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Patogenia do megaesôfago brasileiro e europeu
... A megaesophagus can reach 26 times its normal weight and hold up to 2 liters of fluid (130). Histologically, there is epithelial thickening with cornification, leukocytic infiltration (occasionally deep into the muscularis mucosa and submucosa), and hypertrophy of the muscularis mucosa and muscularis propria (131,132,201). The thickened mucosa may have erosions and esophagitis as a result of stagnation. ...
... In asymptomatic patients, the sphincter relaxes following 75 to 85% of initiated swallows irrespective of the presence or absence of dilation. Pessoa (195) has shown that in 50% of asymptomatic chagasic patients, the lower esophageal sphincter fails to relax after swallowing (132). Collectively, these data suggest that esophageal body abnormalities can occur independently of the lower esophageal sphincter dysfunction. ...
Chagas' disease, caused by Trypanosoma cruzi, is an important cause of morbidity in many countries in Latin America. The important modes of transmission are by the bite of the reduviid bug and blood transfusion. The organism exists in three morphological forms: trypomastigotes, amastigotes, and epimastigotes. The mechanism of transformation and differentiation is currently being explored, and signal transduction pathways of the parasites may be involved in this process. Parasite adherence to and invasion of host cells is a complex process involving complement, phospholipase, penetrin, neuraminidase, and hemolysin. Two clinical forms of the disease are recognized, acute and chronic. During the acute stage pathological damage is related to the presence of the parasite, whereas in the chronic stage few parasites are found. In recent years the roles of tumor necrosis factor, gamma interferon, and the interleukins in the pathogenesis of this infection have been reported. The common manifestations of chronic cardiomyopathy are arrhythmias and thromboembolic events. Autoimmune, neurogenic, and microvascular factors may be important in the pathogenesis of the cardiomyopathy. The gastrointestinal tract is another important target, and "mega syndromes" are common manifestations. The diagnosis and treatment of this infection are active areas of investigation. New serological and molecular biological techniques have improved the diagnosis of chronic infection. Exacerbations of T. cruzi infection have been reported for patients receiving immuno-suppressive therapy and for those with AIDS.
... 79,81,82 The parasympathetic denervation of the digestive tract and the consequent morphological and functional alterations have been extensively described. [83][84][85][86] The involvement of the glands and secondary organs of the digestive tract in Chagas disease has not been studied much. 81,82,87 When ESN is destroyed, the bile secretion is blocked, increasing the gallbladder size. ...
Hydroxymethylnitrofurazone (NFOH) is a nitrofurazone prodrug effective in vivo during acute infections, and it has less hepatotoxicity effect than the standard drug benznidazole (BZN) which has been used during short‐ and long‐term treatment. In the present study, we induced the indeterminate form of Chagas disease in mice with a Y strain of Trypanosoma cruzi and analysed the histopathological data about the effects of NFOH and BZN on different tissues, including the heart, skeletal muscle, liver, kidney, colon, spleen and brain. After infection, BALB/c mice were treated with NFOH (150 mg/kg) and BZN (60 mg/kg) for 60 days and then submitted to immunosuppression using dexamethasone (5 mg/kg) for 14 days. Two trained analysts, as part of a blind evaluation, examined the results using serial sections of 3 mm diameter in two different moments. The results showed reactivation of the disease only in the infected nontreated group (POS). After treatment, amastigote nests were found in the heart, colon, liver and skeletal muscle in the POS group and in the heart and liver of the BZN group. Interestingly, amastigote nests were not found in the NFOH and NEG groups. The histopathological analysis showed fewer tissue lesions and parasite infiltrates in the NFOH group when compared with the BZN and POS groups. We have not observed any increase in the levels of hepatocellular injury biomarkers (AST/ALT) in the NFOH group. These in vivo studies show the potential for NFOH as an effective and safe compound useful as an anti‐T. cruzi agent.
... According to Gabella 11 , the loss of neurons of the myenteric plexus of the small intestine of the guinea pig was of 40 and 60%. On the other hand, for the human esophagus, Koberle 26 and Wada 27 observed a neuronal reduction of about 55% in the myenteric plexus due to age which would be responsible for malfunctions in the esophagus confirmed in the presbiesophagus. In a work on the aging of the myenteric plexus of the guinea pig colon, Alves 17 observed a neuronal drop of around 46%. Santer and Baker 25 observed a reduction of 64% in the rat colon for myenteric neurons. ...
To study the aging of submucous plexus of the small intestine (jejunum-ileum) of the guinea pigs from the quantitative, structural and ultrastructural perspective.
