ARMI News - Part 63

Gallbladder polyps: CLINICAL SIGNIFICANCE OF GALLBLADDER POLYPS Part 1

CLINICAL SIGNIFICANCE OF GALLBLADDER POLYPSThe frequency of symptoms in patients with PLG is difficult to evaluate due to inadequacies of studies in the available literature. Symptoms were not assessed in most of the population-based, ultrasonographic prevalence studies. In a study evaluating the natural history of PLG diagnosed via cholecystography, only 6% of patients were thought to have symptoms referable to the gallbladder. Surgical studies, on the other hand, have found a higher frequency of symptoms in patients with documented PLG, likely due to selection bias. For example, Terzi et al reported symptoms in 91% of 74 patients who had undergone cholecystectomy for benign PLG. The most frequently cited complaints included right upper quadrant or epigastric pain (98%), nausea and vomiting (51%), and dyspepsia (26%). Right upper quadrant tenderness was the most common physical finding (61%). There were no significant differences in symptoms between patients with benign PLG and those with malignant PLG, a finding that has been confirmed in other studies. Gallbladder polyps have also been implicated in cases of obstructive jaundice, acalculous cholecystitis and massive hemobilia. They may increase the risk of acute pancreatitis. Buy cheap drugs online fast – buy antibiotics online for you to enjoy a reliable pharmacy.

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Gallbladder polyps: RISK FACTORS FOR GALLBLADDER POLYPS Part 2

Gallbladder polypsSimilarly, there is no evidence of a relationship between PLG and biochemical parameters such as plasma lipid profile, hepatitis B virus carrier status and liver function. Chen et al found that glucose intolerance, but not overt diabetes mellitus, is a risk factor for the development of gallbladder polyps. They suggested that gallbladder dys-motility due to hyperglycemia may predispose glucose-intolerant patients to the formation of gallbladder polyps. However, because of the absence of a similar finding in the overtly diabetic patients in their study and in other prevalence studies, the validity of this association is questioned.

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Gallbladder polyps: RISK FACTORS FOR GALLBLADDER POLYPS Part 1

Gallbladder polypsMany studies have attempted to determine individual risk factors that predispose patients to the formation of PLG. The impact of demographic factors such as patient age and sex have been variable. Although most reports have documented the highest prevalence of gallbladder polyps in the third to fifth decades of life, consistent associations with patient age have not been reported. For example, using multivariate analysis, Chen et al failed to show an effect of age on the development of PLG in Chinese subjects. Other investigators have found similar findings. Conversely, Segawa and colleagues reported a significant age-dependent prevalence of PLG in Japanese men and in women under the age of 70 years, with the highest prevalence occurring in 40- to 50-year-old men. The impact of sex on the formation of PLG also has been discordant across studies. Some reports find that gallbladder polyps are more common in males, whereas others note an increased frequency in females or no difference between the sexes. Overall, PLG seem to predominate in males, unlike gallstone disease. In the largest screening study to date involving 194,767 Japanese participants, Okamoto et al reported PLG in 6.9% of males and 4.5% of females. Best quality drugs are waiting – diabetes drugs to spend less time and money.

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Gallbladder polyps: PREVALENCE

GallbladderThe prevalence of PLG has been estimated to range from 0.03% to 9.5% of the adult population, depending on the type of study and the population of interest. Many of the large population studies have been performed in Asian populations, often as part of mass screening programs for unrelated conditions. In an ultrasonographic study of 3647 Chinese subjects, gallbladder abnormalities were reported in 701 subjects (19.2%). Specifically, PLG were identified in 243 subjects (6.7%) — a prevalence similar to that of gallstones in this study (7.8%). Further analysis of these data, after excluding subjects who had previously undergone cholecystectomy, those with coexistent gallstones and polyps, and those with unsatisfactory sonographic examinations, revealed an overall frequency of PLG of 6.9%(Table 1). Similar large Japanese studies have reported prevalence rates of 2.6% (4) and 5.6%. Gallbladder polyps were more common among males (6.3%) than females (3.5%, P<0.001). The largest study to date assessing ultrasonography in asymptomatic patients was recently reported by Okamoto et al. Among 194,767 Japanese patients, gallstones were identified in 4.1%, whereas gallbladder polyps were found in 5.6%.

