Thyroid Nodules in Children With Familial Adenomatous Polyposis.

INTRODUCTION: Ultrasound screening for thyroid cancer is recommended in familial adenomatous polyposis (FAP). This study investigated the prevalence of thyroid neoplasia in children with FAP. METHODS: Cross-sectional study of children with FAP at an academic hospital. Clinical and ultrasound data were analyzed for the prevalence of thyroid nodules and cancer. RESULTS: Of 37 children with FAP, 8 (22%) had thyroid nodules and 2 (5%) had thyroid cancer. Nodules (30%) and cancer (9%) were more common among female subjects and rare among male subjects. DISCUSSION: Thyroid ultrasound screening in adolescence may benefit female subjects with FAP but has limited utility in male subjects.

Mutational screening through comprehensive bioinformatics analysis to detect novel germline mutations in the APC gene in patients with familial adenomatous polyposis (FAP).

BACKGROUND: Familial adenomatous polyposis (FAP) as a colon cancer predisposition syndrome is an autosomal-dominant inherited condition and is diagnosed by the progress of hundreds or thousands of adenomatous colonic polyps in the colon. This study aims at the nature and effect of Adenomatous Polyposis Coli (APC) gene mutations in FAP tumorigenesis. METHODS: The genetic screening of 59 FAP Iranian patients in 10 families was performed by polymerase chain reactions and the direct sequencing of the entire coding exons of the APC gene. To do linkage haplotype analysis and multiplex PCR-based microsatellite examination, six short tandem repeat loci were selected in this gene. To evaluate and predict the potentially deleterious effects, comprehensive bioinformatics pathogenicity assays were used. RESULTS: A total of 12 germline heterozygous and homozygous nucleotide variations were identified. They included two missense mutations, four nonsense mutations, which would lead to the truncated and nonfunctional protein products, four synonymous or silent variations, and two nucleotide deletions of 1 to 5 bp or frameshift mutations. In addition, three novel heterozygous nonsense mutations were found in exons 10, 14, and 15 of the gene. There was also p.Arg653Met as a novel heterozygote mutation in exon 14 of the gene. CONCLUSIONS: Bioinformatics analysis and three-dimensional structural modeling predicted that these missense and nonsense mutations generally are associated with the deleted or truncated domains of APC and have functional importance and mainly affected the APC protein. These findings may provide evidence for the progress of potential biomarkers and help to understand the role of the APC gene in FAP.

Resorting the function of the colorectal cancer gatekeeper adenomatous polyposis coli.

As a large number of cancers are caused by nonsense mutations in key genes, read-through of these mutations to restore full-length protein expression is a potential therapeutic strategy. Mutations in the adenomatous polyposis coli (APC) gene initiate the majority of both sporadic and hereditary colorectal cancers (CRC) and around 30% of these mutations are nonsense mutations. Our goal was to test the feasibility and effectiveness of APC nonsense mutation read-through as a potential chemo-preventive therapy in Familial Adenomatous Polyposis (FAP), an inherited CRC syndrome patients. Ten FAP patients harboring APC nonsense mutations were treated with the read-through inducing antibiotic erythromycin for 4 months. Endoscopic assessment of the adenomas was performed at baseline, after 4 and after 12 months. Adenoma burden was documented in terms of adenoma number, maximal polyp size and cumulative polyp size per procedure. Tissue samples were collected and subjected to molecular and genetic analyses. Our results show that in the majority of patients the treatment led to a decrease in cumulative adenoma burden, median reduction in cumulative adenoma size and median reduction in adenoma number. Molecular and genetic analyses of the adenomas revealed that the treatment led to a reduced number of somatic APC mutations, reduced cellular proliferation and restoration of APC tumor-suppressing activity. Together, our findings show that induced read-through of APC nonsense mutations leads to promising clinical results and should be further investigated to establish its therapeutic potential in FAP and sporadic CRCs harboring nonsense APC mutations.

