The clinical presentation of biliary strictures is broad, ranging from incidental imaging findings and laboratory results to symptoms of jaundice, abdominal pain, pruritus, and cholangitis. Therefore, a detailed clinical history can provide important information about its etiology.

Biliary stricture is considered a narrowing of the biliary tree that can be caused by a myriad of etiologies, some benign, others life-threatening.

• There are three classes of biliary strictures: benign, malignant, and indeterminate.
• Unfortunately, only a minority of them (15% to 24%) are benign.

Differentiation between benign and malignant requires a complex diagnostic evaluation, with Endoscopy being an indispensable tool, especially for allowing tissue sampling.

Malignant Biliary Stricture:

• The most common cause of malignant biliary stricture is pancreatic adenocarcinoma. As pancreatic cancer is often diagnosed at an advanced stage, 70% of patients already present with stricture at the time of diagnosis.
• The second most common cause is cholangiocarcinoma, a primary tumor of the biliary duct itself.

Regarding the topography of biliary strictures:

• Distal – pancreatic malignancy should always be the most important consideration, regardless of whether there is an identifiable mass on cross-sectional imaging or not.
• Proximal – suspicion of cholangiocarcinoma should be the most considered.

Benign Biliary Stricture:

• The most common cause is iatrogenic injury, especially post-cholecystectomy or post-liver transplant.
• Several inflammatory conditions can also result in strictures, mainly Primary Sclerosing Cholangitis and IgG4-related Sclerosing Cholangitis. However, as most biliary strictures turn out to be malignant upon investigation, it is always essential to rule out malignancy in these patients.

Indeterminate Biliary Stricture (IBS):

• Concept: in most publications, it is postulated that the term refers to a stricture whose etiology has not been established by radiology, whether Computed Tomography or Magnetic Resonance Imaging (due to the fact that there is no obvious mass on cross-sectional images) AND ERCP with transpapillary biopsy and/or cytological brushing also failed to elucidate.
• Note that we highlighted the “AND” because, despite being the most commom definition understanding, there are disagreements on whether to consider that these two steps would be additive.

• However, it is a fact that ERCP with transpapillary biopsy (guided by fluoroscopy) and/or brushing continues to be the standard procedure in many services in these cases, especially due to the unavailability of Cholangioscopy. However, given the currently published and very promising results with direct biopsies guided by Cholangioscopy, there may be a change in this diagnostic sequence.

IBS continue to present a diagnostic challenge for physicians and represent 20% of all biliary strictures after initial evaluation. Although most biliary strictures are considered malignant, up to 20% of surgical specimens are found to be benign, thus, incorrect diagnosis can lead to unnecessary surgeries or delays in treatment (when actually malignant).

A brief overview of the most accessible technologies that can help establish the etiology of indeterminate strictures

ERCP with cytological brushing and/or transpapillary biopsy guided by fluoroscopy:

• continues to be the initial approach for evaluation, however the diagnostic yield is often disappointing
• Navaneethan et al. conducted a meta-analysis showing that the sensitivity of cytological brushing is 45%, with a specificity of 99% for the diagnosis of malignant strictures, while the sensitivity of biopsy was 48.1% and the specificity was 99.2%. The combination of the two methods only increases the sensitivity to 59.4%. Similarly, recent prospective studies have shown a sensitivity of 46-56% and specificity of 100% with associated biopsies and brushing. This suggests that both brushing and biopsy result in similar accuracy, and the combination of strategies only modestly increases sensitivity.

Cholangioscopy:

• The direct Cholangioscopy system was introduced in 2007, being developed for single-operator examination. Currently, there are cholangioscopes with better image resolution, visibility, better maneuverability, and versatility in the use of accessories.
• A recent randomized controlled study (Gerges et al.) of 57 patients compared the use of single-operator digital cholangioscopy with direct biopsies to ERCP with brushing in patients with IBS. The sensitivity of Cholangioscopy was 68.2% vs. 21.4% for ERCP with brushing (p < 0.01). Similarly, a meta-analysis by Navaneethan et al. of 10 studies (456 patients) calculated a combined sensitivity of 60.1% and specificity of 98% with biopsies guided by Cholangioscopy.

Endoscopic Ultrasound (EUS)

• Unlike other endoscopic modalities, EUS also offers the opportunity to evaluate the pancreatic parenchyma and regional lymphadenopathy for potential FNA. It has been frequently used for the evaluation of diseases of the biliary tree and its surrounding structures.
• In two systematic reviews, the sensitivity of fine needle aspiration guided by EUS after a non-diagnostic ERCP was 77% and 89%, with a specificity of 100%. A meta-analysis by Chiang et al. of 10 studies (1,162 patients) showed a 14% increase after a non-diagnostic ERCP. The diagnostic yield of EUS depends in part on the location of the stricture. A 2016 meta-analysis of 13 studies reported a combined sensitivity of 83% for fine needle aspiration of distal biliary strictures compared to a combined sensitivity of 76% for proximal biliary strictures.

Despite current technology aiding in defining the etiology of IBS in many cases, there are still some others considered “negative” during the investigation, but which persist with suspicion of malignancy and end up undergoing surgery. Thus, new technologies are expected to provide not only high diagnostic precision but also a high negative predictive value, precisely to avoid unnecessary surgeries. This is especially true for Cholangioscopy, whose endoscopic criteria are not yet fully established and there is a lack of consensus on terminology and description of findings, which is why histology continues to be the gold standard for diagnosis.

References

1. Nichol S. Martinez et al. Determining the Indeterminate Biliary Stricture: Cholangioscopy and Beyond. Current Gastroenterology Reports (2020) 22:58.
2. Robert Dorrell et al. The Diagnostic Dilemma of Malignant Biliary Strictures. Diagnostics 2020, 10, 337.
3. Chencheng Xie et al. Indeterminate biliary strictures: a simplified approach. Expert Review Of Gastroenterology & Hepatology, 2018.
4. Petko Karagyozov et al. Role of digital single-operator cholangioscopy in the diagnosis and treatment of biliary disorders. World J Gastrointest Endosc 2019 January 16; 11(1): 31-40. DOI: 10.4253/wjge.v11.i1.31.

