Studies show that the size of the polyp is the main risk factor for the development of cancer, especially when adenomatous polyps are 10 millimeters or more, presenting a chance of malignancy between 37% and 55%.

However, it is difficult to differentiate between adenomatous polyps and polyps without malignant potential in preoperative exams. Therefore, it is important for the gastroenterologist to know the correct indication for surgery in patients with gallbladder polyps in order to avoid an unnecessary surgical procedure in patients without risk and, mainly, correctly indicating the procedure in the population with a higher risk of malignancy.

In this article, we will summarize the indications for follow-up and treatment of gallbladder polyps.

SYMPTOMATIC PATIENTS

Gallbladder polyps rarely cause symptoms, however some studies have reported an association between gallbladder polyps and undetected stones on ultrasound and/or cholecystitis. The joint European guideline of 2022 recommends cholecystectomy for patients who present symptoms such as biliary colic or complications (example: pancreatitis) and who have favorable clinical conditions for surgery [1]. The rate of symptom improvement is variable in the literature (40-90% improvement).

Patients with nonspecific dyspeptic symptoms without biliary colic should be treated conservatively (unless there are other indications for polyp removal), since the pathogenesis of these symptoms is not clear and cholecystectomy may not relieve symptoms. These patients should be treated symptomatically, as with other patients with functional dyspepsia.

ASYMPTOMATIC PATIENTS WITH RISK FACTORS FOR GALLBLADDER CANCER

Risk factors for gallbladder cancer include:

• age >60 years
• primary sclerosing cholangitis
• Asian ethnicity
• sessile polyps with focal gallbladder wall thickness >4 mm

The approach will depend on the size of the polyp:

• Polyps ≤5 mm: surveillance ultrasound at 6 months, 1 year, and 2 years. Follow-up can be discontinued if there is no growth during this period.
• Polyps 6 to 9 mm: cholecystectomy is recommended if the patient is clinically fit and accepts surgery.
• Polyps 10 to 20 mm: Polyps 10 to 20 mm should be considered as possibly malignant. Laparoscopic cholecystectomy is recommended.
• Polyps >20 mm: are generally malignant. Patients should undergo preoperative staging with computed tomography or endoscopic ultrasound. Radical treatment consists of extended cholecystectomy with lymph node dissection and partial hepatic resection at the gallbladder bed.

ASYMPTOMATIC PATIENTS WITHOUT RISK FACTORS FOR GALLBLADDER CANCER

In asymptomatic patients without risk factors for gallbladder cancer, surveillance recommendations vary according to the size of the polyp.

• For polyps ≤ 5 mm: no follow-up is necessary. *
• For polyps 6 to 9 mm: perform abdominal ultrasound at 6 months, 1 year, and 2 years. Surveillance can be discontinued if there is no growth during this period.

* This strategy is aligned with the practices of the American College of Radiology [2] and the Canadian Association of Radiologists Incidental Findings Working Group [3], which recommend that polyps smaller than 7 mm do not require follow-up.

IMPORTANT CONSIDERATIONS IN PATIENTS UNDERGOING SURVEILLANCE

1. Increase in polyp size

The joint European guideline of 2017 recommended that:

• An increase in size greater than 2 mm in the images probably represents a clinically significant increase and should prompt referral to a surgeon for cholecystectomy.

The update of this guideline in 2022 recommends that:

• If the polypoid lesion grows 2 mm or more during the 2-year follow-up period, then the current size of the polypoid lesion should be considered along with the patient’s risk factors. Multidisciplinary discussion should be held to decide whether to continue surveillance or if cholecystectomy is indicated.

An important retrospective study published in 2019 including more than 600,000 adults undergoing cholecystectomy showed that:

• The growth of 2 mm or more seems to be part of the natural history of gallbladder polyps.
  • The likelihood of a polyp growing at least 2 mm in 10 years was 66% for polyps smaller than 6 mm and 53% for polyps between 6-10mm.
  • Important: this growth does not seem to be associated with future gallbladder cancer. None of the 507 patients with polyps that grew to 10 mm or more were subsequently diagnosed with cancer.
• The first year is the most important:
  • Most cases of gallbladder cancer were diagnosed in the first year, probably representing neoplasms already present at the time of diagnosis.
  • Polyps initially smaller than 10 mm were almost never associated with future cases of gallbladder cancer (rate 1.05 per 100,000 person-years)
  • Polyps with ≥ 10 mm at diagnosis were rarely associated with gallbladder cancer after the first year.

The cherry on top of this study:

• In addition, we observed that similar proportions of adults were diagnosed with gallbladder Ca (0.053% vs. 0.054%), whether an initial ultrasound showed a gallbladder polyp or not. These findings suggest that there may not be a general link between gallbladder polyps and gallbladder neoplasia, and that gallbladder polyps are an incidental finding.

2. Duration of surveillance

The duration of surveillance in patients with gallbladder cancer is not clear. The updated joint European guidelines recommend discontinuing surveillance in two years if there is no growth of the polyps. Some authors recommend maintaining surveillance for at least five years. However, in patients with risk factors for gallbladder cancer, we should maintain surveillance for gallbladder cancer with abdominal USG indefinitely.

3. Adenomyomatosis

Patients with typical features of adenomyomatosis on ultrasound do not require surveillance or cholecystectomy.

4. If the gallbladder polyp disappears during follow-up

If the gallbladder polyp disappears during follow-up, the follow-up surveillance can be discontinued.

References

1. Foley KG, Lahaye MJ, Thoeni RF, Soltes M, Dewhurst C, Barbu ST, Vashist YK, Rafaelsen SR, Arvanitakis M, Perinel J, Wiles R, Roberts SA. Management and follow-up of gallbladder polyps: updated joint guidelines between the ESGAR, EAES, EFISDS and ESGE. Eur Radiol. 2022 May;32(5):3358-3368. doi: 10.1007/s00330-021-08384-w. Epub 2021 Dec 17. PMID: 34918177; PMCID: PMC9038818.
2. Sebastian S, Araujo C, Neitlich JD, Berland LL (2013) Manag- ing incidental findings on abdominal and pelvic CT and MRI, Part 4: white paper of the ACR Incidental Findings Commit- tee II on gallbladder and biliary findings. J Am Coll Radiol 10(12):953–956
3. Bird JR, Brahm GL, Fung C, Sebastian S, Kirkpatrick IDC (2020) Recommendations for the management of incidental hepatobiliary findings in adults: endorsement and adaptation of the 2017 and 2013 ACR Incidental Findings Committee White Papers by the Canadian Association of Radiologists Incidental Findings Working Group. Can Assoc Radiol J 71(4):437–447
4. Szpakowski JL, Tucker LY. Outcomes of Gallbladder Polyps and Their Association With Gallbladder Cancer in a 20-Year Cohort. JAMA Netw Open. 2020 May 1;3(5):e205143. doi: 10.1001/jamanetworkopen.2020.5143. PMID: 32421183; PMCID: PMC7235691.