Surveillance for pathology associated with cancer on endoscopy (SPACE): criteria to identify high-risk gastric polyps in familial adenomatous polyposis.

BACKGROUND AND AIMS: Gastric cancer is an extracolonic manifestation of familial adenomatous polyposis (FAP) and is associated with high-risk gastric polyps. There are no known endoscopic criteria to identify these high-risk polyps. Our aim was to develop endoscopic criteria to identify high-risk polyps on endoscopy in FAP. METHODS: We prospectively collected 150 gastric polyps in consecutive patients undergoing surveillance EGD at the Cleveland Clinic. Pictures were taken of each polyp under narrow-band imaging and high-definition white light. In an exploratory phase, 5 endoscopists developed consensus criteria using the images to distinguish high-risk (pyloric gland adenoma, tubular adenoma, hyperplastic) from low-risk (fundic gland with low-grade or no dysplasia) polyps. In the assessment phase, endoscopists were blinded to polyp pathology and used the criteria to predict the individual polyp risk category. To measure diagnostic accuracy, we reported the mean sensitivity, specificity, and interrater agreement (κ). RESULTS: Consensus criteria were developed based on 16 low-risk and 9 high-risk polyps. The final 149 polyps consisted of 128 low-risk and 22 high-risk polyps (1 polyp was excluded from analysis). Using the criteria, the 5 endoscopists distinguished high- from low-risk polyps with a mean sensitivity and specificity of 79% (16.3%) and 78.8% (10.8%), respectively. The κ coefficient was .45, indicating moderate agreement. CONCLUSIONS: We developed endoscopic criteria to distinguish between high- and low-risk polyps associated with gastric cancer in FAP. The criteria provide guidance to endoscopists in targeting high-risk polyps while surveying the stomach of patients with proximal gastric polyposis.

Sessile Serrated Polyposis: Not an Inherited Syndrome?

