in those who had CMV disease (levels were increased at a mean of 7 days before diagnosis of CMV disease) and in those who had acute rejection episodes (levels were increased a mean of 7 days before the clinical diagnosis of rejection). Factors that did not cause an increase in SIL-2R level included acute pancreatitis, wound infection, operative procedures, and CsA nephrotoxicity. SIL-2R level can be useful for monitoring pancreaticoduodenal allograft recipients. Increases predict impending rejection or CMV disease, prior to the onset of organ dysfunction. When SIL-2R level increases, we recommend cultures of blood and urine to exclude CMV and pancreaticoduodenal allograft biopsy to confirm early rejection prior to the initiation of potentially dangerous antirejection therapy.
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Present methods of monitoring for allograft dysfunction in pancreaticoduodenal transplantation (urinary amylase, scintigraphy) give indirect evidence and do not consistently allow recognition of early, potentially reversible rejection from other causes of allograft dysfunction. For better diagnosis of allograft dysfunction, adequate tissue specimens must be obtained without trauma to the allograft. We devised a cystoscopically directed needle biopsy technique to obtain tissue from the canine pancreaticoduodenal allograft. This technique is made feasible by a duodenocystostomy similar to that in human pancreaticoduodenal transplantation. The duodenum acts as a port of entry for the biopsy instruments, providing access to the pancreas. A 24F side-viewing nephroscope is used to view the duodenum. The tissue specimen is obtained with an 18-gauge, 350 mm Menghini aspiration needle inserted by way of the nephroscope through the duodenum and into the pancreas. Pancreaticoduodenal allotransplantation with a duodenocystostomy for exocrine drainage was performed in 18 dogs. Of 59 serial biopsy specimens obtained, 41 (69.5%) were adequate for pathologic evaluation. The principal complication associated with the technique was minimal bleeding at the biopsy site, occurring in 22 of the 59 biopsy procedures. This cystoscopically directed biopsy technique appears to be safe, often obtains adequate tissue for diagnosis, and may be directly applicable for distinguishing causes of allograft dysfunction in human pancreaticoduodenal transplantation.
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To determine the histologic features of rejection and to identify nonrejection causes of human pancreatic allograft dysfunction, we analyzed 31 needle biopsy specimens (17 pancreatic, 14 duodenal) obtained under cystoscopic direction from 15 dysfunctional pancreatoduodenal allografts with exocrine drainage into the bladder. Eight allografts undergoing rejection showed the most common histologic features of rejection to be diffuse mixed inflammatory infiltrates of pancreatic acinar tissue and duodenum wall. Diffuse infiltration of pancreatic acinar tissue by neutrophils was the earliest histologic change in rejection. Seven dysfunctional allografts not undergoing rejection ("nonrejection") showed a normal pancreas or various changes including acinar dilation with inspissation of secretions, fibrosis, cytomegalovirus inclusions, and enzymatic necrosis. The histologic changes in the duodenum paralleled those in the pancreas in both rejection and nonrejection allografts. We conclude that the histologic features of rejection in pancreatoduodenal allografts are distinctive. The changes seen in biopsy specimens accurately reflect the state of the graft and can be used to diagnose rejection and to identify other causes of graft dysfunction. Biopsy samples from the duodenum as well as the pancreas are diagnostically useful. The biopsy findings can be used to guide the clinical management of rejection and in the development of other noninvasive tests for rejection.
This study documents the affinity of hematoporphyrin derivative (HpD) for human colorectal cancer by analysis of surface fluorescence. Ten patients undergoing elective surgery for primary colorectal cancer received intravenous HpD (2-5 mg/kg) either 3 or 72 hours preoperatively. Fluorescent photographs were taken of freshly resected specimens and analyzed using a computerized videodensitometric technique. This technique subtracted contaminating non-HpD fluorescence and facilitated estimation of HpD tissue levels. The HpD-specific fluorescence localized to tumors in all cases, and the mean HpD concentration was six-fold greater in malignant tissue than in surrounding normal mucosa (0.6 microgram/g versus 0.1 microgram/g, P less than 0.001). The authors conclude that HpD preferentially localizes to human colorectal cancer and this is relevant to the photodetection and phototherapy of colorectal neoplasia.