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Gallbladder polyps: Epidemiology, natural history and management

GallbladderOver the past 20 years, the increased availability and improved image quality of abdominal ultrasonography have led to a dramatic increase in the detection of abnormalities of the biliary tree, including polypoid lesions of the gallbladder (PLG). Defined sonographically as immobile echoes protruding from the gallbladder wall into the lumen, PLG comprise several histopathological entities. In 1970, Christensen and Ishak proposed a simple classification of benign PLG that allowed separation of neoplastic from non-neoplastic conditions. Based on an analysis of 180 cases of benign gallbladder polyps, the authors classified benign PLG into pseudotumours, including, most commonly, cholesterol polyps, adenomyomatosis and inflammatory polyps, and true tumours, including adenomas, leiomyomas and lipomas. Distinguishing these benign PLG from malignant and potentially malignant lesions is a major diagnostic dilemma with important clinical implications. The present review highlights the epidemiology, modes of diagnosis and natural history of gallbladder polyps in the adult population. The differentiation of benign from malignant PLG is discussed, and evidence-based recommendations for the management of these lesions are provided. Find best deals online – asthma inhalers can be available every time you visit.

NSAID-induced small bowel diaphragms and strictures diagnosed with intraoperative enteroscopy: SUMMARY

Small bowel NSAID-induced damage in the small intestine may manifest as ulceration, strictures and enteropathy. These lesions should be considered in any patient who has taken NSAIDs and presents with acute obscure gastrointestinal hemorrhage, small bowel obstruction, or chronic occult gastrointestinal blood loss and iron-deficiency anemia. Results of routine endoscopic evaluation of the stomach, duodenum and colon are often negative in this setting and do not predict the presence or absence of small bowel lesions. In addition, radiographic assessment of the small intestine is usually not diagnostic. A high index of suspicion and the judicious use of endoscopic techniques, including push enteroscopy and intraoperative enteroscopy, may permit an accurate diagnosis in many cases.

NSAID-induced small bowel diaphragms and strictures diagnosed with intraoperative enteroscopy: DISCUSSION Part 3

DISCUSSIONThe two cases presented here emphasize the difficulty in diagnosing NSAID-induced small bowel diaphragms and ulcers. A high degree of clinical suspicion should be maintained in the patient taking NSAIDs who presents with obscure gastrointestinal bleeding or unexplained small bowel obstruction. Routine upper and lower endoscopy should be performed in all patients with obscure gastrointestinal bleeding. If these test results are negative, then a small bowel contrast radiographic study (small bowel follow-through or enteroclysis) should be performed. However, the diagnostic yield of a small bowel series is relatively low. It has been estimated that only approximately 5% of small bowel follow-through examinations detect an intestinal bleeding site. Enteroclysis has an increased sensitivity over the standard small bowel follow-through examination, with reported yields of 10% to 25% for obscure gastrointestinal bleeding. However, entero-clysis is more time consuming, has more side effects and involves more radiation exposure than routine small bowel series. Therefore, many experts still recommend small bowel follow-through examinations as the initial test of choice for suspected small bowel lesions, with enteroclysis reserved for difficult diagnostic dilemmas.

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NSAID-induced small bowel diaphragms and strictures diagnosed with intraoperative enteroscopy: DISCUSSION Part 2

DISCUSSION Ulceration in the small intestine can lead to hemorrhage or perforation. A common scenario involves a patient with acute gastrointestinal hemorrhage while taking NSAIDs who has no obvious source of bleeding in the stomach, duodenum or colon after routine endoscopic evaluation. As in the first case, the patient is often suspected of having a small bowel source of bleeding. Morris and colleagues in 1991 reported a prospective enteroscopic study of 15 patients with rheumatoid arthritis taking NSAIDs who presented with chronic occult gastrointestinal bleeding. Seven patients (47%) were found to have jejunal or ileal ulceration that might explain their chronic blood loss. The authors suggested that small bowel enteroscopy may be a valuable technique for the investigation of obscure gastrointestinal bleeding. Further evidence that NSAIDs cause small bowel ulceration comes from an autopsy study of 713 patients. Of these patients, 249 had used NSAIDs in the preceding six months. Nonspecific small bowel ulceration was found in 8.4% of patients who had used NSAIDs compared with only 0.6% of nonusers. Three patients who were long term NSAID users died of perforated small intestinal ulcers (1% of all deaths in NSAID users). There was no relation between the presence of gastroduodenal ulceration and small bowel lesions, suggesting that the presence or absence of small bowel lesions cannot be predicted based on endoscopic assessment of the stomach and duodenum alone. In a retrospective study of surgical complications of NSAID use in the small intestine, 283 patients who underwent small bowel resection were evaluated. Eleven patients (4%) had 12 small bowel complications associated with NSAID use (defined as daily use of one or more NSAIDs). These complications included bleeding in six patients, perforation in four patients and obstruction in two patients. The ulcer location was variable but occurred most commonly in the terminal ileum (67%) and at multiple sites in 50% of patients.