BACKGROUND: Researchers are searching in vain for a coherent genetic explanation for serrated polyposis. We hypothesize that there is no consistent monogenetic inheritance. OBJECTIVE: The purpose of this study was to describe the serrated polyposis phenotype, assessing features of mendelian inheritance, and to compare these features with patients with a solitary sessile serrated lesion. DESIGN: This was a retrospective review of a prospectively maintained database comparing patients with serrated polyposis versus solitary sessile serrated lesions. SETTINGS: The study was conducted at a single-institution tertiary referral center. PATIENTS: Patients with serrated polyposis meeting World Health Organization criteria type I (≥5 serrated polyps proximal to the sigmoid, ≥2 of which are ≥10 mm in diameter) and isolated sessile serrated lesions were included MAIN OUTCOME MEASURES:: Disease phenotype was the main outcome measured. RESULTS: A total of 46 serrated polyposis patients were identified. Median age of first sessile serrated lesion was 66 years (interquartile range, 42-70 y). A total of 60.3% were current or past smokers (mean = 38.6 packs per year). Serrated polyposis patients had a higher number of all types of polyps (26.3 vs 4.4) and a higher rate of high-grade dysplasia (19.6% vs 3.7%) compared with patients with a solitary sessile serrated lesion. A total of 36.2% of patients had personal history of noncolorectal cancers, including skin, prostate, breast, thyroid, and renal cell cancers and leukemia. In addition, 32.6% had a family history of colorectal cancer in first- or second-degree relatives; these cancers were not young age of onset. Breast and prostate cancers were also common (family history of any cancer, 83.0%). Ten patients underwent genetic testing: 4 had negative panels, 1 had a pathogenic variant in MSH2, 1 an IVS7 deletion in PTEN, 2 negative APC sequencing (1 negative MYH), and 1 a pathogenic variant in Chek2. LIMITATIONS: RNF4 was not sequenced. Genetic analysis was performed on a subset of patients. CONCLUSIONS: The rate of associated cancers suggests an underlying genetic predisposition to disordered growth, but serrated polyposis does not have typical features of dominant inheritance. The association with smoking suggests that familial/environmental factors play a role. See Video Abstract at http://links.lww.com/DCR/B84. POLIPOSIS SERRADA SÉSIL: ¿NO ES UN SÍNDROME HEREDITARIO?: Los investigadores están buscando en vano una explicación genética coherente para la póliposis serrados. Suponemos que no existe una herencia monogenética consistente.1) Describir el fenotipo de póliposis serrada, evaluando las características de la herencia mendeliana, 2) comparar estas características con pacientes con una lesión serrada sésil solitaria.Revisión retrospectiva de una base de datos mantenida prospectivamente que compara pacientes con póliposis serrada versus lesiones serradas sésiles solitarias.Institución única, centro de referencia terciario.Pacientes con póliposis serrada que cumplen con los Criterios de la Organización Mundial de la Salud Tipo I (≥ 5 pólipos serrados proximales al sigmoideo, ≥2 de los cuales tienen ≥10 mm de diámetro) y lesiones serradas sésiles aisladas.Fenotipo de la enfermedad.Se identificaron un total de 46 pacientes con póliposis serrada. La edad mediana de la primera lesión serrada sésil fue de 66 años (RIC: 42-70 años). El 60.3% eran fumadores actuales o pasados (medio 38.6 paquetes / año). Los pacientes con póliposis serrada tuvieron un mayor número de todos los tipos de pólipos (26.3 versus 4.4) y una mayor tasa de displasia de alto grado (19.6% versus 3.7%) en comparación con los pacientes con una lesión serrada sésil solitaria. El 36.2% de los pacientes tenían antecedentes personales de cánceres no colorectales, incluyendo los cánceres de piel, próstata, mama, tiroides, células renales y leucemia. El 32.6% tenía antecedentes familiares de cáncer colorectal en familiares de primer o segundo grado; estos cánceres no eran de inicio de edad temprana. El cáncer de mama y próstata también fue frecuente (antecedentes familiares de cualquier tipo de cáncer: 83.0%). 10 pacientes se sometieron a pruebas genéticas: 4 tenían paneles negativos, 1 tenía una variante patogénica en MSH2, 1 una eliminación IVS7 en PTEN, 2 secuenciación APC negativa (1 MYH negativa) y 1 variante patogénica en Chek2.RNF4 no fue secuenciado. El análisis genético se realizó en un subconjunto de pacientes.La tasa de cánceres asociados sugiere una predisposición genética subyacente al crecimiento desordenado, pero la póliposis serrada no tiene características típicas de herencia dominante. La asociación con el tabaquismo sugiere que los factores familiares / ambientales juegan un papel. Consulte Video Resumen en http://links.lww.com/DCR/B84. (Traducción-Dr. Yesenia Rojas-Khalil).

Colonic Surgery in Patients With Familial Adenomatous Polyposis.

CASE SUMMARY: A 34-year-old woman is referred after a colonoscopy that revealed >100 polyps throughout her colon and rectum (). A random selection of 3 polyps is biopsied and reported as adenomas. She is adopted and is unaware of her biological family. She is found to have a deleterious germline variant in APC (c.1967-1974del). She works as a nurse and is married with 4 children (age: 17, 13, 11, and 6 years). She has had no prior abdominal operations.

Assessment of Duodenal Adenomas and Strategies for Curative Therapy.

