Figure 2- - available via license: Creative Commons Attribution 4.0 International
Content may be subject to copyright.
Colonic inertia in a constipated patient with Chagas' disease (ChC). An X-ray obtained on day 7 shows stasis of the radiopaque markers in the ascending colon.
Source publication
Manometric and pharmacological tests have shown that motor abnormalities may occur in the non-dilated colons of chagasic patients. In order to investigate the presence of abnormalities of colonic function in constipated patients with Chagas' disease (ChC) without megaesophagus or megacolon, studies of total and segmental colonic transit time with r...
Context in source publication
Context 1
... upper limits of normality for total and segmental CTT were: total colonic tran- sit time = 65 h; right colonic transit time = 25 h; left colonic transit time = 31 h, and rec- tosigmoid transit time = 32 h. No statistically when a decrease of markers was observed on the X-ray. IC and ChC patients were divided according to total CTT into those with nor- mal transit and those with slow transit, the latter when total CTT was longer than 65 h (Figure 1). Slow colonic transit was shown in 65% of IC (11 out of 17, 10 females) and 27% of ChC (4 out of 15, 3 females; P = 0.03). There was no difference between slow transit IC and slow transit ChC patients in total CTT (Table 2). In addition, all patients with prolonged transit reported the chronic use of laxatives. Segmental CTT. The study of the seg- mental CTT classified slow colonic transit patients into the subgroups previously de- fined (Figures 2-4). Among IC patients, 41% (7 of 17) had a pattern of colonic inertia, 12% (2) had hindgut dysfunction, 6% (1) had outlet obstruction, and 6% (1) showed a prolonged total CTT with normal segmental transit time. Among ChC patients, 13% (2) showed a pattern of colonic inertia, 7% (1) had hindgut dysfunction and 7% (1) had outlet ...
Citations
... Compared to control values, this non-dilated oral segment has a higher relative percentage of nitrergic myenteric neurons (Jabari et al. 2011), lower muscle tissue density and intramuscular nerve fibre density (Jabari et al. (Jabari et al. 2014a). Taken together with neural and motor abnormalities similarly seen in the colon of chagasic patients without megacolon (Meneghelli et al. 1982;Santos et al. 2000), these data suggest that EEC abnormalities can take place in T.cruzi-affected patients independently of the occurrence of megacolon. ...
Chagas disease is caused by the parasite, Trypanosoma cruzi that causes chronic cardiac and digestive dysfunction. Megacolon, an irreversible dilation of the left colon, is the main feature of the gastrointestinal form of Chagas disease. Patients have severe constipation, a consequence of enteric neuron degeneration associated with chronic inflammation. Dysmotility, infection, neuronal loss and a chronic exacerbated inflammation, all observed in Chagas disease, can affect enteroendocrine cells (EEC) expression, which in turn, could influence the inflammatory process. In this study, we investigated the distribution and chemical coding of EEC in the dilated and non-dilated portion of T. cruzi-induced megacolon and in non-infected individuals (control colon). Using immunohistochemistry, EECs were identified by applying antibodies to chromogranin A (CgA), glucagon-like peptide 1 (GLP-1), 5-hydroxytryptamine (5-HT), peptide YY (PYY) and somatostatin (SST). Greater numbers of EEC expressing GLP-1 and SST occurred in the dilated portion compared to the non-dilated portion of the same patients with Chagas disease and in control colon, but numbers of 5-HT and PYY EEC were not significantly different. However, it was noticeable that EEC in which 5-HT and PYY were co-expressed were common in control colon, but were rare in the non-dilated and absent in the dilated portion of chagasic megacolon. An increase in the number of CgA immunoreactive EEC in chagasic patients reflected the increases in EEC numbers summarised above. Our data suggests that the denervation and associated chronic inflammation are accompanied by changes in the number and coding of EEC that could contribute to disorders of motility and defence in the chagasic megacolon.
... According to Lopes et al. (2013), who examined the longest radiological series of chagasic patients from endemic areas in Brazil and the Andes, the megacolon mostly starts with the lengthening of the sigmoid associated with an increase in the colon's diameter, at advanced stages of the disease. As shown for the esophagus (de Oliveira et al., 1995), colonic motility may reflect functional abnormalities in a stage preceding colon dilation (Santos et al., 2000). Studies using pharmacological tests (Meneghelli et al., 1983;Vieira et al., 1996) or manometry (Habr-Gama et al., 1970;Meneghelli et al., 1982) have shown the presence of neural and motor abnormalities in nondilated colons. ...
There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite's DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.
... M. J. I. Salemans, 1993;Linnet, 1983;Sonne et al., 2013;Suzuki et al., 2014;Tobiasson et al., 1981) Time of maximal value 7 143 3 (Ahmad et al., 2013;Angelin and Björkhem, 1977;De Barros et al., 1982;De Giorgi et al., 2014;Heuman et al., 1982;J. M. J. I. Salemans, 1993;LaRusso et al., 1978;Sonne et al., 2013;Suzuki et al., 2014;Tobiasson et al., 1981) Transit Fasting SI transit 1* 114 1 (Pišlar et al., 2015) Postprandial SI transit 1* 36 1 (Pišlar et al., 2015) Colon transit 9 405 1 (Arhan et al., 1981;Bouchoucha et al., 2006;Danquechin Dorval et al., 1994;Metcalf et al., 1987;Notghi et al., 1994;Pomerri et al., 2009;Santos et al., 2000;Yuan et al., 2012) TOTAL ...
