Relevancia de la PET/TC con [18F]FDG en la detección de enfermedad localizada en el colon en pacientes estudiados por bacteriemia o endocarditis infecciosa causadas por microorganismos enteropatógenos / Relevance of [18F]FDG-PET/CT in the detection of colon pathology in patients studied by bacteriemia or infectious endocarditis caused by enteropathogenic microorganisms

Objetivo La asociación entre la endocarditis infecciosa (EI) por Streptococcus gallolyticus y las lesiones malignas del tracto gastrointestinal está bien descrita. Asumimos que otros microorganismos enteropatógenos, como el Streptococcus viridans y Enterococcus faecalis también pueden estar relacionados con la enfermedad colorrectal. Nuestro objetivo fue determinar la frecuencia de depósitos focales de la [18F]FDG en localización colorrectal, sugestivos de lesiones tumorales, y su correlación con la enfermedad de colon y recto en pacientes con infección causada por diferentes microorganismos comensales del tracto gastrointestinal. Métodos Examinamos retrospectivamente 61 pacientes con diagnóstico de bacteriemia y de EI (posible o concluyente) según los criterios de Duke y causada por microorganismos enteropatógenos, y que fueron sometidos a una PET/TC de cuerpo entero con [18F]FDG en nuestra institución. Buscamos depósitos de la [18F]FDG en localización colorrectal, así como la presencia de lesiones morfológicas. A todos los pacientes con EI se les realizó una colonoscopia completa y los resultados histológicos se clasificaron según 4 grupos: lesión maligna, lesión premaligna, lesión benigna y ausencia de lesión. Se evaluó la correlación existente entre los hallazgos de la PET/TC con [18F]FDG y el diagnóstico histopatológico y el microorganismo implicado. Resultados La PET/TC detectó 20 depósitos de [18F]FDG en localización colorrectal (32,79%-OR: 47,28), 2 de ellos en pacientes con bacteriemia (16,7%) confirmados como lesiones malignas y premalignas y 18 en el grupo con EI (36,6%), 17 de ellos correspondientes a enfermedad colorrectal: 11 lesiones malignas, 5 premalignas y una benigna. En el subgrupo con EI la colonoscopia detectó lesiones colorrectales en el 51,02% de los pacientes: 11 malignas, 8 premalignas y 6 benignas. En el subgrupo de Streptococcus spp. se detectó una mayor incidencia de depósitos de [18F]FDG en localización colorrectal (AU)

Objective Association between Streptococcus gallolyticus infective endocarditis (IE) and malignant lesions of the gastrointestinal tract is well described. We hypothesize that other enteropathogenic microorganisms, such as Streptococcus viridans and Enterococcus faecalis are also related with colorectal pathology. Our aim is to determine the frequency of focal colorectal FDG deposits, suggestive of tumoral lesions and their correlation with colorectal pathology, in patients with infection caused by different commensal microorganisms of the gastrointestinal tract. Methods We retrospectively examined 61 patients diagnosed with bacteremia (BSI) and IE (possible or definite) according to Duke's criteria, caused by enteropathogenic microorganisms, who underwent a full-body [18F]FDG-PET/CT in our institution. We looked for colorrectal FDG deposits and morphological lesions. All IE patients underwent a complete colonoscopy and the histological results were classified into four groups: malignant lesion, premalignant lesion, benign lesion and no lesion. We evaluated the correlation between the findings of the [18F]FDG-PET/CT with the histopathological diagnosis and the involved microorganism. Results PET/CT detected 20 colorectal FDG deposits (32.79%-OR: 47.28), 2 within bacteriemic patients (16.7%) confirmed as malignant and premalignant lesions and 18 in IE group (36.6%), 17 of them corresponding to colorrectal pathology: 11 malignant, 5 premalignant and 1 benign lesions. In the IE subgroup, the colonoscopy detected colorectal lesions in 51.02% of the patients: 11 malignant, 8 premalignant and 6 benign. We found a higher incidence of colorectal FDG deposits in Streptococcus spp. subgroup. Regarding the anatomopathological colonic findings there was a predominance of patients affected by S. viridans, followed by E. faecalis and S. gallolyticus (AU)

Therapeutic targeting of the oncogenic Wnt signaling pathway for treating colorectal cancer and other colonic disorders.