Chemical preparations of membrane of the jejunum-ileum of old and young animals with the use of light and electronic microscope.
The ganglia of young animals presented between 1 and 56 neurons and the old animals presented from 1 to 30 neurons. The mean density of the ganglia by cm(2) in the young jejunum-ileum was of 551±36.89 and in the old one 413±11.86. The density of the neurons was 5011±291.11 neurons/cm(2) average in young animals and 2918±120.70 neurons/cm(2) in the old ones. The size of the neurons varied in both age groups. The collagen fibers in the ganglia of old animals they were condensed. Degenerated mitochondrias in the interior of the cell were frequent in the old animals.
In submucous plexus of the jejunum-ileum there is a loss of 38% of the neurons with aging.
... material from patients in the chronic phase is expected as, According to this hypothesis, megaesophagus, megacolon according with which we will describe latter, it seems and cardiac dilation in Chagas' disease are consequences necessary to examine several different sections of the heart of the denervation of the parasympathetic autonomous to detect the parasite in this phase of the disease. system, whereas the myocardial inflammation should not be considered as an important element for cardiac failure [19][20][21]. Several authors have demonstrated [17,[22][23][24][25] a 4 . ...
Cardiomyocyte apoptosis as well as proliferation have been described in congestive heart failure, but their clinical relevance remains unclear. In order to clarify whether apoptosis and cell proliferation occur in patients with idiopathic dilated cardiomyopathy and whether their degree in left ventricle fragments resected during partial left ventriculectomy has any influence on the outcome after this surgery, we compared their occurrence in four groups of patients: group A, short-term survivors (n = 18); group B, deaths within 6 months of the surgery (n = 13); group C, long-term survivors (n = 12); and Group D, deaths within 60 months (n = 19).
Apoptotic cardiomyocytes and interstitial cells were quantified in left ventricle fragments from 31 patients with idiopathic-dilated cardiomyopathy using the TUNEL assay. Cell proliferation was quantified in parallel sections by KI-67 immunohistochemistry.
Apoptotic cells were present in the majority of cases (n = 24) and proliferative cells in all cases. Whereas there was no significant difference regarding all parameters examined between Groups A and B, there was a highly significant difference between Groups C and D in the number of apoptotic cardiomyocytes (P = 0.012) and apoptotic interstitial cells (P = 0.006). There was no significant relationship between apoptotic cardiomyocytes and KI-67-positive cardiomyocytes, but a negative correlation between apoptotic interstitial cells and KI-67-positive interstitial cells (r = -0.383; P = 0.028).
Cardiomyocyte apoptosis and proliferation occur in the majority of patients with idiopathic-dilated cardiomyopathy. High numbers of apoptotic cardiomyocytes and apoptotic interstitial cells are significantly related to a bad late outcome after partial left ventriculectomy.
... abdominal esophagus is resected while its cervical segment is preserved. Since the myenteric plexuses destroyed by the parasite are almost nonexistent in this segment, this region is not affected by the disease [14], with no decrease in the number of myenteric plexuses and/or their replacement with fibrous tissue, pathognomonic findings of chagasic esophagus, being observed in this segment [15]. ...
Chagas' disease affects about 5 to 8 million individuals in Brazil, with 5% to 8% of them developing megaesophagus. In view of the transformation of the esophagus into an inert tube unable to propel food to the stomach, and in order to prevent complications, the elected treatment for advanced megaesophagus is subtotal esophagectomy. We evaluate here the outcome of laparoscopic transhiatal subtotal esophagectomy in the treatment of advanced megaesophagus.
Thirty patients with advanced esophagopathy, 26 with chagasic and 4 with idiopathic megaesophagus, were submitted to transhiatal subtotal esophagectomy without thoracotomy through laparoscopy and left cervicotomy. Contrast exams of the esophagus, stomach, and duodenum (ESD), upper digestive tract endoscopy (UDE), esophageal electromanometry, and 24-hour pHmetry were performed during the preoperative and postoperative period. With respect to the surgical technique, pyloroplasty was not performed. The cervical esophagus was dissected through a left cervicotomy and the esophagogastric anastomosis was performed between the cervical segment of the esophagus and the posterior wall of the stomach.
No death or conversion to open surgery occurred in the present series. Complications were observed in 8 patients (26.7%): 6 cases of pneumothorax (20%), 2 of cervical fistulas (6.7%), 7 of transient dysphonia (23.3%), and 1 of anastomotic esophagogastric stenosis (3.3%). One (3.3%) of the patients developed dysphagia for solid food after 36 months despite normal ESD, UDE, electromanometry, and 24-hour pHmetry.