BACKGROUND: The increasing incidence of duodenal neoplasm has underlined different methods of resection depending on the clinical presentation, endoscopic features and histopathology. In this comprehensive review, we systematically describe the current knowledge concerning the diagnosis and management of duodenal adenomas (DAs) and discuss data considering all possible therapeutic approaches. SUMMARY: Among a variety of duodenal lesions, including neuroendocrine tumors and gastrointestinal stromal tumors, DAs present precancerous lesions of the duodenal papilla or non-ampullary region necessitating removal. DAs can occur sporadically (SDA) as rare lesions or relatively common in polyposis syndromes. The endoscopic resections of DA are associated with an increased degree of complexity due to distinctive anatomical properties of the duodenal wall, luminal diameter and the presence of ampulla with pancreatic and biliary drainage. The endoscopic techniques including cold snare polypectomy (CSP), endoscopic mucosal resection (EMR), and argon plasma coagulation ablation are suggested to be less invasive than surgical treatment, associated with shorter hospital stay and lower cost. According to the current clinical practice, surgery has been accepted as standard therapeutic approach in familial adenomatous polyposis patients with severe polyposis or DA not amenable to endoscopic resection. Key Messages: The strategy for endoscopic resection of DAs depends on the lesion size, morphology, location, and histopathology findings. Small adenomas are most frequently diagnosed and removed by standard CSP techniques, while large laterally spreading lesions and ampullary adenoma are referred for EMR or endoscopic papillectomy respectively. Screening colonoscopy is indicated in patients with SDA. Additional studies for new endoscopic strategies and techniques for curative therapy of DAs are needed to refine future management decisions. Complete resection of DA is considered curative, but nevertheless, long-term endoscopic follow-up is still required to detect and treat any recurrent arising lesions.

Web-Based Model for Predicting Time to Surgery in Young Patients with Familial Adenomatous Polyposis: An Internally Validated Study.

INTRODUCTION: The timing of prophylactic colorectal surgery in patients with familial adenomatous polyposis (FAP) is based on the immediacy of the colorectal cancer risk. The ability to predict the need for surgery may help patients and their families plan in the context of life events and CRC risk. We created a model to predict the likelihood of surgery within 2 and 5 years of first colonoscopy at our institution. METHODS: A single institution hereditary colorectal syndrome (Cologene™) database was interrogated for all patients with FAP having a deleterious APC mutation. Patients with first colonoscopy after age 30 and before year 2000 were excluded. Cox regression analysis was done to assess multiple factors associated with surgery, followed by stepwise Cox regression analysis to select an optimal model. Receiver operator curve (ROC) analysis was performed to assess the model. RESULTS: A total of 211 (53% female) patients were included. Forty-five percent underwent surgery after an average of 3.8 years of surveillance. The final model was created based on initial clinical characteristics (age, gender, BMI, family history of desmoids, genotype-phenotype correlation), initial colonoscopic characteristics (number of polyps, polyp size, presence of high-grade dysplasia); and on clinical events (chemoprevention and polypectomy). AUC was 0.87 and 0.84 to predict surgery within 2 and 5 years, respectively. The final model can be accessed at this website: http://app.calculoid.com/#/calculator/29638 . CONCLUSION: This web-based tool allows clinicians to stratify patients' likelihood of colorectal surgery within 2 and 5 years of their initial examination, based on clinical and endoscopic features, and using the philosophy of care guiding practice at this institution.

Natural history of colonic polyposis in young patients with familial adenomatous polyposis.

BACKGROUND AND AIMS: Proctocolectomy prevents colorectal cancer in familial adenomatous polyposis (FAP). Colorectal polyp progression is one of the indications for surgery. No data exist regarding the natural history of colorectal polyposis in young patients with FAP. This study examined the rate of polyposis progression and factors associated with it. METHODS: Patients with FAP <30 years old who had undergone ≥2 colonoscopies since 2000 were identified. Rate of polyposis progression was calculated by review of polyp counts obtained from baseline and last colonoscopy, accounting for any polyps removed during the observation period. Endoscopic and non-endoscopic factors affecting the rate of polyposis progression were evaluated. Multivariate analysis was performed to identify factors associated with rate of polyposis progression. RESULTS: One hundred sixty-eight patients (52% female; median age, 13.5 years) were included. Median rate of polyposis progression was 25.4 polyps/year (interquartile range, 9.5-69.8). Highest median rate of polyposis progression (89 polyps/year) was associated with mutation in codon 1309. The rate of polyposis progression was independently associated with the location of mutation in the adenomatous polyposis coli gene, the number of polyps at the initial colonoscopy, and exposure to chemoprevention. Of the 39.9% of patients who underwent surgery, an increase in polyp number was the most common indication (53.7%). CONCLUSIONS: The rate of polyposis progression in young patients with FAP varies with a median of about 25 new polyps per year. Progression is associated with distinct factors, which can be used in discussion with patients regarding the need for and timing of prophylactic colorectal surgery.