How to cite this article

Brasil, G. Indeterminate biliary stricture – important concepts you need to know. Endoscopy News 2022. Available at:  https://endoscopy.news/general-topics/indeterminate-biliary-stricture-important-concepts-you-need-to-know/

Colon obstructions can be mechanical or non-mechanical and constitute about 25% of all intestinal obstructions. Among the mechanical causes, the most common are:

1. obstructive tumor in the colon or rectum (60%);
2. stenosis due to previous diverticulitis (10%);
3. volvulus of the colon (15 to 20%).

Colon volvulus is the twisting of a redundant segment of the colon on its mesentery that can lead to luminal occlusion of the twisted segment and ischemia by rotation of the mesocolon and, consequently, to perforation.

Although colon volvulus can occur in any redundant segment, it most commonly involves the sigmoid (60%–75% of all cases) and cecum (25%–40% of all cases).

Sigmoid volvulus occurs mainly during the 6th to 8th decades of life, being more common in men, institutionalized patients, patients with chronic constipation, neuropsychological impairment, or decompensated comorbidities. On the other hand, cecal volvulus usually presents in younger patients and has a female predominance.

Acute pseudo-obstruction of the colon, or Ogilvie’s syndrome, is a non-mechanical functional cause of obstruction that is believed to be a consequence of dysregulation of the autonomic impulses of the colon’s innervation. There is significant distension of the colon without an obstructive factor, but it can also evolve into ischemia and perforation. Clinical presentations vary according to the degree of distension, whether the ileocecal valve is competent or not, and the clinical condition of the patient. More commonly, Ogilvie’s syndrome affects elderly patients or patients hospitalized for unrelated reasons, including elective surgery, trauma, or treatment of an acute medical condition.

Here we present some recommendations from the guidelines of the American Society of Colon and Rectal Surgeons for the management of these cases.

Colon Volvulus

• Initial evaluation with history, physical examination, and basic laboratory tests. Symptoms may include cramping, nausea, vomiting, abdominal discomfort. Sigmoid volvulus usually has a more indolent presentation, while cecal volvulus tends to have a more acute presentation. On physical examination, there is generally abdominal distension with varying degrees of tenderness to palpation, up to peritonitis. Rectal examination reveals an empty rectal ampulla. Presentation in the emergency room with peritonitis and signs of shock occurs in 25 to 35% of cases.

• In hemodynamically stable patients, an abdominal radiograph aids in the initial evaluation (finding of “coffee bean” and, in patients with incompetent ileocecal valve, small bowel distension). Computed tomography is used to confirm the diagnosis.

Sigmoid Volvulus

• Hemodynamically stable patients without signs of peritonitis or evidence of perforation should undergo rectosigmoidoscopy to assess the viability of the sigmoid, untwist the torsion, and decompress the colon, effective therapy in 60 to 95% of cases. It is possible to maintain a decompression tube after rectosigmoidoscopy. The recurrence rate is 43 to 75% in cases not subjected to subsequent surgical intervention.

• Urgent sigmoidectomy is indicated when endoscopic detorsion is unsuccessful and in cases of colon suffering or perforation, as well as in patients with signs of peritonitis or septic shock. After resection of the twisted segment, the decision to perform a primary anastomosis, terminal colostomy, or anastomosis with diversion should be individualized considering the clinical context of the patient at the time of surgery, the conditions of the remaining colon, and comorbidities.

• Patients who undergo successful endoscopic detorsion are candidates for segmental colectomy during the same hospital admission to prevent recurrent volvulus and its complications. Non-resection operations, including only detorsion, sigmoidopexy, and mesosigmoidoplasty, are inferior to colectomy for the prevention of recurrent volvulus.

• Endoscopic fixation of the sigmoid may be considered in selected patients in whom surgical intervention is prohibitively risky.

Cecal Volvulus

• Attempts at endoscopic reduction of cecal volvulus are not recommended.

• Segmental resection is the treatment of choice for patients with cecal volvulus. Nonviable or ischemic cecum is present in 18% to 44% of patients with cecal volvulus and is associated with a significant mortality rate.

• In the case of cecal volvulus with viable intestine, the use of non-resection surgical procedures should be limited to patients without clinical conditions for resection.

Acute Colonic Pseudo-Obstruction (Ogilvie’s Syndrome)

• The initial evaluation should include history and physical examination, laboratory tests, and imaging diagnosis.
  In the absence of fever, leukocytosis, peritonitis, pneumoperitoneum, or cecal diameter > 12 cm, initial therapy consists of correcting hydroelectrolytic disorders, volume replacement, avoiding or minimizing the use of opioids, avoiding anticholinergic medications, and identifying and treating concomitant infections. Deambulation, fasting, positioning maneuvers (knee-chest or prone) to promote intestinal motility, and decompression with nasogastric and rectal tubes are also recommended. Oral osmotic laxatives should be avoided as they can worsen colon dilation. Abdominal radiographs are part of the daily evaluation, accompanied by physical examination.

• The initial treatment is clinical support and includes the exclusion or correction of conditions that predispose patients to the condition or prolong its course.

• Pharmacological treatment with neostigmine is indicated when the condition does not resolve with supportive therapy.

• Endoscopic decompression of the colon should be considered in patients with Ogilvie’s syndrome in whom neostigmine therapy is contraindicated or ineffective.

• Surgical treatment is recommended in cases complicated by ischemia or perforation of the colon or refractory to pharmacological and endoscopic therapies.