The present results show that laparoscopic transhiatal subtotal esophagectomy is a feasible and safe procedure with an excellent postoperative outcome.
parasitic zoonoses diseases in human and animals
A brief overview of the evolution of knowledge about Chagas disease since its discovery by Carlos Chagas in 1909 until the mid-1940s is presented. The trajectory of physician Pedreira de Freitas and his growing involvement in research in the area led to his contributions to laboratory diagnosis – which lent consistency and security to epidemiological surveys of Chagas disease – and the redefinition of the scale of the disease in Brazil and the Americas with its terrible social and economic impact. His proposal for the disease prevention model – based on selective purging in the application of insecticide – was adopted nationally and internationally and made it possible to bring the disease under control in Brazil and other countries. He devoted himself with equal intensity to enhancing the teaching of medical practices in the community and was a pioneer in the implementation of preventive medicine in medical education in Brazil.
Data were recorded on the mean nucleolar areas of neurons from the megacolon of chagasic patients, and neurons from the colon of non-chagasic subjects. The significant differences obtained were indicative of a higher level of nucleolar activity in the megacolon neurons of the chagasic, than in the colon of non-chagasic, patients. Chagasic and non-chagasic individuals in the samples analysed were not significantly different in their nucleolar/nuclear ratios, due to an increase of nuclear areas in parallel with an increase of nucleolar areas in chagasic subjects.
In the acute phase of Chagas disease the nests of Trypanosoma cruzi amastigote forms are found in tissues, especially in cardiac, skeletal and smooth muscle cells from human body. However the most important element of severe injuries formation in the heart and digestive tube tissues is the lymphocyte and macrophage cells infiltration triggering the destruction of normal, non-parasitized heart muscles, and ganglia from the intestine and peripheral nervous system. The non-parasitized target cells destruction caused by lymphocytes and macrophages from the immune system is particularly evident during the chronic phase of the chagasic infection. The severe inflammation weakens the organs, leading to dilatation and to insufficiency. The cellular death implies in replacement by fibrous scars which are only a sequelae from the rejection of the "self" tissue.
Die amerikanische Trypanosomose, verursacht durch das Trypanosoma cruzi (Chagas, 1909), war ursprünglich eine auf Wirbellose (Triatominae) beschränkte Parasitose, die sich nach Einbeziehung von Vertebraten in den parasitären Entwicklungscyclus auf zahlreiche Wirbeltierarten ausdehnte. Nachdem sich einige Überträger an die menschlichen Behausungen angepaßt hatten und dadurch auch der Mensch in den Entwicklungskreislauf des Trypanosoms eingeschlossen worden war, nahm sie schließlich den Charakter einer typischen Zoonose an (Chagas, 1912).
Silver stainings (Masson-Fontana and Sevier- Munger methods) were applied to sections from surgical specimens of chagasic megasigmoid. The distribution and the number of both enterochromaffin (EC) cells and EC plus argyrophyl (ARG) cells were studied. Both of them, EC and ARG cells presented a predominantly basal localization in mucosal glands of megasigmoids (n = 16) and Controls (n= 8) The counting of EC cells and EC plus ARG cells has shown that only the group EC plus ARG cells was significantly increased. Morphometric studies revealed a significant increase in the thickness of the muscle and mucosa layers of the megasigmoid when compared to the Controls.
One thousand seven hundred and eight chronic chagasic post-mortem examinations studied from a total of4690 autopsies perfomed at our Institution. Two hundred and seventy-three chagasic had megas. Megacolon was the most frequent, followed by megaesophagus. Megacolon associated with megaesophagus was, the third mostcommom finding. Our data are discussed and compared with the literature. Megacolon and megaesophagus were more prevalent in man, as shown by other workers. Higher parasitemia perhaps could explain this finding.
Os autores descrevem o caso de um recém-nascido anencéfalo com oito dias de vida, que à autópsia apresentava grande dilatação do cólon descendente, acompanhada de alterações degenerativas e inflamatórias dos plexos mioentéricos e parasitismo de células volumosas, de núcleos gigantes e vacuolados, por formas amastigotas de Trypanosoma cruzi, exclusivamente no intestino grosso. As alterações colônicas foram as únicas manifestações da doença de Chagas.The authors report the case of an anencephalic neonate, who presented at autopsy extreme dilatation of the left colon accompanied by degenerative and inflammatory alterations of the myenteric plexus and parasitism of large vacuolated cells by amastigote forms of T. cruzi, exclusively in large bowel. The large bowel alterations were the sole manifestation of Chagas' disease.