... Assim com relatado por outros autores, não observamos em nossos pacientes diferença estatística significante com relação ao sexo 5,15,16 . No entanto, alguns estudos tem mostrado diferenças o que tem sido atribuído à presença de síndrome do intestino irritável não diagnosticado previamente 3,8 . ...
OBJETIVO: Com a introdução de marcadores radiopacos para avaliação do tempo de trânsito intestinal, tornou-se possível mensurar não apenas o tempo de trânsito total, como também o segmentar. Visando a simplificação da técnica, especialmente no que diz respeito à diminuição da exposição à irradiação, foi descrito novo método com número menor de radiografias. Os autores apresentam estudo do tempo de transito colônico total e segmentar em indivíduos normais. MÉTODO: Quinze voluntários adultos e assintomáticos, oito do sexo feminino e sete do masculino, foram submetidos a exame radiológico com marcadores radiopacos para medida do tempo de trânsito colônico total e segmentar (cólon direito, esquerdo e retossigmóide). RESULTADOS: A média do tempo de trânsito colônico total foi de 36,61 ± 3,48 horas. Dos tempos de trânsito segmentares obtivemos as médias de 11,51 ± 2,28 horas para o cólon direito; de 12,14 ± 2,19 horas para o cólon esquerdo; e de 12,96 ± 2,23 horas para o retossigmóide. CONCLUSÕES: A técnica descrita é método simples e útil para a avaliação do tempo de trânsito colônico total e segmentar e quando aplicada a indivíduos assintomáticos reproduziu resultados comparáveis aos da literatura e aos obtidos a partir de outras técnicas.
... En ellos se analizan: presencia o no de cardiopatía, basados principalmente en el electrocardiograma 9,10 y algunos se preocupan sólo de las complicaciones digestivas proponiendo 28,7% de megacolon en la población chagásica 11 . Los estudios existentes no brindan información sobre la presencia de estreñimiento sin megacolon o sintomatología esofágica v gr, asociación de disfagia y dolor torácico; sin acalasia radiológica, condiciones posibles en el espectro clínico del Chagas [12][13][14] . ...
... Parece sugerente, desde el punto de vista costo-beneficio, realizar enema baritada, más bien, a los pacientes estreñidos que a todos los portadores de T Cruzi. En coincidencia con otros autores 13 , podemos afirmar que no todos los sujetos chagásicos estreñidos tienen megacolon. Respecto a los pacientes con cardiopatía, reportes clásicos informan 23,8% de prevalencia en un grupo chagásico estudiado, sólo con clínica y ECG 22 . ...
Trypanosoma cruzi infection is endemic in Northern/Central Chile. Aim: To perform a clinical assessment of patients infected with Trypanosoma cruzi. Patients and methods: Two hundred sixty three subjects with a positive serology for Trypanosoma cruzi, were invited by mail to a clinical assessment in a Regional Hospital. In a subsample of these, a polymerase chain reaction for Trypanosoma cruzi, was done. Results: Of all the invited subjects, 183 responded and were assessed at the hospital. Of these, 60 had cardiac affections, 52 had colon problems and 17, esophageal disease. Seventy four were asymptomatic. Of the 64 patients in whom polymerase chain reaction was done, 35 had a positive result. Conclusions: A high percentage of subjects infected with Trypanosoma cruzi, had clinical consequences of the infection. Polymerase chain reaction showed persistency of the parasite in more than half of the infected patients (Rev Méd Chile 2003; 131: 881-6)
The canonical Wnt pathway is one of the key cellular signaling cascades that regulates, via the transcriptional co-activator β-catenin, numerous embryogenic developmental processes, as well as tissue homeostasis. It is therefore not surprising that misregulation of the Wnt/β-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.
Background: Trypanosoma cruzi infection is endemic in Northern/Central Chile. Aim: To perform a clinical assessment of patients infected with Trypanosoma cruzi. Patients and methods: Two hundred sixty three subjects with a positive serology for Trypanosoma cruzi, were invited by mail to a clinical assessment in a Regional Hospital. In a subsample of these, a polymerase chain reaction for Trypanosoma cruzi, was done. Results: Of all the invited subjects, 183 responded and were assessed at the hospital. Of these, 60 had cardiac affections, 52 had colon problems and 17, esophageal disease. Seventy four were asymptomatic. Of the 64 patients in whom polymerase chain reaction was done, 35 had a positive results. Conclusions: A high percentage of subjects infected with Trypanosoma cruzi, had clinical consequences of the infection. Polymerase chain reaction showed persistency of the parasite in more than half of the infected patients.
Autonomic nerve fibers are affected in most generalized peripheral neuropathies. Although this involvement is often mild or subclinical, there are a group of peripheral neuropathies in which the small or unmyelinated fibers are selectively or prominently targeted. These include the autonomic neuropathies associated with diabetes and amyloid, immune-mediated autonomic neuropathies including those associated with a paraneoplastic syndrome, inherited autonomic neuropathies, autonomic neuropathies associated with infectious diseases, and toxic autonomic neuropathies. The presenting features include impairment of cardiovascular, gastrointestinal, urogenital, thermoregulatory, sudomotor, and pupillomotor function. The accurate diagnosis of the autonomic neuropathies has been enhanced by the availability of physiological tests that measure autonomic function, and more recently, structural studies of the autonomic cutaneous innervation. With the help of these investigations and the judicious use of laboratory testing, many autonomic neuropathies can be accurately diagnosed and their clinical progression monitored.