The impact of chromoendoscopy for surveillance of the duodenum in patients with MUTYH-associated polyposis and familial adenomatous polyposis.

BACKGROUND AND AIMS: Duodenal polyposis and cancer have become a key issue for patients with familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). Almost all patients with FAP will develop duodenal adenomas, and 5% will develop cancer. The incidence of duodenal adenomas in MAP appears to be lower than in FAP, but the limited available data suggest a comparable increase in the relative risk and lifetime risk of duodenal cancer. Current surveillance recommendations, however, are the same for FAP and MAP, using the Spigelman score (incorporating polyp number, size, dysplasia, and histology) for risk stratification and determination of surveillance intervals. Previous studies have demonstrated a benefit of enhanced detection rates of adenomas by use of chromoendoscopy both in sporadic colorectal disease and in groups at high risk of colorectal cancer. We aimed to assess the effect of chromoendoscopy on duodenal adenoma detection, to determine the impact on Spigelman stage and to compare this in individuals with known pathogenic mutations in order to determine the difference in duodenal involvement between MAP and FAP. METHODS: A prospective study examined the impact of chromoendoscopy on the assessment of the duodenum in 51 consecutive patients with MAP and FAP in 2 academic centers in the United Kingdom (University Hospital Llandough, Cardiff, and St Mark's Hospital, London) from 2011 to 2014. RESULTS: Enhanced adenoma detection of 3 times the number of adenomas after chromoendoscopy was demonstrated in both MAP (P = .013) and FAP (P = .002), but did not affect adenoma size. In both conditions, there was a significant increase in Spigelman stage after chromoendoscopy compared with endoscopy without dye spray. Spigelman scores and overall adenoma detection was significantly lower in MAP compared with FAP. CONCLUSIONS: Chromoendoscopy improved the diagnostic yield of anomas in MAP and FAP 3-fold, and in both MAP and FAP this resulted in a clinically significant upstaging in Spigelman score. Further studies are required to determine the impact of improved adenoma detection on the management and outcome of duodenal polyposis.

The clinical significance and synchronous polyp burden of large (≥ 20 mm) sessile serrated polyps in patients without serrated polyposis syndrome.

BACKGROUND: Sessile serrated polyps (SSPs) are important precursors of colorectal carcinoma and interval cancer. Large SSPs (≥ 20 mm) outside the definition of serrated polyposis syndrome (SPS) have not been studied in comparison with SPS. We aimed to describe the characteristics of patients with large SSPs in this context. METHODS: Patients with at least one SSP (≥ 20 mm) were eligible. Data from three consecutive colonoscopies were used to compare clinical and endoscopic characteristics in three patient groups: SPS, a solitary large SSP, and patients with at least two SSPs without fulfilling the criteria for SPS (oligo-SSP). Data on the diagnostic colonoscopy were collected retrospectively, whereas the remaining data was collected prospectively. RESULTS: 67/146 patients (45.9 %) had SPS, 53/146 (36.3 %) had a solitary SSP, and 26/146 (17.8 %) were categorized as oligo-SSP. Personal (16.4 %, 9.4 %, and 11.5 %, respectively) and family (17.9 %, 17.0 %, and 23.1 %, respectively) history of colorectal carcinoma did not differ significantly between groups. Polyp burden was greater in SPS compared with solitary SSP but was not different from oligo-SSP (advanced adenomas: SPS 32.8 % vs. solitary SSP 9.4 % [P = 0.002] vs. oligo-SSP 34.6 % [P = 0.87]; ≥ 10 conventional adenomas: 11.9 % vs. 0 % [P = 0.01] vs. 3.8 % [P = 0.44], respectively). Dysplasia in large SSPs was frequent in all groups (41.1 % overall). SPS was recognized by referring endoscopists in only 9.0 % of cases. CONCLUSION: Patients with oligo-SSPs have similar synchronous polyp burden and clinical characteristics as patients with SPS and may require similar surveillance. Modification of the criteria for the diagnosis of SPS to include this group seems warranted. Patients with a solitary SSP have a lower risk of synchronous polyps, including advanced adenomas. Larger studies are warranted to determine whether these patients may return to standard surveillance following complete examination and clearance of the colon.