References:

1. Alavi K, Poylin V, Davids JS, Patel SV, Felder S, Valente MA, Paquette IM, Feingold DL; Prepared on behalf of the Clinical Practice Guidelines Committee of the American Society of Colon and Rectal Surgeons. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Colonic Volvulus and Acute Colonic Pseudo-Obstruction. Dis Colon Rectum. 2021 Sep 1;64(9):1046-1057. doi: 10.1097/DCR.0000000000002159. PMID: 34016826.
2. Yeo HL, Lee SW. Colorectal emergencies: review and controversies in the management of large bowel obstruction. J Gastrointest Surg. 2013;17:2007–2012.
3. Bauman ZM, Evans CH. Volvulus. Surg Clin North Am. 2018;98:973–993.
4. Quénéhervé L, Dagouat C, Le Rhun M, et al. Outcomes of first-line endoscopic management for patients with sigmoid volvulus. Dig Liver Dis. 2019;51:386–390.

How to cite this article

Camargo MGM. Treatment of Colonic Volvulus and Acute Colonic Pseudo-Obstruction (Ogilvie’s Syndrome). Endoscopy News, 2024, vol1. Available at: https://endoscopy.news/2024/02/05/treatment-of-colonic-volvulus-and-acute-colonic-pseudo-obstruction-ogilvies-syndrome/

The Helicobacter pylori

The Helicobacter pylori is a gram-negative bacterium that induces cellular and chemical reactions in the stomach, being considered a human carcinogen. Its diagnosis and treatment play an important role in the prevention of associated diseases, such as gastric cancer, ulcers, MALT lymphoma, and hyperplastic polyps. (To learn more about H. PYLORI, visit this post 1 and this post 2)

There are several diagnostic tests, from non-invasive (serology, breath test, and fecal antigen) to invasive (urease, culture, and histology). Non-invasive methods have high accuracy, but do not assess changes in the gastric mucosa. To learn more about diagnostic tests visit this article.

Due to the focal nature of bacterial colonization, the accuracy of invasive methods depends on the location, number, and size of biopsies. These, when poorly directed, can result in false negatives. Thus, it is important to evaluate the endoscopic predictors of the presence or absence of H. pylori in order to direct biopsies to areas with a higher probability of infection, as well as to avoid them when the positive predictive value is high.

Studies have shown that, although not pathognomonic, some endoscopic findings are associated with the presence of H. pylori. Recently, new chromoendoscopy and magnification technologies have allowed the analysis of the microstructure of the gastric mucosa and, consequently, greater accuracy in determining the infection status (absence, active infection, and post-eradication).

The aim of this article is to assist endoscopists in assessing endoscopic findings related to H. pylori both with white light, as well as chromoendoscopy and magnification.

So let’s go!

2. Findings of the non-infected stomach

2.1 With white light

The normal stomach has a pinkish-red and shiny color, and the mucosal folds are present uniformly. The mucus should be hyaline and often forming a small pool. In the body and fundus, the folds are more concentrated on the greater curvature, in a tent shape and tend to disappear with insufflation. The antrum is flat, with a clear hue.

2.2 With chromoscopy and magnification

To understand the changes visualized in endoscopic magnification, we first need to know the histomorphology of the normal gastric mucosa.

To learn more about the normal histology of the stomach Click here

In summary, the mucosa of the gastric body is composed of cryptic orifice (OC), marginal epithelium of the crypt (MCE), subepithelial capillary network (SECN), collecting vessels, and intervening spaces (between the crypts), as shown in the following scheme:

In the stomach not infected by H. pylori, the subepithelial capillary network is present, regularly throughout the body, called RAC (regular arrangement of collecting venules). The negative predictive value of this finding is greater than 90%, which means that its presence in the distal body’s lesser curvature and incisura is strongly associated with the condition of non-infection by H. pylori.

We can also observe that both the crypt orifice and the marginal epithelium are oval, regular, and symmetrical. The subepithelial capillary network (SECN) is regular and fine, in a honeycomb pattern.

3. Findings of the infected stomach

3.1- With white light

With white light, the endoscopic findings most associated with H. pylori infection are: diffuse hyperemia, petechial redness (“speckled”) of the fundus and proximal body, thickened and tortuous folds, mucosal edema, fibrinous exudate in the body, and antral nodularity. With the persistence of the infection, there is a decrease in the folds and the submucosal vessels become more visible, findings of atrophic gastritis.

In a prospective multicenter study, the sensitivity and specificity of the endoscopic findings described above were 94.3% and 62.8% (KATO,2013). Diffuse hyperemia was considered the most reliable characteristic by experienced endoscopists.

We know that this infection starts in the antrum and progresses to the body. However, in the antrum, the diagnostic accuracy is lower, as the vessels are located more deeply, hindering their visualization. Therefore, we must first assess the presence or absence of hyperemia in the body. When this assessment is difficult, we should pay attention to petechial redness, edema, folds, and fibrinous exudate.

As previously described, the absence of the regular pattern of collecting venules (RAC negative) may be associated with active infection by H. pylori, but the specificity of this finding is low. In a Brazilian study (Fiuza F, Martins BC, 2021), the absence of RAC was associated with only 50.6% positivity of H. pylori. In other words, the absence of RAC has high accuracy for the presence of the bacterium, but the infection is not always what causes its loss.

It is important to remember that, in H. pylori infection, the RAC initially disappears in the distal body’s lesser curvature and incisura, being these the most specific places to be analyzed. However, in chronic gastritis, when antral atrophy extends precisely through the incisura and lesser curvature of the distal body, there may be disappearance or deformity of the RAC, even in eradicated patients, making its analysis difficult. In these cases, we need to look for the RAC in the distal body mucosa away from atrophy.

Another important fact is that the last region where the RAC is preserved is in the proximal body and gastric fundus, places that are not recommended for evaluating bacterial infection.