How to cite this article

Martins BC. Management of Gallbladder Polyps: When to Follow Up and When to Recommend Cholecystectomy? Gastropedia 2024; vol 1. Available at: https://gastropedia.pub/en/surgery/management-of-gallbladder-polyps-when-to-follow-up-and-when-to-recommend-cholecystectomy

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How do you know if triglycerides (TG) are the cause or just an epiphenomenon present in an acute pancreatitis of another etiology?

Concept

Hypertriglyceridemia is defined as an increase in serum triglyceride levels above 150 mg/dL. This increase can be categorized into:

• Mild HTG: 150-199 mg/dL
• Moderate HTG: 200-999 mg/dL
• Severe HTG: 1000-1999 mg/dL
• Very severe HTG: > 2000 mg/dL

HTGs are classified into:

• Primary – patients with genetic alterations that do not allow the correct metabolism of triglycerides. These causes were cataloged by Friderickson into types I to V. The types most associated with acute pancreatitis are: types I, IV and V.
• Secondary: some patients raise TG due to: obesity, poorly controlled diabetes, hypercaloric and hyperlipidic diet, pregnancy and alcohol use. In addition, some medications are known to cause HTG and should be researched in this context (eg: retinoids, protease inhibitors, anti-psychotics, calcineurin inhibitors, diuretics and estrogens)

The risk of acute pancreatitis (PA) occurring in individuals with HTG is considered when TG rises > 1000 mg/dL (around 5%) and increases greatly when TG > 2000 mg/dL (risk becomes 10-20%). When analyzing the population with severe hypertriglyceridemia, about 20% reported a previous history of acute pancreatitis, a value much higher than the prevalence found in the population.

Pathophysiology

The pathophysiology of pancreatitis by HTG is complex, and to this day not completely understood. It is known that TG in the microcirculation induces the release of pancreatic lipase, which cleave the molecules into free fatty acids (which are lipotoxic to pancreatic cells). These, in turn, lead to endothelial injury with capillary extravasation. TG also activate substances such as tramboxane, phospholipase A and prostaglandins that lead to vasoconstriction and pancreatic ischemia.

Triglycerides and free fatty acids also tend to group together in the form of micelles, which increases plasma viscosity and leads to gland ischemia.

Added to this we also have the imbalance in intracellular calcium, oxidative stress in organelles, which also precipitate the early activation of trypsin, still within the pancreas.

Diagnosis

The diagnosis of PA by HTG is given in the same way as other etiologies, with the Atlanta criteria, when 2 of the 3 criteria are present (upper abdominal pain, elevation of pancreatic enzymes > 3 the limit of the method and compatible imaging exam) associated with elevation of TG > 1,000 mg/dL.

Here it is important to remember that PAs originating from other causes (biliary, alcoholic and drug) can raise TG in the acute phase, but rarely at levels > 1000 mg/dL. This elevation is seen as an epiphenomenon.

As for severity, in studies conducted, it was observed that PA by HTG tends to be more severe compared to other etiologies. In meta-analyses and systematic reviews, it was observed that these patients evolved with higher severity scores, higher recurrence rates, more ICU admissions, and higher mortality.

Treatment

The initial treatment is based on support, as in any pancreatitis: hydration, analgesia and nutritional support (especially for severe PAs).

Among the specific approaches, the following stand out:

• Heparin pump: heparin can be used in monotherapy or associated with other modalities (such as the insulin pump). The anticoagulant initially increases the degradation of TG into free fatty acids. This effect, however, is temporary and hepatic consumption of plasma lipoprotein lipase causes a rebound increase in TG after discontinuation of the infusion. In addition, heparin infusion increases hemorrhagic events, especially in severe PAs with local complications.
• Insulin pump: continuous insulin infusion also increases the activation of lipoprotein lipase and decreases the release of free fatty acids by adipocytes and promotes the metabolism of these fatty acids by hormone-sensitive cells. It can be used in conjunction with heparin therapy, but the studies that evaluated the results are small. This modality has the potential to reduce TG levels by 50-75% in 3 days.
• Plasmapheresis: this therapy mechanically removes excess chylomicrons from the bloodstream. Similarly, it appears to reduce the levels of pro-inflammatory cytokines, which are determinants for severity in the initial phase of PA. However, the results regarding relevant outcomes (multiple organ dysfunction, mortality) did not favor plasmapheresis over supportive therapy. In addition, these patients had higher ICU admission rates (since it is a procedure performed in an intensive care unit), always need central catheter placement and may present an infusion reaction to plasma. It is a safe therapy to be performed in pregnant women.
• Hemofiltration: this is another controversial therapy, which tends to remove lipids and cytokines from plasma. Although it removes TG quickly and effectively, there was no difference in relevant clinical outcomes, in addition to having a high cost.

Follow-up

Patients who have already had PA by HTG need follow-up after discharge to reduce the risks of recurrence. The use of hypolipidemic agents (such as fibrates) is recommended as soon as the patient is already able to resume the diet orally, still in the hospital. The goal in outpatient treatment is to keep TG levels < 500 mg/dL.

Patients with primary HTGs should be followed by specialists in the lipid area.

In summary, HTG is a relevant cause of PA, especially in patients with primary hypertriglyceridemias. Triglyceride dosage should be done in the first few hours, as levels tend to drop significantly with fasting. The therapeutic approach is similar to that of other pancreatitis, and specific therapies can be associated for short-term TG reduction. Patients should always be referred for follow-up post discharge, to reduce the risk of a new event.

References

1. Yang, AL & McNabb-Blatar, J. Hypertriglyceridemia and acute pancreatitis. Pancreatology 20 (2020) 795-800
2. Qiu, M et al. Comprehensive review on the pathogenesis of hypertriglyceridaemia associated acute pancreatitis. Annals of Medicine 2023, VOL. 55, No. 2, 2265939
3. de Pretis, N et al. Hypertriglyceridemic pancreatitis: Epidemiology, pathophysiology and clinical management. United European Gastroenterology Journal 2018, Vol. 6(5) 649–655
4. Bálint, ER et al. Assessment of the course of acute pancreatitis in the light of aetiology: a systematic review and meta?analysis. Sci Rep 2020 Oct 21;10(1):17936.