Specimen Identification Errors in Breast Biopsies: Age Matters. Report of Two Near-Miss Events and Review of the Literature.

The consequences of patient identification errors due to specimen mislabeling can be deleterious. We describe two near-miss events involving mislabeled breast specimens from two patients who sought treatment at our institution. In both cases, microscopic review of the slides identified inconsistencies between the histologic findings and patient age, unveiling specimen identification errors. By correlating the clinical information with the microscopic findings, we identified mistakes that had occurred at the time of specimen accessioning at the original laboratories. In both cases, thanks to a timely reassignment of the specimens, the patients suffered no harm. These cases highlight the importance of routine clinical and pathologic correlation as a critical component of quality assurance and patient safety. A review of possible specimen identification errors in the anatomic pathology setting is presented.

The "Studded" Rectum: Phenotypic Evidence of MYH-Associated Polyposis.

BACKGROUND: MYH-associated polyposis is a recessively inherited syndrome of colorectal cancer predisposition attributed to biallelic germline mutations in the base excision repair gene MYH. Clinically it overlaps with attenuated familial adenomatous polyposis, sporadic oligopolyposis, serrated polyposis, familial colorectal cancer type X, and Lynch syndrome. There is no specific phenotypic feature of MYH-associated polyposis. We have noticed that a proportion of patients with MYH-associated polyposis presenting for yearly colonoscopy surveillance have rectums that are studded with small hyperplastic polyps. OBJECTIVE: We report this as a possible unique phenotypic feature of the syndrome. DESIGN: This was a descriptive study. SETTINGS: The study was conducted at a department of colorectal surgery in a tertiary referral center. PATIENTS: Patients affected with oligopolyposis or MYH-associated polyposis presenting for endoscopic surveillance and polyp control were included. INTERVENTIONS: Interventions included colonoscopy or proctoscopy with excision or biopsy of mucosal lesions. MAIN OUTCOME MEASURES: The presence of rectal studding was measured. RESULTS: There were 49 patients, 16 with biallelic germline mutations of MYH; 10 of these had rectal studding. A sampling of rectal polyps was biopsied and all were hyperplastic. Five patients with biallelic MYH mutations had no studding, and 1 had not been prospectively examined. The studding was independent of the nature of the MYH mutation(s). The 33 patients other patients included 21 with serrated polyposis, 2 with a germline APC mutation, 1 with a PTEN mutation, 2 with mixed polyposis, 3 with oligoadenomatous polyposis and no germline mutation, and 4 patients with oligoadenomatous polyposis who had not been genetically tested. Only 1 of these (oligoadenomatous polyposis, not tested) had studding. LIMITATIONS: The study was limited by its small number of biallelic MYH mutation carriers. CONCLUSIONS: Rectal studding may be a sign of MYH-associated polyposis and raises questions about the biology of abnormal base excision repair.

Inducible loss of one Apc allele in Lrig1-expressing progenitor cells results in multiple distal colonic tumors with features of familial adenomatous polyposis.