The canonical Wnt pathway is one of the key cellular signaling cascades that regulates, via the transcriptional co-activator ß-catenin, numerous embryogenic developmental processes, as well as tissue homeostasis. It is therefore not surprising that misregulation of the Wnt/ß-catenin pathway has been implicated in carcinogenesis. Aberrant Wnt signaling has been reported in a variety of malignancies, and its role in both hereditary and sporadic colorectal cancer (CRC), has been the subject of intensive study. Interestingly, the vast majority of colorectal tumors harbor mutations in the tumor suppressor gene adenomatous polyposis coli (APC). The Wnt pathway is complex, and despite decades of research, the mechanisms that underlie its functions are not completely known. Thus, although the Wnt cascade is an attractive target for therapeutic intervention against CRC, one of the malignancies with the highest morbidity and mortality rates, achieving efficacy and safety is yet extremely challenging. Here, we review the current knowledge of the Wnt different epistatic signaling components and the mechanism/s by which the signal is transduced in both health and disease, focusing on CRC. We address some of the important questions in the field and describe various therapeutic strategies designed to combat unregulated Wnt signaling, the development of targeted therapy approaches and the emerging challenges that are associated with these advanced methods.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine Induced Colon Injury by Disrupting the Intestinal Bacterial Composition and Lipid Metabolic Pathways in Rats.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), one of the most abundant heterocyclic amines, is a common carcinogen produced in thermally processed protein-rich foods. Studies have demonstrated that PhIP could induce colon tumors in rodents, leaving mechanisms uncovered. This study aims to investigate the mechanism of PhIP-induced colon injury in a rat model. The results of 16S rRNA gene sequencing and metabolomics showed that PhIP disrupted intestinal bacterial composition and affected the glycerophospholipid metabolism and linoleic acid metabolism. Simultaneously, the lipid metabolism function in the intestinal flora was inhibited by PhIP. Notably, transcriptomics revealed that PhIP remarkably inhibited the expression of gene sets associated with steroid hormone biosynthesis, fatty acid elongation, fatty acid degradation, and glycerolipid metabolism pathways in the colon. The results provide new perspectives to study the mechanism of PhIP-induced colon injury and theoretical bases for further understanding the toxicity of PhIP.

An Overview of Gut Microbiota and Colon Diseases with a Focus on Adenomatous Colon Polyps.

It is known and accepted that the gut microbiota composition of an organism has an impact on its health. Many studies deal with this topic, the majority discussing gastrointestinal health. Adenomatous colon polyps have a high prevalence as colon cancer precursors, but in many cases, they are hard to diagnose in their early stages. Gut microbiota composition correlated with the presence of adenomatous colon polyps may be a noninvasive and efficient tool for diagnosis with a high impact on human wellbeing and favorable health care costs. This review is meant to analyze the gut microbiota correlated with the presence of adenomatous colon polyps as the first step for early diagnosis, prophylaxis, and treatment.

Colonic mucormycosis in solid organ transplantation: Case report and review of the literature (colonic mucormycosis after DDLT).

Mucormycosis is an opportunistic fungal infection that can occur throughout the body and carries a high mortality. Colonic mucormycosis is an uncommon form of the disease whose successful treatment relies upon a high degree of clinical suspicion and early, often empiric, therapy. We report colonic mucormycosis in a liver transplant patient and review the literature on colonic mucormycosis in solid organ transplant recipients.

[Novel insight into the role of gut microbiome in colorectal surgery].

Colorectal surgery is a major therapeutic approach for various colorectal diseases. Surgery and perioperative management, such as fasting, mechanical bowel preparation, and antibiotics use, have an impact on the composition and function of gut microbiome. Abnormal microbiome reconstruction may lead to multiple complications, including infection, gastrointestinal dysfunction, anastomotic leak and disease recurrence. The aim of this review is to elucidate the roles and mechanisms of perioperative interventions of colorectal surgery on gut microbiome, which may provide a novel insight into the microbe-based therapies in the perioperative period of colorectal surgery.

[Pay attention to the diagnosis and treatment of intestinal infectious diarrhea after colorectal surgery].

Colorectal surgery patients have severe intestinal flora disorders and antibiotic resistant bacteria due to the disease itself and preoperative treatment, as well as the influence of dietary structure and environmental factors. Perioperative anesthesia and operative stress can cause gastrointestinal motility disorders. In addition, the widespread use of prophylactic broad-spectrum antibiotics and antiacids aggravate intestinal flora disorders and induces severe postoperative infectious diarrhea, such as pseudomembranous enteritis and fatal enteritis. The clinical manifectation are severe infectious diarrhea with high fever and abdominal distension after surgery. The disease progresses rapidly. When the diagnosis and treatment are delayed, the patient can quickly develop shock and other serious complications such as anastomotic leakage, even die of multiple organ failure. Therefore, early diagnosis and treatment are crucial.