3.2- With magnification

From a histomorphological perspective, with H. pylori infection, the crypts become larger and irregular, surrounded by erythema and grooves. We can no longer see the subepithelial capillary network, as inflammatory cells, edema, degenerated epithelium, and rupture of the microvascular network prevent its adequate visualization. The crypt orifices become asymmetrical and white due to the deposit of inflammatory content inside the glands. As atrophy expands, the marginal epithelium of the crypts becomes enlarged and has an irregular and elongated/curved shape. This is what we call “antralization” of the gastric body.

In a Brazilian study (Fiuza F, Martins BC, 2021), it was found that it is possible to identify these changes in the gastric mucosa (especially the presence or absence of RAC) using near focus technology, since gastroscopes with magnification are not yet widely available.

4. Findings of the treated stomach (post-eradication)

It still remains controversial whether H. pylori treatment can reverse atrophic gastritis and intestinal metaplasia. Moreover, it can take up to 10-15 years for the mucosa to recover and return to normal.

After eradication, the non-atrophic areas dissipate the inflammation and the atrophic areas become relatively reddish when compared to the adjacent mucosa. This confers the “map-like” pattern. This pattern may be associated with the development of both primary and metachronous gastric cancer even after effective treatment of H. pylori.

Another characteristic described is the “cracked” pattern, where grooves appear in the antral mucosa, indicating reparative mucosa.

Studies have shown that eradication therapy can alter the characteristics of the repaired stomach, causing difficulty in diagnosing early gastric cancer. That is why the post-eradication status must be distinguished from the negativity of H. pylori.

References

1. Anagnostopoulos GK, Yao K, Kaye P, Fogden E, Fortun P, Shonde A, Foley S, Sunil S, Atherton JJ, Hawkey C, Ragunath K. High-resolution magnification endoscopy can reliably identify normal gastric mucosa, Helicobacter pylori-associated gastritis, and gastric atrophy. Endoscopy. 2007 Mar;39(3):202-7.
2. Yao K. The endoscopic diagnosis of early gastric cancer. Ann Gastroenterol. 2013;26(1):11-22. 
3. Yagi K, Nakamura A, Sekine A. Comparison between magnifying endoscopy and histological, culture and urease test findings from the gastric mucosa of the corpus. Endoscopy. 2002 May;34(5):376-81. 
4. Yuan C, Lin XM, Ou Y, Cai L, Cheng Q, Zhou P, Liao J. Association between regular arrangement of collecting venules and Helicobacter pylori status in routine endoscopy. BMC Gastroenterol. 2021 Oct 20;21(1):389. 
5. Glover B, Teare J, Patel N. A systematic review of the role of non-magnified endoscopy for the assessment of H. pylori infection. Endosc Int Open. 2020 Feb;8(2):E105-E114.
6. Qi Q, Guo C, Ji R, Li Z, Zuo X, Li Y. Diagnostic Performance of Magnifying Endoscopy for Helicobacter pylori Infection: A Meta-Analysis. PLoS One. 2016 Dec 19;11(12):e0168201.
7. Weng CY, Xu JL, Sun SP, Wang KJ, Lv B. Helicobacter pylori eradication: Exploring its impacts on the gastric mucosa. World J Gastroenterol. 2021 Aug 21;27(31):5152-5170.  
8. Nishikawa Y, Ikeda Y, Murakami H, et al. Classification of atrophic mucosal patterns on Blue LASER Imaging for endoscopic diagnosis of Helicobacter pylori-related gastritis: A retrospective, observational study. PLoS One. 2018;13(3):e0193197.
9. Toyoshima O, Nishizawa T, Koike K. Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis. World J Gastroenterol. 2020 Feb 7;26(5):466-477.
10. Ono S, Dohi O, Yagi N, Sanomura Y, Tanaka S, Naito Y, Sakamoto N, Kato M. Accuracies of Endoscopic Diagnosis of Helicobacter pylori-Gastritis: Multicenter Prospective Study Using White Light Imaging and Linked Color Imaging. Digestion. 2020;101(5):624-630.
11. Kato T, Yagi N, Kamada T, Shimbo T, Watanabe H, Ida K; Study Group for Establishing Endoscopic Diagnosis of Chronic Gastritis. Diagnosis of Helicobacter pylori infection in gastric mucosa by endoscopic features: a multicenter prospective study. Dig Endosc. 2013 Sep;25(5):508-18.
12. Fiuza F, Maluf-Filho F, Ide E, Furuya CK Jr, Fylyk SN, Ruas JN, Stabach L, Araujo GA, Matuguma SE, Uemura RS, Sakai CM, Yamazaki K, Ueda SS, Sakai P, Martins BC. Association between mucosal surface pattern under near focus technology and Helicobacter pylori infection. World J Gastrointest Endosc. 2021 Oct 16;13(10):518-528.

How to cite this article

Nobre R, Baba E. ENDOSCOPIC FINDINGS RELATED TO H. PYLORI INFECTION. Endoscopy News; 2024, vol1. Available on: https://endoscopy.news/2024/01/27/endoscopic-findings-related-to-h-pylori-infection

Authors: Marcus Fernando Kodama Pertille Ramos and Ítalo Beltrão Pereira Simões

The majority of gastric cancer (GC) cases are sporadic, but about 10% present familial aggregation and 1 to 3% have a hereditary cause. Knowledge of hereditary syndromes as a causal factor for colorectal cancer (CRC) is well estabilished, but for GC this is less publicized, which can impair early diagnosis and proper follow-up.

Hereditary GC can occur with or without the presence of polyposis, as in the case of Hereditary Diffuse Gastric Cancer, Li-Fraumeni, BRCA1, BRCA2, and Lynch syndromes. In this article, we will briefly describe the main hereditary GC syndromes associated with polyposis, leaving those not associated for a future article.

1. HEREDITARY GC ASSOCIATED WITH POLYPOSIS

1.1 FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

FAP results from a mutation in the APC tumor suppressor gene causing a very high risk of CRC.