How to cite this article

Marzinotto M. Acute Pancreatitis by Hypertriglyceridemia Gastropedia 2024, vol 1. Available at: gastropedia.com.br/gastroenterology/pancreas/acute-pancreatitis-by-hypertriglyceridemia/

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Introduction

The pelvic floor is a peculiar muscular structure, with an important function in maintaining anal continence and influence on defecation, and its dysfunction, whether for functional, anatomical and/or neurological reasons, results in morbidities with significant social, emotional, psychological and economic impact. Urinary incontinence, prolapse of pelvic organs, anal incontinence, evacuatory dysfunction and sexual disorders, among others, are considered abnormalities of the pelvic floor.

The evacuation disorders, whether fecal incontinence (FI) or chronic intestinal constipation (CIC), represent alterations of the pelvic floor quite frequent in the general population more commonly in those with risk factors, that is, elderly, women with obstetric past, comorbidities (such as scleroderma, hypothyroidism, diabetes mellitus), history of pelvic radiotherapy, bedridden patients or with locomotion deficits, history of orificial surgeries, chronic use of analgesics, opioids and psychiatric medications, among others.

Fecal incontinence has a very variable incidence and fundamentally dependent on the age of the study population, so that the incidence oscillates between 1.4 to 18%, with an average of 2 to 8.4%. On the other hand, chronic intestinal constipation (CIC) is one of the most common functional gastrointestinal disorders with high prevalence in the population, affecting 16% of adults and up to 33% of those over 60 years of age, more specifically females with a prevalence of 2 to 3:1 when compared to males.

Anorectal manometry can assist the attending physician, whether he is a gastroenterologist, digestive tract surgeon, coloproctologist or other medical specialty to better understand the disorder being evaluated and assist in its management. We will discuss the indications, concepts and techniques of anorectal manometry below.

Indications

Anorectal manometry (MNAR) can be indicated mainly for cases of:

• fecal incontinence (FI);
• intestinal constipation;
• dysinergia of the pelvic floor;
• prolapse of pelvic organs: rectocele, enterocele, mucosal prolapse, rectal procidence and cystocele;
• chronic pelvic pain: endometriosis, proctalgia fugax;
• pre-operative of orificial surgeries and reconstruction of intestinal transit;
• post-operative of colorectal surgery, notably in patient with the syndrome of anterior resection of the rectum.

Technique for execution

About 2-3 hours before the exam, retrograde intestinal preparation is indicated with a bottle of phosphoenema® or two of Minilax® (evacuatory enemas). No dietary restriction is necessary. At the time of the exam, the patient is positioned in left lateral decubitus with the lower limbs semi-flexed (Simms position) and then anal inspection is performed followed by rectal touch with the aim of:

• assessing whether there is an excess of feces in the rectal ampulla;
• measuring subjectively the tone of the internal and external sphincters of the anus, respectively during rest and anal contraction;
• assessing the relaxation of the puborectal muscle and the force of rectal propulsion;

In addition, the rectal touch has the final purpose of guiding the adequate and careful insertion of the anorectal manometry catheter.

Parameters evaluated

The following data are evaluated during the MNAR:

• Resting pressure: provided fundamentally by the action of the internal anal sphincter muscle (EAI – values in mmHg);
• Functional anal canal length: normally between 2-3 cm in females and a little longer in males;
• Contraction pressure: action performed by the anorectal striated musculature, that is, by the external anal sphincter (EAE) and puborectal muscle (PR – values in mmHg);
• Action of the sphincter musculature during the Valsalva maneuver or evacuatory effort in order to observe adequate relaxation of the same or signs suggestive of paradoxical contraction of the PR muscle, also described as pelvic floor dysinergia;
• Ability to sustain contraction: corresponds to the fatigue index during 30 seconds of the anorectal striated musculature with measurement in percentage and in duration time;
• Rectoanal inhibitory reflex: demonstrates the relaxation of the EAI to the stimulation of the nerve receptors in the anorectal ring from the stepped insufflation of air in the balloon, positioned at the distal end of the manometry catheter (it can be positive, negative or indeterminate);
• Sensitivity and capacity of the rectum: measurement made with the instillation of water inside this same balloon (values measured in ml);
• Sphincter asymmetry index at rest and during contraction: measures the symmetry of the anorectal sphincter complex in its circumference, in percentage.

After obtaining these data, it is recommended to perform the rectal balloon expulsion test, primarily in patients with clinical symptoms of intestinal constipation and those with manometric signs suggestive of paradoxical contraction of the puborectal muscle to MNAR.

For this, about 50 to 60 ml of water is left inside the rectal balloon with the probe positioned just above the anorectal ring and the patient is asked, mainly in the sitting position on a toilet, to eliminate the balloon, simulating an evacuation. The test is considered negative if there is elimination in up to three attempts with a maximum time of 60 seconds each. If the balloon containing water is not eliminated after 3 attempts, the test is positive, and may corroborate with pelvic floor dysinergia.

Conventional x High resolution

The conventional MNAR had, in our environment, its dissemination and execution methodology from 1993. For this, a probe with eight radial holes located at its end is used and through which the sphincter pressures are measured through the resistance offered to the flow of water at 0.3-0.5 ml/minute/channel. For its execution, the probe is inserted up to 6 cm from the anal edge and the catheter is pulled at each centimeter in a stationary manner.

On the other hand, the most recent MNAR devices, known as high resolution, have 24 or 36 channels, distributed radially and staggered from 1 to 6 cm from the end of the catheter. For its execution, the probe is inserted 6 cm from the anal edge, leaving it static with successive measurements of the above mentioned data, following a specific protocol known as the London Protocol, which better standardized the high resolution MNAR in relation to the conventional one.

This new MNAR execution technology has as main advantages:

• graphs with better spatial visualization;
• less discomfort to the patient, notably those with anal pain, such as chronic fissure;
• better technical standardization;
• less need for the participation of the nursing technician who assists the exam;

However, despite these advantages and a greater performance of the technological system in the preparation of reports, any of the available techniques does not replace the importance of the correct execution and interpretation of the data by the doctor who performs the exam.

Conclusion

The anorectal manometry exam, whether conventional or high resolution, is an important propaedeutic resource in the approach of patients with pelvic floor disorders, especially in anal incontinence and refractory intestinal constipation, and can also be used as a method in the pre-operative of colorectal and/or orificial surgeries in specific situations.

Also read: Screening for anal intraepithelial neoplasia and prevention of anal cancer

How to cite this article

Pinto RA, Neto IJFC, Marques CFS. Anorectal Manometry: concepts, indications and technique Gastropedia 2023, vol. 2. Available at: https://gastropedia.com.br/cirurgia/manometria-anorretal-conceitos-indicacoes-e-tecnica

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Causes of chronic pancreatitis

What is currently being discussed in the literature are the possible causes for this pathology. Alcohol is already well established as the main environmental risk factor for the onset of CP (42-77% of cases). Patients considered moderate or severe drinkers (35-48 drinks per week) have a relative risk of 2.7 to 3.3 for the development of the disease in a Danish observational study.