Acute changes in the colonic microbiota are associated with large intestinal forms of surgical colic.

BACKGROUND: Horses that undergo surgery for treatment of primary large colon disease have been reported to be at increased risk of developing recurrent colic episodes postoperatively. The reasons for this are currently unknown. The aim of the current study was to characterise the faecal microbiota of horses with colic signs associated with primary large colon lesions treated surgically and to compare the composition of their faecal microbiota to that of a control group of horses undergoing emergency orthopaedic treatment. Faecal samples were collected from horses in both groups on admission to hospital, during hospitalisation and following discharge from hospital for a total duration of 12 weeks. Additionally, colonic content samples were collected from surgical colic patients if pelvic flexure enterotomy was performed during laparotomy. A total of 12 samples were collected per horse. DNA was extracted from samples using a commercial kit. Amplicon mixtures were created by PCR amplification of the V1 - V2 regions of the bacterial 16S rRNA genes and submitted for sequencing using the Ion Torrent PGM next-generation sequencing system. Multivariate data analysis was used to characterise the faecal microbiota and to investigate differences between groups. RESULTS: Reduced species richness was evident in the colonic samples of the colic group compared to concurrent sampling of the faeces. Alpha and beta diversity differed significantly between the faecal and colonic microbiota with 304 significantly differentially abundant OTUs identified. Only 46 OTUs varied significantly between the colic and control group. There were no significant differences in alpha and beta diversity of faecal microbiota between colic and control horses at admission. However, this lack of significant differences between groups should be interpreted with caution due to a small sample size. CONCLUSIONS: The results of the current study suggest that faecal samples collected at hospital admission in colic cases may not accurately represent changes in upper gut microbiota in horses with colic due to large colon disease.

E-cadherin Beyond Structure: A Signaling Hub in Colon Homeostasis and Disease.

E-cadherin is the core component of epithelial adherens junctions, essential for tissue development, differentiation, and maintenance. It is also fundamental for tissue barrier formation, a critical function of epithelial tissues. The colon or large intestine is lined by an epithelial monolayer that encompasses an E-cadherin-dependent barrier, critical for the homeostasis of the organ. Compromised barriers of the colonic epithelium lead to inflammation, fibrosis, and are commonly observed in colorectal cancer. In addition to its architectural role, E-cadherin is also considered a tumor suppressor in the colon, primarily a result of its opposing function to Wnt signaling, the predominant driver of colon tumorigenesis. Beyond these well-established traditional roles, several studies have portrayed an evolving role of E-cadherin as a signaling epicenter that regulates cell behavior in response to intra- and extra-cellular cues. Intriguingly, these recent findings also reveal tumor-promoting functions of E-cadherin in colon tumorigenesis and new interacting partners, opening future avenues of investigation. In this Review, we focus on these emerging aspects of E-cadherin signaling, and we discuss their implications in colon biology and disease.

[Immunohistochemical diagnosis of colonic spirochetosis with anti-treponema antibody in patients consulting for chronic diarrhea. Results of a prospective study conducted in 137 patients]. / Diagnostic immunohistochimique de la spirochétose colique avec l'anticorps anti-tréponème chez les patients consultant pour une diarrhée chronique. Résultats d'une étude prospective menée chez 137 patients.

AIM: To assess the incidence of colonic spirochetosis, diagnosed by immunohistochemical stain with anti-Treponema pallidum antibody, in a prospective study of colonic biopsies of patients presenting with chronic diarrhea. MATERIAL AND METHODS: From March 2017 to March 2018 the colonic biopsies of patients presenting with chronic diarrhea were stained with Hematoxylin Eosin and anti-Treponema pallidum antibody. The positive cases were also stained with Steiner stain. RESULTS: A total of 137 colonic biopsies were assessed and 3 cases were positive for immunohistochemical stain with anti-Treponema pallidum antibody (2% of the patients). One case was easy to diagnose with HE stain but the 2 other cases were not. The bacteria were stained with Steiner stain, but less easily seen than with the immunohistochemical stain. No patient was treated with antibiotics. DISCUSSION AND CONCLUSION: The colonic spirochetosis can be easily diagnosed by pathologists with immunohistochemical stain with anti-Treponema pallidum antibody. The bacteria are more easily diagnosed with immunohistochemical stain than with HE stain or Steiner stain. However, colonic spirochetosis is rarely diagnosed on colonic biopsies of patients presenting with chronic diarrhea (2% of the patients in our study). Due to the rarity of the entity, and the cost of immunohistochemical stain and the weak benefit for the patient (no patient in our study was treated with antibiotics for colonic spirochetosis) we cannot advise to perform systematic immunohistochemical stain with anti-Treponema pallidum antibody in all the colonic biopsies of patients presenting with chronic diarrhea.