About 51 to 88% of patients have gastric polyps, mainly fundic gland polyps (FGP). The incidence is high even in attenuated FAP. They tend to be numerous, and the term gastric polyposis can be used only when more than 20 are present.

Low-grade dysplasia may be present in up to 44% of fundic gland polyps. Adenomatous polyps are detected in about 20% of patients with FAP.

Upper endoscopic screening is recommended at the time of colonic polyposis manifestation or from the age of 25. The interval of performance will depend on the findings and also according to the need for follow-up of papillary adenoma, when present, according to the Spigelman score.

1.2 PEUTZ-JEGHERS SYNDROME (PJS)

PJS is an autosomal dominant disorder, characterized by the development of gastrointestinal hamartomatous polyposis mainly in the jejunum associated with the presence of melanocytic macules.

The clinical diagnosis is based on the confirmation of the presence of hamartomatous polyps associated with a positive family history and hyperpigmentation of mucous membranes, fingers, and external genitalia.

Gastric polyps are detected in 25% of cases, compared with 70-90% found in the small intestine and 50% in the colon. The morphological appearance of the gastric polyp in PJS resembles a villous pattern of hyperplastic epithelial proliferation, making it difficult to distinguish from juvenile and hyperplastic polyps.

Dysplasia is rarely detected in the polyps, but individuals with PJS have a 29% risk of developing GC, mainly of the intestinal type.

Screening should be started early in childhood with initial endoscopy, with frequency depending on the findings. From the age of 50, the risk of GC increases and the frequency should be more frequent between 1 to 2 years.

1.3 JUVENILE POLYPOSIS SYNDROME

An autosomal dominant syndrome that leads to the development of polyps throughout the gastrointestinal tract mainly in the colon and rectum.

Criteria for clinical suspicion of the syndrome include more than 5 colorectal juvenile polyps, juvenile polyps throughout the gastrointestinal tract, or more than 1 juvenile polyp with a positive family history. The definitive diagnosis is made from one of the clinical suspicion criteria in the presence of the BMPR1A and SMAD4 genes in the genetic test.

Juvenile polyps are hamartomatous polyps that develop from normal tissue of the gastrointestinal tract. The usual endoscopic appearance is of a pedunculated, multilobed, soft polyp ranging from small polyps to giant polyps. In up to 75% of cases, other types of polyps are present together. Severe gastric polyposis can occur causing anemia, hematemesis, protein-losing enteropathy, and obstructive symptoms. Progression to GC occurs in up to 21% of cases with an average age of 58 years.

Endoscopic screening is recommended from adolescence with annual endoscopies.

Learn more about juvenile polyposis by clicking this post

1.4 MUTYH-ASSOCIATED POLYPOSIS (MAP)

MAP is a rare syndrome, autosomal recessive, associated with mutation in the MUTYH gene that participates in DNA repair processes. Patients with MAP are predisposed to CRC, breast, and ovarian cancer.

Gastric polyps are detected in about 10 to 33% of cases and the majority are adenomas and FGP.

The risk of GC is low (2%) but occurs in younger patients (median age of 38 years). On the other hand, the risk of duodenal cancer is high and can occur in 17% of cases.

1.5 GASTRIC ADENOCARCINOMA WITH PROXIMAL POLYPOSIS (GAPPS)

This syndrome is characterized by the development of proximal gastric polyposis including the fundus and body forming a carpet of small polyps usually smaller than 1 cm. The histological type of the polyps is varied and can be FGP, hyperplastic, adenomas, and mixed.

The criteria for clinical diagnosis include detection of more than 100 polyps or more than 30 polyps with a positive family history in a first-degree relative, polyps restricted to the body and fundus without the presence of colorectal polyps, morphology of FGP with areas of dysplasia or carcinoma, exclusion of other syndromes, and use of proton pump inhibitors.

Case series have reported an incidence of 12.7% of GC, all of the intestinal type.

Endoscopic follow-up should be performed, but in cases with multiple polyps, the evaluation of polyps with signs of degeneration may be impaired, indicating total gastrectomy.

References

1. Clauditz TS, Moore M, Setia N, et al. Syndromic gastric polyposis and hereditary gastric cancers. Diagnostic Histopathologic 2019; 26(1):39-46.
2. Mahon SM. Hereditary Polyposis Syndromes. Gentics and Genomics 2018; 22(2): 151-6
3. Cardoso DM. Síndromes de polipose colorretal. Endoscopia Terapêutica; 2020. Disponível em: http://endoscopiaterapeutica.com.br/assuntosgerais/sindromes-de-polipose-colorretal/

How to cite this article

Kodama, MFKP and Simoes IBP. Hereditary gastric cancer. Gastropedia 2022. Available at: https://endoscopiaterapeutica.com.br/assuntosgerais/cancer-gastrico-hereditario

The sessile serrated lesion (SSL) is the new term for lesions previously called sessile serrated adenoma (SSA) and SSL with dysplasia is the term used for lesions previously called SSA with dysplasia. A detailed review of serrated lesions can be found in this other article.

Based on this, Serrated Polyposis Syndrome (SPS) is a rare condition characterized by multiple colorectal serrated lesions and increased risk of colorectal cancer.

• The prevalence varies from 0.03% to 0.5% in patients undergoing colonoscopy.
• The diagnosis usually occurs between 50-55 years, although it ranges from 20-70 years.
• Similar prevalence in men and women.

Click here to learn about other colorectal polyposis syndromes.

Updated Criteria for Serrated Polyposis:

Compared to the previous edition, the WHO in 2019 updated the diagnostic criteria, keeping only 2 of the 3 clinical criteria for the definition of SPS:

1. Criterion: At least 5 serrated lesions/polyps proximal to the rectum, all measuring ? 5 mm, with at least 2 measuring ? 10 mm.
2. Criterion: More than 20 serrated lesions/polyps of any size distributed throughout the colon, with at least 5 of them proximal to the rectum.