Another environmental risk factor is smoking, which is very prevalent in patients with CP, and is currently considered an independent risk factor for the onset of the pathology. It is a potent risk factor, including, for cases of recurrent acute pancreatitis, which sometimes culminate in the appearance of CP. In the case of smoking, the relative risk is 1.93 for current smokers compared to people who have never smoked.

Other causes of CP include autoimmune etiologies (both type I autoimmune pancreatitis – IgG4-related disease – and type II autoimmune pancreatitis are considered etiologies of chronic pancreatitis), obstructive etiologies (as in cases of neoplasms, cysts, scarring stenoses of the main pancreatic duct, oddi sphincter dysfunctions and pancreas divisum), Recurrent Acute Pancreatitis (RAP) and genetic etiologies.

Even after genetic study, about 10-15% of CPs still remain idiopathic, suggesting that there is much unknown in this field.

Pancreatic genetics and risk of neoplasia

The genetics of pancreatic pathologies is extremely complex, with several genes possibly involved in the phenotypes presented. Many mutations can lead to a RAP picture, which culminates with gland fibrosis, and other mutations or polymorphisms that lead directly to the appearance of CP.

The main genes involved in the pathogenesis of CP are listed below:

• PRRS-1: cationic trypsinogen gene – autosomal dominant inheritance mutation, responsible for Hereditary Chronic Pancreatitis.
• SPINK-1: gene that, in the absence of pathogenic mutations, prevents the activation of trypsinogen.
• CFTR: gene that encodes the chloride channels in the membrane of ductal cells – mutations in this gene can result in the phenotypes of Cystic Fibrosis
• CTRC: gene that promotes the degradation of trypsinogen and that mutated loses this protection mechanism

There are several other genes listed as coadjuvants in the pathological processes of the pancreas, and probably others that we are not yet aware of. The fact is that, in pancreatitis associated with one or more genetic mutations, the risk of Ductal Adenocarcinoma of the Pancreas is higher than other pancreatitis and much higher than the population risk. Patients with PRRS-1 and SPINK-1 mutations have a cumulative risk of 53% of pancreatic neoplasia at 75 years of age, while alcoholic CPs have this same calculated risk of 4%.

However, it was observed that this risk may be even higher in smoking patients. Cigarette smoking is the main risk factor for pancreatic neoplasia not associated with CP, and when the risks of mutated genes are added to smoking

Other mutations (such as CFTR and CTRC) do not seem to contribute to a significant increase in the incidence of pancreatic cancer. Just as other causes of CP, such as autoimmune pancreatitis or rarer causes, also do not confer a significant additional risk of neoplasia.

Although there is a higher incidence of ductal adenocarcinoma of the pancreas in the population with CP, there are no studies suggesting an efficient screening strategy for all patients. For patients with PRSS-1 mutations (or with suspicion of the mutation, in cases with more than two family members affected by CP) the international group recommends annual screening with imaging examination (computed tomography or magnetic resonance imaging). The use of echoendoscopy was not recommended, as it can be falsified by inflammation, fibrosis or calcifications. More studies are needed for recommendations regarding other mutations and other etiologies.

Despite recent advances, there is still a vast unknown field regarding the etiology and risk factors for CP, and more studies are needed so that we can unravel all the mysteries about this topic.

References

1. Singh, VK et al. Diagnosis and Management of Chronic Pancreatitis A Review. JAMA. 2019;322(24):2422-2434.
2. Hart, PA et al. Chronic Pancreatitis: Managing a Difficult Disease. Am J Gastroenterol. 2020 January ; 115(1): 49–55.
3. Aune, D et al. Tobacco smoking and the risk of pancreatitis: a systematic review and meta-analysis of prospective studies. Pancreatology, 2019 Dec;19(8):1009-1022.
4. Gardner, TB et al. ACG Clinical Guideline: Chronic Pancreatitis. Am J Gastroenterol 2020;115:322–339.
5. Le Cosquer, G et al. Pancreatic Cancer in Chronic Pancreatitis: Pathogenesis and Diagnostic Approach. Cancers 2023, 15, 761.
6. Greenhalf, G et al. International consensus guidelines on surveillance for pancreatic cancer in chronic pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club. Pancreatology 2020, 20, 910-918

How to cite this article

Marzinotto M. Chronic Pancreatitis – main etiologies and associated risk of Pancreatic Neoplasia Gastropedia 2023, vol 2. Available at: gastropedia.com.br/gastroenterologia/pancreatite-cronica-principais-etiologias-e-risco-associado-de-neoplasia-pancreatica/

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How can we diagnose portal hypertension?

The gold standard for defining portal hypertension is the measurement of the hepatic venous pressure gradient (HPVG). Values above 5mmHG define portal hypertension. When this gradient exceeds 10mmHg, we consider that portal hypertension is clinically significant (HPCS), with the patient prone to the appearance of decompensations. The presence of esophageal varices in patients diagnosed with cirrhosis also implies the presence of clinically significant portal hypertension regardless of the venous gradient measurement.

As the measurement of the hepatic venous pressure gradient is not a routine practice, in addition to being an invasive examination, it is admitted that, liver stiffness values ? 25 kPa obtained through transient hepatic elastography, are defining of HPCS, with specificity and positive predictive value > 90%. As it is a non-invasive examination, capable of providing such information, transient hepatic elastography has been increasingly used in the follow-up of compensated cirrhotic patients in order to provide data so that the pharmacological treatment of portal hypertension can be instituted early, without the need for serial endoscopies or even the measurement of the hepatic venous pressure gradient.

And what is the role of beta-blockers in the treatment of patients with liver cirrhosis?

Non-selective beta-blockers (propranolol, nadolol and carvedilol), have been used routinely, with proven benefits in the primary prophylaxis of bleeding from risk varices and as an adjunct in the secondary prophylaxis of varicose bleeding.

Patients at high risk for bleeding are those with thin-caliber esophageal varices with red color signs, medium and large caliber varices, gastric varices and decompensated patients in ascites with varices of any size.

Carvedilol is a non-selective beta-blocker, with alpha-1 blocking activity and appears to be more effective than traditional beta-blockers in reducing portal hypertension, having been recommended in the last Baveno VII consensus, as the beta-blocker of choice in the treatment of portal hypertension. Its currently recommended dose is 12.5mg/day, divided into two doses and patients should be monitored for their main adverse effects such as asthenia, dyspnea and low blood pressure (SBP< 90mmHG).