Individuals with familial adenomatous polyposis (FAP) harbor a germline mutation in adenomatous polyposis coli (APC). The major clinical manifestation is development of multiple colonic tumors at a young age due to stochastic loss of the remaining APC allele. Extracolonic features, including periampullary tumors, gastric abnormalities, and congenital hypertrophy of the retinal pigment epithelium, may occur. The objective of this study was to develop a mouse model that simulates these features of FAP. We combined our Lrig1-CreERT2/+ mice with Apcfl/+ mice, eliminated one copy of Apc in leucine-rich repeats and immunoglobulin-like domains protein 1 (Lrig1)-positive (Lrig1(+)) progenitor cells with tamoxifen injection, and monitored tumor formation in the colon by colonoscopy and PET. Initial loss of one Apc allele in Lrig1(+) cells results in a predictable pattern of preneoplastic changes, culminating in multiple distal colonic tumors within 50 days of induction, as well as the extracolonic manifestations of FAP mentioned above. We show that tumor formation can be monitored by noninvasive PET imaging. This inducible stem cell-driven model recapitulates features of FAP and offers a tractable platform on which therapeutic interventions can be monitored over time by colonoscopy and noninvasive imaging.

Multiple colon polyposis.

INTRODUCTION: Familial adenomatous polyposis (FAP) is a rare autosomal, dominant hereditary disease, which affects both sexes equally (1-10). FAP accounts for less than 1% of all colon cancers and is estimated to occur in one of 8,300 live births. It is characterized by numerous adenomas scattered throughout mucosa of the colon and rectum. CASE REPORT: The patient is a 62 years old man, admitted at the Surgical Department of the General Hospital in Konjic on May 18 2010 with gastrointestinal problems including: hard stool, often splattered with fresh blood, irregular and that causes the patient a lot of problems. The final diagnosis was median laparatomy supra et infraumibilicalis. Exploratio cavi abdominalis. Colectomy totalis et ileo-recto anastomosis TT cum staypler (33Ch). Loop ileostomy. Drainage cavi abdominalis N I (uno). Early postoperative course was generally regular. Control laboratory findings show the reference value. After ten days of hospitalization, the patient was discharged on the home recovery, with practically given instructions for care and use of stoma bags. For the secondary surgery was planned ileostomy closure, and regular post-operative endoscopic control. CONCLUSION: Most of the listed surgical intervention in case of FAP treatment localized in the colon can be performed by open (classic), or laparoscopic methods. Duration of postoperative stay in the hospital depends on the patient's general condition and the type of performed surgery. It is usually about 7 days. After hospital treatment, recovery at home is from 4-6 weeks. Patients can usually return to work or school 6-8 weeks after surgery. After surgery, patients lives will be completely normal. Sexual and social activities remain the same, while either procedure does not affect the ability of a man or woman to have offspring.

Role of 68 Ga-FAPI PET/CT in Screening Malignancy of Familial Adenomatous Polyposis.

ABSTRACT: A 57-year-old man with familial adenomatous polyposis (FAP) and newly diagnosed colonic adenocarcinoma was referred to 18 F-FDG PET/CT for staging and 68 Ga-FAPI-04 PET/CT for ongoing trial. 18 F-FDG PET/CT showed equal intense 18 F-FDG uptake in the tumor and multiple hypermetabolic polypoid lesions in the entire colorectum. 68 Ga-FAPI-04 PET/CT showed intense 68 Ga-FAPI-04 uptake only at the colonic tumor, without uptake at polypoid lesions.

MRI of the ileal pouch.

Ileal pouch surgery is the surgical gold standard treatment for patients with ulcerative colitis (UC) and familial adenomatous polyposis (FAP). However, ileal pouch surgery is a technically challenging procedure and is associated with high morbidity. Clinical presentations of pouch complications are often nonspecific but imaging can identify many of these complications and is essential in clinical management. This paper will focus on magnetic resonance imaging (MRI) of the ileal pouch, including recommended MRI protocol and approach to imaging interpretation with an emphasis on those ileal pouch complications particularly well evaluated with MRI.