Systematized study was made in 56 esophagi of chronic chagasics (17 with and 39 without megas) aiming to: 1) to avaluate the esophageal caliber and thickness ranges; 2) analyse qualitative and quantitatively, the myenteric plexuses, trying to evaluate the relation of their lesions and the development of megaesophagus (ME); 3) study the lesions of the muscularis propria to verify if they contribute or not to the beginning of the process; 4) search for T. cruzi and its eventual relationship with the inflammation; 5) identify the principal mucosal alterations. It was confirmed that the severest lesions were found in the muscularis propria and in the plexures of Auerbach ganglia. In the former, the main alterations were myositis and fibrosis. The myentric plexuses showed inflammation and neuronal depopulation when compared with non-mega chagasic esophagi and even more when compared with the controls. On the other hand, there were normal caliber esophagi with severe denervation. It is possible that several factors may lead to the esophagopathy, especially to the ME. The search for T. cruzi was found positive in four out of eight esophagi with mega and in none of eight chagasic esophagi without mega. Mucosal and submucosal lesions were unremarkable and do not seem to be involved with the development of the process.
This study was made with the objective of reevaluating the colon denervation in chronic Chagas' disease. The diameters of neuron perikaryons of the myenteric plexus were measured on paraffin sections in a ring from the sigmoid in Chagas' disease patients, 17 with and 10 without megacolon and in 10 non-chagasic controls. All neurons were counted in ten en-echelon sections. Neuron hypertrophy only occurred in the group with megacolon, and the average increase in diameter was 69.3%. This could generate an error factor in the neuron count by increasing the probability of neurons being seen in a greater number of histological sections. The original result of the neuron count gave medians of 1264, 1961, and 2665 in the groups of chagasic patients with megacolon, without megacolon, and in the control, respectively. The denervation was greater than 55% in only seven megacolon cases (41.2%). After applying a correction factor, the median in the group with megacolon was 746, and the denervation was greater than 55% in 13 cases (76.5%). This occurrence demonstrates the need to apply a correction factor when the neuron count in chagasic megacolon is being evaluated and in the other pathologies where neuron hypertrophy may be found.
Eight adult patients with visceral Chagas' disease were studied twice within an interval of 64 months. In each case the esophagus was evaluated radiologically and manometrically. None of the patients had esophageal symptoms and no significant change in resting gastroesophageal sphincter pressure was observed during the study. However in 3 patients incomplete sphincteric relaxation was noted. Normal progressive contractions did not change. The importance of these findings are discussed.
In Chagas' disease, the degeneration of the nerve cells of the intramural parasympathetic ganglia of the stomach causes a wide range of motor and secretory disturbances of the organ. To assess and to correlate the alterations of these two gastric functions, electromanometric and secretory studies were performed in 22 chagasic patients and in 12 control individuals. The gastric antrum electromanometric records were carried out in basal conditions and under the stimulation of methacholine chloride (Mecholyl). Gastric secretory studies were carried out in two sessions with a Kay's test: in the first, with the test alone; in the second, associated with bethanechol chloride (Urecholine). The chagasic patients were divided into two groups according to their gastric motor response to methacholine. It was concluded that the parasympathetic denervation in Chagas' disease changes both acid and pepsin secretions in the same direction but that as the disease worsens, the responsiveness of pepsin secretion to cholinergic action tends to disappear earlier than that of acid secretion.
Acute Trypanosoma cruzi infections can be asymptomatic, but chronically infected individuals can die of Chagas' disease. The transfer of the parasite mitochondrial kinetoplast DNA (kDNA) minicircle to the genome of chagasic patients can explain the pathogenesis of the disease; in cases of Chagas' disease with evident cardiomyopathy, the kDNA minicircles integrate mainly into retrotransposons at several chromosomes, but the minicircles are also detected in coding regions of genes that regulate cell growth, differentiation, and immune responses. An accurate evaluation of the role played by the genotype alterations in the autoimmune rejection of self-tissues in Chagas' disease is achieved with the cross-kingdom chicken model system, which is refractory to T. cruzi infections. The inoculation of T. cruzi into embryonated eggs prior to incubation generates parasite-free chicks, which retain the kDNA minicircle sequence mainly in the macrochromosome coding genes. Crossbreeding transfers the kDNA mutations to the chicken progeny. The kDNA-mutated chickens develop severe cardiomyopathy in adult life and die of heart failure. The phenotyping of the lesions revealed that cytotoxic CD45, CD8(+) γδ, and CD8α(+) T lymphocytes carry out the rejection of the chicken heart. These results suggest that the inflammatory cardiomyopathy of Chagas' disease is a genetically driven autoimmune disease.