The PREDESCI study showed that the use of beta-blockers, especially carvedilol, in cirrhotic patients with clinically significant portal hypertension (HPVG> 10mmHG) reduced the chance of decompensation in ascites by up to 40% in a subgroup of patients with thin-caliber varices without red color signs, implying an improvement in survival.

The use of beta-blockers in patients with portal hypertension without varices has no clearly proven benefits. Pre-primary prophylaxis, that is, the use of this medication in compensated cirrhotic patients, did not show benefit in the appearance of varices, however, the use in patients with HPCS, even in the absence of varices, has been an increasingly routine practice, suggested in the latest consensuses, with the aim of reducing long-term decompensation.

In summary…

In patients diagnosed with liver cirrhosis, the use of beta-blockers, preferably carvedilol, is indicated in:

• patients without ascites with thin-caliber esophageal varices without red color signs – for prevention of decompensation in ascites;
• decompensated patients in ascites with thin-caliber esophageal varices without red color signs – for primary prophylaxis of bleeding;
• thin-caliber varices with red color signs, medium and large caliber varices and gastric varices– as primary prophylaxis;
• thin-caliber varices with red color signs, medium and large caliber varices and gastric varices – as secondary prophylaxis associated with elastic ligation;
• recurrent bleeding from portal hypertensive gastropathy;
• patients with clinically significant portal hypertension ( LMS ? 25 kPa).

References

1. Turco L, Reiberger T, Vitale G, La Mura V. Carvedilol as the new non-selective beta-blocker of choice in patients with cirrhosis and portal hypertension. Liver Int. 2023 Jun;43(6):1183-1194. doi: 10.1111/liv.15559. Epub 2023 Apr 17. PMID: 36897563.
2. Wong YJ, Zhaojin C, Tosetti G, Degasperi E, Sharma S, Agarwal S, Chuan L, Huak CY, Jia L, Xiaolong Q, Saraya A, Primignani M. Baveno-VII criteria to predict decompensation and initiate non-selective beta-blocker in compensated advanced chronic liver disease patients. Clin Mol Hepatol. 2023 Jan;29(1):135-145. doi: 10.3350/cmh.2022.0181. Epub 2022 Sep 5. PMID: 36064306; PMCID: PMC9845679.
3. Gralnek IM, Camus Duboc M, Garcia-Pagan JC, Fuccio L, Karstensen JG, Hucl T, Jovanovic I, Awadie H, Hernandez-Gea V, Tantau M, Ebigbo A, Ibrahim M, Vlachogiannakos J, Burgmans MC, Rosasco R, Triantafyllou K. Endoscopic diagnosis and management of esophagogastric variceal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline. Endoscopy. 2022 Nov;54(11):1094-1120. doi: 10.1055/a-1939-4887. Epub 2022 Sep 29. PMID: 36174643.
4. de Franchis R, Bosch J, Garcia-Tsao G, Reiberger T, Ripoll C; Baveno VII Faculty. Baveno VII – Renewing consensus in portal hypertension. J Hepatol. 2022 Apr;76(4):959-974. doi: 10.1016/j.jhep.2021.12.022. Epub 2021 Dec 30. Erratum in: J Hepatol. 2022 Apr 14;: PMID: 35120736.
5. Katarey D, Jalan R. Non-selective beta blockers in cirrhosis: time to extend the indications? Ann Transl Med. 2019 Dec;7(Suppl 8):S355. doi: 10.21037/atm.2019.09.56. PMID: 32016073; PMCID: PMC6976476.
6. Villanueva C, Albillos A, Genescà J, Garcia-Pagan JC, Calleja JL, Aracil C, Bañares R, Morillas RM, Poca M, Peñas B, Augustin S, Abraldes JG, Alvarado E, Torres F, Bosch J. ? blockers to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension (PREDESCI): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet. 2019 Apr 20;393(10181):1597-1608. doi: 10.1016/S0140-6736(18)31875-0. Epub 2019 Mar 22. Erratum in: Lancet. 2019 Jun 22;393(10190):2492. PMID: 30910320.
7. Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology. 2017 Jan;65(1):310-335. doi: 10.1002/hep.28906. Epub 2016 Dec 1. Erratum in: Hepatology. 2017 Jul;66(1):304. PMID: 27786365

How to cite this article

Ramos JSD, When is the use of beta-blockers recommended in patients with liver cirrhosis? Gastropedia 2023 Vol 2. Available at: gastropedia.com.br/gastroenterology/when-is-the-use-of-beta-blockers-recommended-in-patients-with-liver-cirrhosis/

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Gallbladder polyps are usually incidental findings diagnosed during abdominal ultrasound exams or during cholecystectomy. They usually do not present symptoms, but occasionally they can cause discomforts similar to those caused by gallstones.

Most of these lesions are not neoplastic, but rather hyperplastic or represent lipid deposits.

With the widespread use of ultrasound, polypoid lesions in the gallbladder are being increasingly detected. However, often the image is not enough to rule out the possibility of neoplasia or pre-malignant adenomas. In this article, we will review the clinical importance and differential diagnosis of gallbladder polyps.

Classification

Polypoid lesions in the gallbladder can be categorized as benign or malignant. Benign lesions can be subdivided into neoplastic and non-neoplastic.

Non-neoplastic benign polyps

The most common benign non-neoplastic lesions are cholesterol polyps, followed by adenomyomatosis and inflammatory polyps.

• Cholesterol polyps and cholesterosis:
  • it is a benign condition characterized by the accumulation of lipids in the mucosa of the gallbladder wall.
  • they are the most common types of gallbladder polyps, reaching up to 10% or more.
  • It can be of the diffuse or polypoid type.
  • The term cholesterosis refers to the diffuse type, which is usually diagnosed incidentally during cholecystectomy, causing the appearance of a “strawberry gallbladder” due to the contrast it makes with the gallbladder mucosa.
  • Cholesterol polyps are the polypoid form of cholesterosis, being the most common gallbladder polyp, usually diagnosed incidentally on ultrasound.
  • Although usually asymptomatic, in some patients it can cause symptoms and complications similar to those caused by gallstones.
• Adenomyomatosis:
  • it is an abnormality of the gallbladder characterized by excessive growth of the mucosa, thickening of the muscular wall and intramural diverticula.
  • The prevalence of gallbladder adenomyosis is low, but it appears to have a higher prevalence in women than in men.
• Inflammatory polyps
  • Inflammatory polyps are the least common non-neoplastic polyps.
  • They appear as sessile or pedunculated and are composed of granulation and fibrous tissue with plasma cells and lymphocytes.
  • The polyps are usually 5 to 10 mm in diameter, although inflammatory polyps larger than 1 cm have been described

Neoplastic benign polyps

• Adenomas:
  • Adenomatous polyps of the gallbladder are the most common benign neoplastic lesions. Although the true incidence is unknown, in most series it is less than 0.5 percent.
  • Gallbladder adenomas are benign epithelial tumors composed of cells that resemble the epithelium of the bile ducts.
  • The risk of cancer increases with the size of the polyp, with larger adenomatous polyps having a risk of malignancy.
• Others — Other neoplastic lesions of the gallbladder such as fibromas, lipomas and leiomyomas, are rare. The natural history of these polyps is not well defined.