"Fungating" tumour? No, it's bacterial!

A fit and healthy 26-year-old woman presented to the general surgical team with epigastric pain and weight loss of 2 stones over 6 months. She has also a positive family history of ulcerative colitis. As her oesophagogastroduodenoscopy and colonoscopy were normal, a contrasted CT was requested, and it detected an inflammatory mass with fat streaking around her transverse colon. An intrauterine contraceptive device (IUCD) was noted. In light of the CT findings, she underwent a diagnostic laparoscopy. As the inflammatory mass was not separable from the transverse colon, a segmental transverse colectomy was proceeded. The histology revealed multiple actinomycosis abscesses in the mesentery. Subsequently, we learnt that her IUCD had been in situ for the last 7 years, and the source of actinomycosis abscesses is likely from her IUCD. The patient was recommended to have the coil removed and commenced on a 6 months course of amoxicillin.

High-fat diet causes psychiatric disorders in mice by increasing Proteobacteria population.

The excessive intake of a high-fat diet (HFD) leads to obesity, including metabolic syndromes, disturbs gut microbiota composition, causes colitis, and increases the plasma concentration of lipopolysaccharide (LPS). In the present study, we examined the role of gut microbiota in the occurrence of HFD-induced psychiatric disorders in mice. C57BL/6 J male mice fed a HFD for 9 weeks were led to obesity; their memory impairment was assessed by the Y-maze and novel object recognition test, and anxiety-like behaviors by the elevated plus maze. The intake of a HFD suppressed brain-derived neurotrophic factor (BDNF) expression in the hippocampus and increased blood TNF-α and LPS levels. HFD treatment more potently increased NF-κB activation and Iba1+ (microglial) cell populations in the hippocampus. Furthermore, HFD feeding increased TNF-α expression, myeloperoxidase activity, and CD11b+/CD11c+ cell (macrophages and dendritic cells) populations in the colon and altered gut microbiota composition including increases in the Proteobacteria population, and increases in fecal LPS levels. The stool lysates of HFD-treated mice suppressed BDNF expression and CREB phosphorylation in SH-SY5Y cells and increased NF-κB activation in BV-2 microglial cells compared to those of low-fat diet-treated mice while these effects were attenuated by treatment with anti-LPS antibody. These findings suggest that excessive intake of HFD can simultaneously cause obesity and psychiatric disorders by suppressing hippocampal BDNF expression with the disturbance of gut microbiota composition, particularly the increase in Proteobacteria population and LPS production.

Actinomicosis primaria intestinal. Informe de un caso en íleon y colon. Revisión de la literatura / Primary intestinal actinomycosis in ilium and colon. A case report and review of the literature

La actinomicosis es una enfermedad crónica, supurativa e inflamatoria granulomatosa causada por bacterias filamentosas grampositivas anaerobias del género Actinomyces, siendo más frecuente Actinomyces israelii. Caso clínico: hombre de 42 años de edad con dolor abdominal, pérdida de peso de 10kg y tumor en epigastrio adherido a planos profundos. La tomografía reveló dilatación de las asas intestinales; así como engrosamiento de las paredes de colon, por lo que se pensó en proceso linfoproliferativo. Se extirparon quirúrgicamente el tumor, fragmento íleon y colon; los cuales se encontraban adheridos por tejido fibroadiposo de la serosa. Microscópicamente se observó abundante infiltrado de leucocitos polimorfonucleares y gránulos de bacterias compatibles con Actinomyces spp

Actinomycosis is a chronic, suppurative, inflammatory granulomatous disease caused by gram positive anaerobic filamentous bacteria of the genus Actinomyces, most frequently Actinomyces israelii. We report a case of a 42-year-old male presenting with abdominal pain, a 10kg weight loss and a fixed mass in the epigastrium. Tomography revealed dilatation of the intestinal loops and thickening of the colon walls; the coexistence of these two findings suggested a lymphoproliferative process. The tumour, ileum fragment and colon were surgically removed; these were adherent to the serosal fibro-adipose tissue. Microscopically, abundant polymorphonuclear infiltrate and grains of bacteria compatible with Actinomyces spp.were seen

Gender Difference and Dietary Supplemental Vitamin B6: Impact on Colon Luminal Environment.