• Patients who meet at least one criterion are diagnosed with serrated polyposis.
• All subtypes of serrated polyps (sessile serrated lesion, hyperplastic polyp, traditional serrated adenoma, unclassified serrated adenoma) are included in the count.
• The count is cumulative over several colonoscopies.
• Studies report a cancer risk between 15–30% in patients with SPS, varying according to age, polyp phenotype, and high-risk histological features.
• Rigorous endoscopic surveillance (annual colonoscopy) is recommended.
• More recent studies have shown that most patients have endoscopic control with a reduction in the number and size of polyps after 2-3 annual colonoscopies, suggesting spacing the surveillance interval to 2 years after this initial stage [1].

Summary of Changes:

Reference

1. MacPhail M.E., Thygesen S.B., Patel N., Broadley H.M., Rex D.K. Endoscopic control of polyp burden and expansion of surveillance intervals in serrated polyposis syndrome. Gastrointest. Endosc. 2019;90:96–100. doi: 10.1016/j.gie.2018.11.016. 

How to cite this article

Martins BC and Tanigawa R. Serrated Polyposis Syndrome (SPS). Endoscopia Terapeutica, 2024 vol. 1. Available at: https://endoscopiaterapeutica.com.br/assuntosgerais/sindrome-de-polipose-serrilhada-sps/

1. Introduction

Colorectal cancer (CRC) is a major public health problem, associated with high morbidity and mortality rates in the West. CRC represents the end point of a wide range of genetic and epigenetic changes that occur in normal colorectal cells.

It is estimated that approximately 85% of CRCs develop from colorectal polyps. Adenomatous polyps and sessile serrated lesions (SSLs) are the most important precursors of CRC. It is estimated that adenomas and SSLs are present in 20% to 50% of individuals over 50 years of age [1].

2. WHO Classification for Colorectal Serrated Lesions

Until 2010, colorectal serrated lesions were generally considered harmless lesions and reported as hyperplastic polyps (HPs) by pathologists and gastroenterologists.

Subsequently, a variety of terms were used to describe these lesions, contributing to misunderstandings about the terminology and classification of serrated lesions.

In 2010, the World Health Organization (WHO) proposed the following classification for colorectal serrated lesions (4th edition = penultimate version until the publication of this article):

Histological Type	Histological Type
Hyperplastic Polyp (HP)	• Microvesicular Type
	• Goblet cell-rich Type
	• Mucin-poor Type
Sessile Serrated Adenoma/Polyp (SSA/P)	• SSA/P with dysplasia
	• SSA/P without dysplasia
Traditional Serrated Adenoma (TSA)

In 2019 the WHO updated the classification of Colorectal Serrated Lesions (5th Edition) [2]. This new classification differentiates serrated lesions into four categories:

Histological Type	Subtype Histological
Hyperplastic Polyp (HP)	• Microvesicular Type
	• Goblet cell-rich Type
Sessile Serrated Lesion (SSL)	• SSL
	• SSL with dysplasia (SSLD)
Traditional Serrated Adenoma (TSA)
Serrated Adenoma, Not Classified

The main change in terminology is the approval of the new term “sessile serrated lesion ” (SSL), which aims to adjust the previous confusing terminologies “sessile serrated adenoma and sessile serrated polyp “. Indeed, the term “adenoma” includes the concept of dysplasia, which is not observed in a significant number of SSLs. Now, when the pathologist observes a dysplastic pattern in SSLs, they should use the terminology “SSL with dysplasia”. Moreover, a large part of SSLs do not have a polypoid appearance, making the term “polyp” inappropriate.

3. Colorectal Serrated Lesions: Histological and Endoscopic Characteristics

Microscopically, colorectal serrated lesions are characterized by the presence of serrated folds similar to saw teeth in the epithelial crypts [1]. The differences between the main subtypes of serrated lesions lie in the architectural characteristics and the location/extent of the proliferative zone.

3.1 – Hyperplastic Polyps (HP)

• HPs are the most common serrated lesions, representing about 75% of all serrated polyps.
• Estimated prevalence in patients undergoing screening colonoscopies is 20–30%.
• In HPs, the crypts are straight and elongated, with a serrated architecture confined to the upper two-thirds of the crypts and the cells show minimal cytological atypia.
• At the base of the crypt, the architecture is regular and not serrated, and the cells do not show signs of atypia.
• HPs are commonly found in the left colon, mainly in the rectosigmoid colon, and usually measure less than 5 mm.
• In white light endoscopy, they appear as raised or sessile lesions, sometimes covered with normal mucosa.
• In chromoendoscopy, a type II star-shaped crypt pattern is observed on the surface of the lesion.

There are two variants of Hyperplastic Polyps:

• microvesicular type hyperplastic polyps:

  • characterized by the presence of small mucus droplets in the cells
  • considered precursors of SSL.

• goblet cell-rich hyperplastic polyps:

3.2 – Sessile Serrated Lesions (SSL)

• SSLs are the second most common type of serrated lesion and are considered precursor lesions of CRC. (More etiopathogenic details)
• The prevalence of SSL in the general population is 5–10%.
• Generally, SSLs are larger than HPs, with an average diameter between 5-7 mm, and their shape is flat or sessile.
• Unlike HPs, SSLs are more frequent in the right colon.
• The histological characteristic that distinguishes SSL from HP is the presence of distorted serrated crypts.
• For the histological diagnosis of SSL, the crypt must show at least one of the following characteristics:

  1. Horizontal growth along the muscularis mucosae.
  2. Dilation of the base of the crypt.
  3. Serration extending to the base of the crypt.
  4. Asymmetric proliferation.

• Endoscopic characteristics:

  • presence of a mucus cap
  • Pale/whitish coloration.
  • Type II-O (open) crypt pattern in magnifying chromoscopy.