Malignant polyps:

• Most malignant polyps in the gallbladder are adenocarcinomas.
• The adenocarcinomas of the gallbladder are much more common than gallbladder adenomas, unlike the colon, where adenomas are much more common than adenocarcinomas.
• Squamous cell carcinoma, mucinous cystadenoma and gallbladder adenoacanthomas are rare

CANCER RISK

Most gallbladder polyps are benign, and most benign polyps, with the exception of adenomas, do not have malignant potential. The overall risk of gallbladder cancer in patients with gallbladder polyps appears to be low.

• In a large cohort study with over 35,000 adults with gallbladder polyps diagnosed by USG, 0.053% had gallbladder cancer, similar to the population without polyps (0.054%). [ref]
• The risk of progression to neoplasia varies according to the size of the polyps, occurring in 128/100,000 people for polyps > 10mm, but only in 1.3/100,000 people for polyps < 6mm.

Established risk factors for cancer

• Polyp size — The incidence of gallbladder cancer varies from 43 to 77% in polyps larger than 1 cm and 100% in polyps larger than 2 cm.
• Sessile polyp — sessile polyps are an independent risk factor for malignancy, with a 7x higher risk of gallbladder cancer. [ref]
• Age > 60 years: this is the cut-off adopted in guidelines for risk stratification and treatment guidance.
• Others: Indian ethnicity, primary sclerosing cholangitis

Conditions with uncertain risk

• Concomitant gallstones
• Adenomyomatosis — There is no evidence that the presence of adenomyosis increases the risk of gallbladder cancer. If the risk is increased, the magnitude of the increase appears to be small.

DIAGNOSIS

Gallbladder polyps are usually discovered incidentally on abdominal ultrasound exams. None of the available imaging modalities can unequivocally distinguish benign from malignant polyps. This can only be confirmed by histopathology after cholecystectomy.

Characteristics of gallbladder polyps on abdominal ultrasound:

• They can be single or multiple
• Sensitivity 84% and specificity 96% (meta-analysis with 16,260 patients)
• CHOLESTEROL POLYPS are usually multiple, homogeneous, polypoid and pedunculated, with echogenicity greater than the liver parenchyma.
  • They may or may not contain hyperechoic points.
  • Cholesterol polyps usually measure less than 1 cm.
  • In contrast to cholesterol polyps, diffuse cholesterosis does not have specific ultrasonographic findings, and its diagnosis is usually made after surgery.
• ADENOMAS are homogeneous lesions, isoechoic in relation to the liver parenchyma, have a smooth surface and usually do not have a pedicle.
  • The sessile morphology and focal thickening of the gallbladder wall greater than 4 mm are risk factors for malignancy.
• ADENOCARCINOMAS are homogeneous or heterogeneous polypoid structures that are usually isoechoic in relation to the liver parenchyma.
• The ADENOMYOMATOSIS can also cause a diffuse thickening with round anechoic f

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Patients with a IBD (Inflammatory Bowel Disease) moderate to severe phenotype and/or with risk factors for a worse prognosis, once elected for advanced therapy with biologics, should undergo preparation for the start of treatment safely.

This stage involves the evaluation of 3 pillars:

• Check if there is a relative or absolute contraindication to the use of such medications;
• Screening for active or latent infections;
• Updating vaccination status

Regarding contraindications or signs of greater attention to the use of biologics, we have:

• Severe ongoing infection, including perianal abscess;
• Untreated latent tuberculosis (a period from the start of treatment should be awaited to start the biologic, preferably a non-anti-TNF);
• Decompensated CHF or EF ? 35% (absolute contraindication to anti-TNF);
• History of severe previous infusion reaction to biologics;
• Multiple sclerosis or other demyelinating diseases; optic neuritis; previous lymphoma (in these conditions anti-TNF has an absolute contraindication, the others weigh risk x benefit);
• Current malignancy;
• Decompensated liver disease (cirrhosis Child B or C);
• Untreated chronic infection by the hepatitis B virus;
• Uncontrolled HIV infection;
• History of melanoma (absolute contraindication to anti-TNF) or recurrent cervical dysplasia (relative contraindication to anti-TNF)

The next step is to carry out the infectious screening, which includes:

• Chest X-ray;
• PPD and/or IGRA (interferon gamma release test);
• Serologies for hepatitis B, C and HIV (also consider adding screening for measles, CMV, varicella zoster and Epstein-Barr – note that primary EBV infection in immunosuppressed patients increases the risk of lymphoproliferative diseases, in this scenario caution should be exercised when prescribing associated thiopurines);
• In the presence of diarrhea, exclude the presence of Clostridium difficile as a mimicking agent;
• In the female population, colpocytology is also recommended for HPV infection screening.

The screening for latent TB should be renewed annually while the patient is using the biologic, especially if it is of the anti-TNF class, as we know how much TNF-alpha is crucial for granuloma stability.

In the case of patients with PPD ? 5mm, or IGRA + or sequelae on chest X-ray suggestive, first the treatment of latent TB should be started and only start the biologic after 30 days from the start of treatment.

Patients with HBsAg + or with isolated anti-HBc + should receive antiviral therapy during the use of biologics or oral immunosuppressants. In the first case, the treatment time will be guided by liver disease. In the second case (hidden infection), for at least 6 months after the end of treatment (if applicable).

Vaccination status

Regarding the vaccination schedule, inactivated vaccines are extremely safe and indicated for all patients with IBD, and ideally should be administered at least 2 weeks before the biologic, so as not to compromise the vaccine response. The attenuated vaccines are contraindicated for patients who are already using immunosuppressants or biologics, or who are planning to start such medications in the next 4 to 6 weeks. They can only use attenuated vaccines after 3 months of suspension of such medications (if applicable).

The inactivated vaccines to be considered in patients with IBD are: Influenza, Pneumococcal, Tetanus/Diphtheria (Adult Double), Meningococcal, Hepatitis A, Hepatitis B (including possibly making 4 double doses aiming for anti-HBs >10), HPV, COVID-19. Recently, the recombinant inactivated herpes zoster vaccine was also launched, allowing use to patients in immunosuppression or planning to start biologics, unlike the vaccine available until then which was attenuated virus.