Colon diseases can be affected by several factors such as gender difference and dietary supplemental vitamin B6 (B6). The nutritional status of B6 is affected by gender difference, leading us to hypothesize that gender difference affects colon luminal environment, which is dependent on B6 status. To investigate this hypothesis, we fed male and female rats a diet containing 1 mg, 7 mg, or 35 mg pyridoxine HCl/kg diet for 6 wk. We found significantly higher fecal mucin levels in female rats compared to those in male rats. Supplemental B6 significantly increased fecal mucins and was particularly profound in the female rats. The abundances of cecal and fecal Akkermansia muciniphila (mucin degrader) were unaffected. The fecal mucin levels were significantly correlated with colonic free threonine and serine and with gene expression of colon MUC16, implying that the combined effect of gender and dietary B6 on fecal mucins was mediated by the alteration in the levels of such amino acids and MUC16 expression. This study further showed the significant effects of gender difference on colonic free amino acids such as threonine, ornithine, asparagine/aspartate ratio, and glutamine/glutamate ratio, cecal and fecal Lactobacillus spp. levels, and colonic gene expressions of MUC16 and TLR8, the factors relating to colon health and diseases. Therefore, our findings suggest that gender difference and dietary B6 may have an impact on colon diseases by modulating these parameters.

Surgical management of colonic basidiobolomycosis among adolescent and adult patients: presentation and outcome.

AIM: The aim of this study was to review retrospectively the clinical presentations, indications for surgery and surgical outcomes of adolescent and adult patients who were diagnosed with colonic basidiobolomycosis in the last 10 years. METHOD: The study was carried out in Aseer Central Hospital, Abha, Saudi Arabia by reviewing the medical files of all patients in the last 10 years who were diagnosed with colonic basidiobolomycosis and required surgical intervention. RESULTS: There were 22 patients. Common findings in all patients were weight loss, abdominal pain and an abdominal mass. The right colon was affected in 21 patients. The initial diagnosis was correct in seven patients while nine were thought to be malignant. All patients underwent colonic resection followed by at least 1 year of antifungal medical treatment. Intra-operatively, all patients had moderate or dense adhesions, an abdominal mass and lymphadenopathy. Most surgeons had the impression intra-operatively that the diagnosis was inflammatory rather than malignant. Postoperatively, three patients died within 6 months of the operation due to progression of the disease. Four patients developed severe wound infections, three of whom had abdominal dehiscence and required re-closure. CONCLUSION: Colonic basidiobolomycosis is a life-threatening fungal infection that should be considered a surgical condition. A high index of suspicion including basidiobolomycosis in the differential diagnosis for the acute abdomen with a colonic mass is required for a proper diagnosis. Early aggressive surgical management followed by a prolonged course of itraconazole postoperatively could improve the outcome of the condition.

Bifidobacteria alleviate experimentally induced colitis by upregulating indoleamine 2, 3-dioxygenase expression.

The goal of this study was explore the role of indoleamine 2, 3-dioxygenase (IDO) in the therapeutic effect of probiotics on inflammatory bowel disease (IBD). Trinitrobenzene sulfonic acid (TNBS) was used to induce colitis in mice and 1-methyltryptophan (1-MT) to block expression of IDO. Clinical manifestations and macroscopic and microscopic colonic changes were assessed using a disease activity index (DAI), the Wallace-Keenan, and Curtner scoring systems, respectively. Expression of colonic IDO was detected by western blot. Immunohistochemistry analysis to evaluate numbers of CD11c+ cells and expression of IL-17 and Foxp3 showed that DAI, Wallace-Keenan, and Curtner scores were lower in the Bifidobacteria treatment group than the control group and that the therapeutic effect of Bifidobacteria was blocked by 1-MT (P < 0.05). Additionally, Bifidobacteria were found to increase expression of IDO and the numbers of CD11c+ cells, CD11c+ and IDO double positive cells and Foxp3+ Treg cells, while decreasing the number of IL-17+ cells (P < 0.05). The generation of Foxp3+ Treg cells induced by Bifidobacteria was abrogated by 1-MT (P < 0.05). These findings study suggest that Bifidobacteria attenuate TNBS-induced colitis by inducing expression of IDO, which further increases generation of Foxp3+ Treg cells.