3.3 – Sessile Serrated Lesions with Dysplasia (SSL-D)

• According to their known carcinogenic potential, SSLs can originate dysplastic foci.
• This histological entity, called SSLD, represents a subgroup of SSLs.
• It is estimated that about 4–8% of SSLs contain dysplasia.
• At least three different morphological types of dysplasia have been described in SSLD:

  • Intestinal dysplasia (similar to adenoma): rare.
  • Serrated dysplasia: more common.
  • Minimal deviation dysplasia: few changes compared to SSL and characteristic loss of MLH1.

• Endoscopically, these lesions usually present nodules on the surface.
• Signs such as (sub)pedunculated morphology, double elevation, central depression, and reddish hue are suspicious signs of dysplasia. [3]
• In magnifying chromoendoscopy, they exhibit an adenomatous pit pattern (Kudo type III, IV). [4]

3.4 – Traditional Serrated Adenoma (TSA)

• Most common in the left colon.
• They are the rarest serrated colorectal lesions with a prevalence of less than 1%.
• Generally, TSA are larger than SSL and have a polypoid or pedunculated appearance.
• Histologically, they show distorted villous architecture and, in many cases, villi with bulbous tips.
• Both adenoma-like dysplasia and serrated dysplasia can be seen in TSA.
• The risk and speed of progression to carcinoma are unknown.
• On endoscopy, they look like reddish, protuberant or pedunculated lesions and, macroscopically, they have a “pine” or “coral” appearance.

Summary of Changes:

• Sessile serrated lesion (SSL) is the new term for lesions previously called sessile serrated adenoma (SSA). The clinical guidelines for the management of SSA apply to SSL.
• SSL with dysplasia is the term used for lesions previously called SSA with cytological dysplasia.
• Unclassified serrated adenoma has been introduced for rare polyps that are difficult to classify as SSL or TSA.

Summary of Histological Criteria for Sessile Lesions and Polyps:

• A single undisputed distorted crypt is sufficient to diagnose a sessile serrated lesion (SSL). Distortion of the crypt architecture can include horizontal growth along the muscularis mucosae, dilation of the crypt base and asymmetrical proliferation.
• Flat serrated lesions/polyps without a typical SSL-type crypt are diagnosed as hyperplastic polyps (HP) by exclusion. Mild symmetrical dilatation of the crypt and goblet cells at the base of the crypts are not sufficient to diagnose SSL.
• Stratification into low-grade and high-grade dysplasia is not recommended.
• The diagnosis of traditional serrated adenoma (TSA) requires two of the following characteristics:
• (1) slit-like serration;
• (2) tall eosinophilic cells with pencil nuclei;
• (3) ectopic crypt formations.

References:

1. Mezzapesa M, Losurdo G, Celiberto F, Rizzi S, d’Amati A, Piscitelli D, Ierardi E, Di Leo A. Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis. Int J Mol Sci. 2022 Apr 18;23(8):4461. doi: 10.3390/ijms23084461. PMID: 35457279; PMCID: PMC9032676.
2. WHO Classification of Tumours Editorial Board . WHO Classification of Tumors: DIGESTIVE System Tumours. 5th ed. International Agency for Research on Cancer; Lyon, France: 2019
3. Murakami T, Sakamoto N, Ritsuno H, Shibuya T, Osada T, Mitomi H, Yao T, Watanabe S. Distinct endoscopic characteristics of sessile serrated adenoma/polyp with and without dysplasia/carcinoma. Gastrointest Endosc. 2017 Mar;85(3):590-600. doi: 10.1016/j.gie.2016.09.018. Epub 2016 Sep 20. PMID: 27663716.
4. Tate D.J., Jayanna M., Awadie H., Desomer L., Lee R., Heitman S.J., Sidhu M., Goodrick K., Burgess N.G., Mahajan H., et al. A standardized imaging protocol for the endoscopic prediction of dysplasia within sessile serrated polyps. Gastrointest. Endosc. 2018;87:222–231. doi: 10.1016/j.gie.2017.06.031.

How to cite this article

Martins BC e Tanigawa R. Colorectal Serrated Lesions. Endoscopy News, 2024 vol. 1. Available on: https://endoscopy.news/2024/01/09/colorectal-serrated-lesions

Introduction

Acute pancreatitis is one of the diseases responsible for the highest number of emergency hospitalizations in gastroenterology. Its incidence is 13 to 45 cases per 100,000 people, accounting for 270,000 hospitalizations per year in the United States ¹. Most cases are mild, but it can evolve into severe forms, requiring intensive care unit admission and even death. Its mortality is close to 5%, being significantly higher when only the most severe cases are analyzed ².

Gallstone disease and alcoholism are the main causative agents, accounting for about 60% to 80% of cases ³. Other less common causes include anatomical changes, metabolic disorders, tumors, autoimmune diseases, among others. However, in a significant percentage of cases, about 10% to 30%, it is not possible to identify a causative factor after initial evaluation ^3-4. It is then defined as idiopathic acute pancreatitis, being the 3rd most common cause in some series ³.

A detailed evaluation in these patients with idiopathic acute pancreatitis is of fundamental importance, since 14% to 26% may present recurrent episodes, evolving to chronic pancreatitis ^5-6. In some cases, after specialized examinations, a treatable causative agent can be identified, thus avoiding new crises.

The endoscopic ultrasound is a minimally invasive procedure and, due to the proximity of the stomach and duodenum to the pancreas and bile ducts, allows a detailed examination of this region. Several studies have shown its benefit in the investigation of patients with idiopathic acute pancreatitis, however, the timing of its performance is not yet well defined ^1,2-8.