Reinforcing, the attenuated vaccines that should not be done in the scenario of immunosuppressed patients are: MMR (measles, mumps and rubella), varicella, yellow fever and the older version of the herpes zoster vaccine composed of live attenuated virus.

References:

1. T. Kucharzik et al. ECCO Guidelines on the Prevention, Diagnosis, and Management of Infections in Inflammatory Bowel Disease. Journal of Crohn’s and Colitis, 2021, 879–913
2. Chebli JMF et al. Preparing Patients With Inflammatory Bowel Diseases For Biological Therapies In Clinical Practice. Journal of Gastroenterology and Hepatology Research 2018; 7(2): 2535-2554
3. Beaugerie et al. Predicting, Preventing, and Managing Treatment-Related Complications in Patients With Inflammatory Bowel Diseases. Clinical Gastroenterology and Hepatology 2020;18:1324–1335
4. S. Riestra et al. Recommendations of the Spanish Working Group on Crohn’s Disease and Ulcerative Colitis (GETECCU) on screening and treatment of tuberculosis infection in patients with inflammatory bowel disease. Gastroenterología y Hepatología 44 2021 51—66
5. R. Ferreiro-Iglesias et al. Recommendations of the Spanish Group on Crohn’s Disease and Ulcerative Colitis on the importance, screening and vaccination in inflammatory bowel disease patients. Gastroenterología y Hepatología 45 (2022) 805—818

How to cite this article

Vilela PBM, Check-list to start biological therapy in IBD Gastropedia 2023, Vol 2. Available at: gastropedia.com.br/sem-categoria/check-list-para-iniciar-terapia-biologica-na-dii/

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The situation I want to put here is that of a patient with cholestatic syndrome due to non-biopsied periampullary malignant neoplasia. He had a very good status, a totally independent athlete for daily activities and with little weight loss even in the presence of symptoms of food intolerance.

Not meeting criteria for neoadjuvant (borderline)¹ and without evidence of metastatic lesions in the staging performed, a resection was chosen as the first treatment (upfront) which took place about 1 month after the first contact with the surgeon.

I expose the intraoperative photo:

The subcentimetric lesion highlighted was resected and sent for freezing biopsy. The finding was malignant neoplasia in the sample sent.

There are several factors at this decision-making moment that induce us to proceed with the surgery: the fallibility of intraoperative freezing, the fact that this patient – the exception of most cases attended in this context – is so physically and nutritionally fit for surgery, the confidence and optimism transmitted in consultation to the patient and family in the face of the precocity of surgical treatment, the experience of previous cases that were “successful”.

For this reason, I share the following studies that aimed to define the real prognosis of this patient.

What do the studies say?

In the first² patients undergoing pancreatectomies associated with hepatic resections at an internationally renowned center were retrospectively analyzed.

The sample size (22 patients) is criticizable and is probably a consequence of high patient selection. This selection is also proven in the sample details: average size of the metastasis (0.6 cm), hepatic resections were mostly nodulectomies. In addition, all cases were similar to ours, an incidental intraoperative finding.

For control, two groups were designated: 1 – conventional resection with the same primary site without association with hepatic metastasis and 2 – palliative surgery performed in the face of hepatic metastasis (bili-digestive + food diversion). The comparison showed interesting but not unexpected results: at a cost of a higher rate of complications, bleeding and length of stay, there was no benefit in the survival of these patients in the long term compared to palliative surgery. It is worth noting that, as in our situation, we are comparing a group selected by optimism, by the expectation of better evolution compared to the usual.

I also highlight this more recent systematic review³ showing a similar survival between patients who underwent combined surgery in the proposed context and patients referred for palliative chemotherapy after metastasis detection in staging (not submitted to surgery). In selected patients, after chemotherapy and systemic control, the survival provided by the same surgery was 3 to 4 times greater.

Conclusion

As seen above, we are not lacking examples that in a few patients the surgery initially thought (resection of hepatic metastasis + duodenopancreatectomy) can bring benefit in survival⁴. However, at the time of surgery this individual has not yet gone through this selection of systemic treatment and, therefore, we do not yet know if he is – or better – will be one of these cases. Therefore, on that day, we proceeded with the bili-digestive diversion – thus solving the biliary obstruction – associated with food diversion due to the food symptoms alleged.

For those who would choose to proceed with the procedure, I invite you to reflect: no matter how optimistic our expectation, our intention and attitude remain subject to data and statistics. Our main function during our patient’s journey is to advise him to take the most advantageous path and not just hope for the best result.

After all, there are less risky surgeries that relieve symptoms and provide a systemic treatment without complications for our patient. In this way, in the light of current knowledge, he will remain with a higher quality of life and for a longer time outside the hospital environment. Remembering that definitive treatment will not cease to be an option if it proves adequate over its evolution.

References

1. Isaji, S. et al. International consensus on definition and criteria of borderline resectable pancreatic ductal adenocarcinoma 2017. Pancreatology 18, 2–11 (2018).
2. Gleisner, A. L. et al. Is resection of periampullary or pancreatic adenocarcinoma with synchronous hepatic metastasis justified? Cancer 110, 2484–2492 (2007).
3. Crippa, S. et al. A systematic review of surgical resection of liver-only synchronous metastases from pancreatic cancer in the era of multiagent chemotherapy. Updates Surg. 72, 39–45 (2020).
4. Nagai, M. et al. Oncologic resection of pancreatic cancer with isolated liver metastasis: Favorable outcomes in select patients. J. Hepatobiliary. Pancreat. Sci. 1–11 (2023) doi:10.1002/jhbp.1303.

How to cite this article

Magalhães DP. Periampullary neoplasia with isolated hepatic metastasis: what would you do? Gastropedia, vol. 2 Available at: gastropedia.com.br/cirurgia/neoplasia-periampular-com-metastase-hepatica-isolada-o-que-voce-faria/

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However, some patients have locally advanced tumors that cannot be resected. The incidence of these varies in the literature from 5 to 30% of GC cases. In these cases, gastrointestinal bypass procedures or the use of endoscopic prostheses may be indicated to improve quality of life, relieve symptoms of gastric obstruction, and thus enable the administration of palliative treatment.