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NSAID-induced small bowel diaphragms and strictures diagnosed with intraoperative enteroscopy: DISCUSSION Part 1

DISCUSSIONNSAIDs are among the most widely used drugs due to their potent analgesic, antipyretic and anti-inflammatory properties. The majority of adverse effects of NSAID use occur within the gastrointestinal tract. Gastroduodenal ulceration, hemorrhage, perforation and gastric outlet obstruction are well-documented side effects of NSAID use. It has been estimated that gastroduodenal ulceration occurs in 15% to 35% of chronic NSAID users. However, NSAID-induced damage can occur throughout the gastrointestinal tract. The present review focuses on the effect of NSAIDs in the small intestine and the difficulty in diagnosing this effect with standard diagnostic techniques. The utility of intraoperative enteroscopy in making this diagnosis are discussed.

The prevalence and variety of NSAID-induced lesions in the small intestine (jejunum and ileum) have been under-appreciated in the past due to the relative inaccessibility of the small bowel to sensitive diagnostic testing. The reported adverse effects of NSAIDs on the small intestine have included ulcers, strictures and enteropathy. The clinical consequences of these lesions include hemorrhage, perforation, small bowel obstruction, iron-deficiency anemia, protein-losing enteropathy and malabsorption.

NSAID-induced small bowel diaphragms and strictures diagnosed with intraoperative enteroscopy: CASE PRESENTATION Part 2

Small bowel stricturesCase 2: A 49-year-old man was referred to the authors’ institution for evaluation of recurrent small bowel obstruction. He reported a total of 26 episodes of partial small bowel obstruction that had responded to conservative treatment over the previous six to seven years. He underwent exploratory laparotomy two years previously with no source of obstruction found, but the jejunum was noted to have an area of active inflammation, and a local reactive mesenteric lymph node was excised. He subsequently underwent an EGD, which revealed a fairly tight postbulbar duodenal stricture that was twice dilated with a balloon dilator to 54 French with good endoscopic results. However, the patient continued to have recurrent episodes of partial small bowel obstruction. Before referral, he underwent a repeat upper endoscopy with a pediatric colonoscope that revealed a widely patent duodenum with no evidence of stricture recurrence and normal findings into the proximal jejunum. In addition, a small bowel follow-through showed no abnormalities. His medical history was significant for an appendectomy as a teenager, rotator cuff injury with arthroscopic surgery two years prior and a motorcycle accident five years prior. He had been using NSAIDs regularly for at least 25 years for various orthopedic injuries. He had been off all NSAIDs for about eight months. He was then referred to the authors’ institution, where he initially underwent a push enteroscopy that was normal to approximately 120 cm beyond the ligament of Treitz. He then underwent an intraoperative enteroscopy that revealed a discrete diaphragm-like stricture approximately 5 mm in diameter in the distal jejunum with an associated ulceration at one border (Figure 2); the enteroscope could not be passed through this stricture. Two other discrete areas of fibrotic-appearing small bowel were noted on external examination. A 30 cm segment of small bowel containing all three areas was resected. The remainder of the small bowel appeared normal. Pathological examination revealed that the area of stricture in the proximal jejunum seen endoscopically contained three successive plicae circulares fused into a thickened circumferential ring covered with granular-appearing mucosa with focal erosion, consistent with an NSAID-induced mucosal diaphragm (Figure 3). In addition, four small (less than 0.8 cm in diameter), nonobstructing carcinoid tumours were noted in the resected specimen extending through the muscularis propria; all seven lymph nodes were negative for tumour. Two of these tumours were associated with the more distal fibrotic areas palpated by the surgeons. One tumour was near but not involving the mucosal diaphragm. There have been no further bouts of intestinal obstruction at a four-month follow-up.

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