Accuracy of Endoscopic Ultrasound

The accuracy of endoscopic ultrasound in identifying a causative agent in patients with idiopathic acute pancreatitis varies greatly among studies, from 29% to 88% ⁴. This large difference is due to the inclusion criteria used in each study. In those where patients underwent a greater number of diagnostic tests before the endoscopic ultrasound, the accuracy was lower. In those where patients were referred earlier for endoscopic ultrasound, the accuracy was higher.

Umans and colleagues in a recent meta-analysis reached an accuracy of 59% ⁷. Biliary lithiasis, presence of stones, microlithiasis or biliary sludge in the gallbladder or common bile duct, was the most common cause, accounting for 30% of cases (Figures 1 and 2). In second place came chronic pancreatitis with 12% and in third pancreas divisum with 5%. It is important to note that in 2% of patients a neoplasm that had not been diagnosed in previous exams was detected. The identified lesions were intraductal papillary mucinous neoplasms (IPMN), pancreatic carcinomas, neuroendocrine tumors (Figure 3), adenomas, and papillary carcinomas. Other less common causes were autoimmune pancreatitis, ascariasis, choledochocele (Figures 4 and 5), biliopancreatic junction anomaly, and diverticulum.

In the same meta-analysis, when comparing the accuracy of endoscopic ultrasound in patients who had previously undergone cholecystectomy with those who had not, the result was different between the two groups, being 50% and 64%, respectively ⁷. Thus demonstrating how gallbladder lithiasis is indeed one of the most common causes.

When to Perform Endoscopic Ultrasound After an Episode of Pancreatitis?

There is controversy in the literature about the ideal timing for endoscopic ultrasound after an episode of acute pancreatitis ⁵. Authors who suggest performing the procedure earlier, sometimes while the patient is still hospitalized, argue that a possible diagnosis could be made more quickly, avoiding the possibility of recurrence and also preventing the patient from losing follow-up ⁵. Those who prefer to perform the procedure later, about 4 weeks after the resolution of the case, argue that the inflammatory changes secondary to pancreatitis could complicate the diagnosis, reducing the accuracy of endoscopic ultrasound ⁵.

In the meta-analysis by Umans and colleagues, the accuracy of endoscopic ultrasound after the improvement of acute pancreatitis and before improvement was 61% and 48%, respectively ⁷.

Perform Endoscopic Ultrasound After the First Episode of Idiopathic Acute Pancreatitis or Only in Recurrent Cases?

There is no consensus in the literature on the ideal indication for performing endoscopic ultrasound ⁵. There seems to be a similar accuracy when performed after the first episode or after recurrent episodes ^5,7. Since many of the identified causes are treatable and would prevent new crises, there is a tendency to already indicate endoscopic ultrasound after the first episode.

Endoscopic Ultrasound vs. MRCP

A meta-analysis by Wan and colleagues, comparing the accuracy of endoscopic ultrasound with MRCP, showed better performance with endoscopic ultrasound, 64% and 34%, respectively ⁸. The main benefit occurred in biliary lithiasis (34% x 9%) and chronic pancreatitis (10% x 1%). In pancreas divisum, the accuracy was similar with both techniques (2% x 2%). When secretin was used, which is not available in Brazil, MRCP was better (12%). Hallenslebem and colleagues demonstrated similar accuracy between endoscopic ultrasound (36%) and MRCP (33%) ⁸.

Conclusion

Endoscopic ultrasound plays a fundamental role in the investigation of patients with idiopathic acute pancreatitis. It presents high accuracy for the diagnosis of causative factors, many of which are treatable, thus avoiding recurrent crises.

It is not yet well established in the literature what would be the ideal timing for the procedure, but most studies tend to wait about 4 weeks after the improvement of pancreatitis for its performance, thus minimizing the diagnostic difficulty secondary to inflammatory changes. Most authors also recommend performing endoscopic ultrasound after the first crisis. It is important to note that the diagnosis of neoplasms not detected by other methods can reach 7% ⁶.

MRCP and endoscopic ultrasound should be used in conjunction. Since biliary lithiasis would be the most common cause and endoscopic ultrasound would have better accuracy for this diagnosis, there is a tendency to indicate it as the first option after an initial negative investigation.

References

1. Working Group IAPAPAAPG. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013; 13: e1–e15.
2. Crockett SD, Wani S, Gradner TB, et al. American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018; 154(4): 1096-1101.
3. Blanco GDV, Gesuale C, Varanese M, et al. Idiopathic acute pancreatitis: a review on etiology and diagnostic work-up. Clin J Gastroenterol 2019; 12(6): 511-524.
4. Tepox-Padrón A, Bernal-Mendez RA, Duarte-Medrano G, et al. Utility of endoscopic ultrasound in idiopathic acute recurrent pancreatitis. BMJ Open Gastroenterol 2021; 8(1): e000538.
5. Somani P, Sunkara T, Sharma M. Role of endoscopic ultrasound in idiopathic pancreatitis. World J Gastroenterol 2017; 14: 6952-6961.
6. Hallensleben ND, Umans DS, Bouwense SA, et al. The diagnostic work-up and outcomes of “presumed” idiopathic pancreatitis: A post-hoc analysis of a multicentre observational cohort. United European Gastroenterol J. 2020; 8(3): 340-350.
7. Umans DS, Rangkuti CK, Weiland CJS, et al. Endoscopic ultrasonography can detect a cause in the majority of patients with idiopathic acute pancreatitis: a systematic review and meta-analysis. Endoscopy 2020; 52(11): 955-964.
8. Wan J, Ouyang Y, Yu C, et al. Comparison of EUS with MRCP in idiopathic acute pancreatitis: a systematic review and meta-analysis. Gastrointest Endosc 2018; 87(5): 1180–8.

How to cite this article

Retes FA. Role of Endoscopic Ultrasound in Idiopathic Acute Pancreatitis. Endoscopia Terapeutica 2023, Vol II. Available at: https://endoscopiaterapeutica.com.br/assuntosgerais/papel-da-ecoendoscopia-na-pancreatite-aguda-idiopatica