The use of endoscopic prostheses has gained popularity for the palliation of digestive tract obstructions, as it has the advantage of being a less invasive option and without the need for use of the operating room with general anesthesia. However, the multicenter randomized study (Sustent Study) reported worse long-term results with the use of the prosthesis compared to gastrojejunostomy. Factors such as prosthesis migration, tumor growth causing new obstruction, and gastric wall erosion, are long-term complications that impair the observed results. Another aggravating factor refers to the cost and immediate unavailability of prostheses by the public system in our country. Currently, the prosthesis is mainly indicated in patients with low clinical performance by the Eastern Cooperative Oncology Group (ECOG) scale, and with a life expectancy of less than 2 months.

Regarding bypass surgical procedures, the most used is gastrojejunostomy, also called gastroentero anastomosis. Gastrojejunostomy consists of performing anastomosis with a wide extension of the posterior wall of the stomach with the first jejunal loop that reaches the stomach without tension (Figure 1). The anastomosis can be performed manually or mechanically, with the use of surgical staplers.

Despite the technical simplicity of performing gastrojejunostomy, a major inconvenience observed in practice is the difficulty of gastric emptying through the anastomosis after the procedure. Literature data refer that 10 to 26% of patients present this complication, as shown in Figure 1. Such occurrence can lead to an increase in hospitalization time and delay the start of palliative chemotherapy, fundamental to prolong survival.

Another inconvenience of this procedure is the maintenance of the tumor in contact with the food ingested by the patient, since the exposure of the tumor predisposes the occurrence of tumor bleeding. Finally, there is also the risk of obstruction of the gastrojejunostomy by the growth of the tumor that is located near the anastomosis, and can thus invade it. This fear can lead the surgeon to perform the anastomosis in a more proximal portion of the gastric body, which further impairs gastric emptying.

With the aim of overcoming these inconveniences, the performance of a partial partition of the stomach associated with gastrojejunostomy in the proximal gastric chamber has been indicated for non-resectable obstructive distal tumors. The rationale for performing the partition involves creating a gastric chamber of smaller dimensions facilitating emptying by gastrojejunostomy and excluding the tumor in the distal chamber reducing the risk of bleeding and preventing the infiltration of the anastomosis by the tumor.

Technical steps of gastric partition

After identifying the proximal limits of the lesion, a point located 3 to 5 cm proximal to the lesion on the greater curvature is selected to start the partition (Figure 2).

A Faucher tube nº 32 or a large nasogastric tube is passed and maintained along the lesser gastric curvature to maintain communication between the two gastric chambers created by the partition (Figure 3). The partial partition of the stomach is performed using a cutting linear stapler.

Subsequently, the gastrojejunostomy is performed in a position anterior to the colon, isoperistaltic in the posterior wall of the stomach with at least 5 cm of extension, using the first jejunal loop about 30-40 cm from the Treitz angle (Figure 4).

The anastomosis can be performed manually or with the use of a cutting linear stapler. The access route can be conventional or laparoscopic, according to the surgeon’s preference.

It is important to note that in cases of proximal tumors or with involvement of the proximal lesser curvature to the angular incisura the partition should be avoided due to the risk of obstruction of the communication between the gastric chambers.

How to cite this article

Ramos MFKP, Gastric partition for the treatment of non-resectable obstructive distal gastric tumors. Gastropedia 2023 Vol 1. Available at: gastropedia.com.br/sem-categoria/particao-gastrica-para-tratamento-de-tumores-gastricos-distais-obstrutivos-nao-ressecaveis/

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Squamous cell carcinoma of the anus and anal canal has a low incidence in the general population (1-2/100,000 people-year). However, when associated with risk factors such as co-infection with HIV, men who have sex with men (MSM), presence of high-grade lesions or carcinoma in the genitals and immunosuppression, this risk can increase considerably:

Anus and anal canal cancer can be screened with a complete proctological examination, with inspection and rectal touch, followed by anoscopy with biopsy in suspicious lesions (3).

High-grade anal intraepithelial lesions (high-grade AIN), as occurs in the cervix, can be identified through exams such as oncotic cytology or genotyping for high-risk oncogenic HPV obtained through the anal smear (Anal-Pap).

When these results come altered, the patient should be referred for a high-resolution anoscopy examination or anoscopy with image magnification, which resembles a colposcopy examination of the anus and anal canal region. Through this examination, it is possible to identify lesions suspicious for high-grade AIN, which, when identified through a biopsy, should be treated, through chemical cauterization or electrocautery or with infrared laser (4)

ANCHOR trial

• Until recently, there was not a robust degree of evidence to indicate the screening and treatment of high-grade anal intraepithelial lesions as a method of prevention for anal and anal canal cancer (2).
• However, in 2022 the results of the ANCHOR trial, (Anal Cancer HSIL Outcomes Research) (5) a prospective multicenter randomized study that evaluated 4446 people living with HIV who were followed up with cytology exams and high-resolution anoscopy were published in the NEJM.
• When high-grade anal intraepithelial lesions (AIN 2 p16+ or AIN3) were identified, the participants were randomized into two groups: one in which these lesions would be treated and another in which these lesions would be followed up every 6 months.
• The rate of progression to anal cancer was 53% lower in the treated group than in the group only followed up (p= 0.03).

Conclusion

• Anus and anal canal cancer is quite rare and should not be screened in the general population.
• Its incidence increases considerably in certain populations such as: people living with HIV, men who have sex with men, women with a history of cancer or high-grade lesions in the genitals and diseases or treatments that course with immunosuppression, which justifies screening in these groups.
• The identification and treatment of high-grade anal intraepithelial lesions in people living with HIV has proven effective in preventing anal and anal canal cancer.

References

1. Clifford, Gary M., et al. “A meta-analysis of anal cancer incidence by risk group: toward a unified anal cancer risk scale.” International journal of cancer 148.1 (2021): 38-47.
2. Stewart, David B., et al. “The American Society of Colon and Rectal Surgeons clinical practice guidelines for anal squamous cell cancers (revised 2018).” Diseases of the Colon & Rectum 61.7 (2018): 755-774.
3. Hillman, Richard John, et al. “International Anal Neoplasia Society guidelines for the practice of digital anal rectal examination.” Journal of lower genital tract disease 23.2 (2019): 138-146.
4. Hillman, Richard John, et al. “2016 IANS international guidelines for practice standards in the detection of anal cancer precursors.” Journal of lower genital tract disease 20.4 (2016): 283-291
5. Palefsky, Joel M., et al. “Treatment of anal high-grade squamous intraepithelial lesions to prevent anal cancer.” New England Journal of Medicine 386.24 (2022): 2273-2282.

How to cite this article

Ribeiro VL. Screening of anal intraepithelial neoplasia and prevention of anal cancer. Gastropedia 2023, vol. 1. Available at: https://gastropedia.com.br/sem-categoria/rastreamento-de-neoplasia-intrapeitelial-anal-e-prevencao-de-cancer-de-anus/

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