In the United States, visceral Kaposi's sarcoma most commonly occurs in association with the acquired immune deficiency syndrome (AIDS). The authors report a unique case of primary colonic Kaposi's sarcoma in a young heterosexual HIV-negative man with chronic ulcerative colitis.
To determine the nature and sequence of the histologic changes in the early rejection of pancreaticoduodenal allografts and to assess the correlation between pancreaticoduodenal biopsy findings and the pathologic changes in the graft, we performed serial cystoscopically directed needle biopsies of pancreaticoduodenal allografts in 18 dogs and compared the findings with the histologic changes in 16 autografts as controls. Tissue adequate for evaluation was obtained by the biopsy technique in 70% of instances. The earliest and most characteristic manifestation of rejection was diffuse mixed inflammatory infiltrates involving the pancreatic acinar tissue and duodenum. The biopsy findings correlated well with the changes in the resected pancreatic specimens. Cellular rejection in the duodenum correlated with rejection in the pancreatic graft. There were no changes in the autografts that resembled cellular rejection. We conclude that, in the canine model, cystoscopically directed needle biopsy of pancreaticoduodenal allografts consistently provides adequate tissue for the diagnosis of rejection; the status of the graft can be monitored by serial biopsies of pancreatic acinar tissue and, possibly, by serial biopsies of the duodenal wall alone.
Most techniques described in animal models of pancreatic transplantation use either segmental or autotransplants. We employ a technique of pancreaticoduodenal allotransplantation in the dog that closely resembles the operation used in humans. The arterial supply of the entire pancreatic graft is preserved by procuring a Carrel patch of aorta encompassing the origin of the celiac and the superior mesenteric arteries. Splenic, inferior pancreaticoduodenal, and superior pancreaticoduodenal arteries remain intact with the graft. Venous drainage is through a short segment of portal vein. A 6-cm cuff of duodenum is taken with the head of the pancreas. Engraftment proceeds by placing the allograft within the peritoneal cavity of the recipient. End-to-side vascular anastomoses are constructed to distal aorta and inferior vena cava. The duodenal cuff is anastomosed to the dome of the bladder for drainage and analysis of exocrine secretions and to provide a port of entry for cystoscopically directed needle biopsy. A total pancreatectomy is performed to induce a state of diabetes. The average operating time is 5 h. Twenty-two dogs have undergone allotransplantation using this technique. Six dogs had no complications and were sacrificed after meeting criteria of their study protocol. There were three technical failures, two arterial thromboses and one exsanguination, yielding an 86% rate of successful engraftment. Three other dogs died of intussusception and three dogs died of sepsis, one secondary to wound dehiscence and one due to inadvertent common bile duct ligation during pancreatectomy. Wound problems, four dehiscences and two superficial infections, occurred only in immunosuppressed dogs.
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Thirty-five CT scans and 23 sonograms of 45 pathologically proved pancreatic cystic neoplasms (16 microcystic adenomas, 17 mucinous [macrocystic] cystadenomas, and 12 mucinous [macrocystic] cystadenocarcinomas) in 43 patients were retrospectively and blindly reviewed. Radiologic findings and their usefulness in differentiating microcystic from mucinous subtypes were assessed. The number of cysts within the tumors (more than six in microcystic adenomas and six or fewer in mucinous cystadenomas and cystadenocarcinomas) and the diameter of the majority of cysts within the tumor (less than or equal to 2 cm in microcystic adenomas and greater than 2 cm in mucinous tumors) were the most helpful radiologic findings in differentiating tumor types. Calcification was present in 38% of microcystic adenomas, 18% of mucinous cystadenomas, and 8% of mucinous cystadenocarcinomas by CT. Calcification was not definitely identified on any of the sonograms. A central scar was identified in only two (13%) of 16 microcystic adenomas. Blind retrospective review was often able to correctly classify tumors as either microcystic (CT, 93%; sonography, 78%) or mucinous (CT, 95%; sonography, 93%). All tumors with a typical appearance on either CT or sonography were categorized correctly. Cystic pancreatic tumors may be difficult to prospectively separate from other types of pancreatic cysts. Assuming a cystic neoplasm is present, it often can be classified correctly as microcystic or mucinous (macrocystic) by using the above criteria.