Dysphagia is the important symptom in achalasia, and surgery is the most common treatment. The Heller-Pinotti technique is the method preferred by Brazilian surgeons. For many years, this technique was performed by laparotomy, and now the laparoscopic method has been introduced. The objective was to evaluate the immediate and long-term results of patients submitted to surgery by either laparotomy or laparoscopy.
A total of 67 patients submitted to surgery between 1994 and 2001 with at least 5 years of follow-up were evaluated retrospectively and divided into two groups: laparotomy (41 patients) and laparoscopy (26 patients). Chagas was the etiology in 76.12% of cases. Dysphagia was evaluated according to the classification defined by Saeed et al.
There were no cases of conversion to open surgery. The mean duration of hospitalization was 3.32 days for laparotomy and 2.54 days for laparoscopy (p < 0.05). An improvement in dysphagia occurred with both groups reporting good or excellent results (laparotomy: 73.17% and laparoscopy: 73.08%). Mean duration of follow-up was 8 years.
There was no difference between the two groups with respect to relief from dysphagia, thereby confirming the safety and effectiveness of the Heller-Pinotti technique, which can be performed by laparotomy or laparoscopy, depending on the surgeon's experience.
A previous study showed that the vas deferens of mice in the acute phase of Chagas' disease had a slight increase in the muscle layer area associated with a small decrease in the luminal area. The vas deferens of chronic chagasic mice, investigated in the present experiment, presented a marked increase in the luminal area in addition to a significant thinning of the muscle and epithelium layers. The structural alterations of the vas deferens observed in the acute and chronic phases of Chagas' disease were compared with the evolution of chagasic esophagopathy.
Patients diagnosed as having chronic chagasic esophagopathy were divided into three groups on the basis of radiologic findings: group I, no dilation; group II, moderate dilation, and group III, extensive dilation. Stasis esophagitis was more frequent in group III, with a significant increase in basal layer thickness when compared with groups I and II. The pathogenesis of basal layer hyperplasia may have been due to stasis of ingested food and to myenteric denervation of the viscera. This hyperplasia may be an intermediate condition explaining the higher frequency of cancer among patients with chagasic megaesophagus.
Chagas' disease is an endemic infectious disease caused by a trypanosome prevalent in South America. An acute illness occurs in childhood (1) and, if the patient survives, an enlarged heart, dilated colon and megaesophagus (2) may develop 30 to 40 years later as manifestations of chronic Chagas' disease. The majority of those infected will always have a positive comple.ment fixation test for trypanosomiasis; only the minority progress to this chronic phase with clinical signs and symptoms. It is established from autopsy incidence that 4 million people in Brazil have trypanosomiasis (3). In Sao Paulo 10% of blood donors have a positive complement fixation text (4). The disease is most prevalent in the Minas Gerais area of Brazil, where about 25% of the population have a positive complement fixation test (5), but it occurs elsewhere in Brazil and to a lesser extent in most South American countries. The trypanosome itself is found in the North American continent (6, 7) but does not usually cause Chagas' disease; the strain of trypanosome is different and the vectors do not have such a close relationship to man as in South America. There is no evidence that it exists in Europe (8) or Asia (9), and the trypanosome of Africa causes sleeping sickness rather than Chagas' disease.
Male Wistar rats were injected i.p. with 2 x 10(5) trypomastigotes of the Bolivia strain. Fifteen days later, few parasite nests were observed in the fibromuscular layer surrounding the seminal vesicle acini of chagasic animals and no parasites were detected in the testis and ventral prostate. A significant decrease was observed in the absolute weight and fructose content of the seminal vesicle and ventral prostate of chagasic rats, which also presented a sharp decrease in plasma testosterone levels.
The pathogenesis of chronic chagasic cardiopathy is still a debated matter. In this review, the main theories raised about it since the first description of the disease in 1909 by Carlos Chagas, are considered. The scarcity of T.cruzi parasites into the myocardium and the apparent lack of correlation between their presence and the occurrence of myocardial inflammatory infiltrate, have originated many theories indicating that chronic Chagas' cardiopathy is an autoimmune disease. Recently however, papers using immunohistochemical technique or PCR have demonstrated a strong association between moderate or severe myocarditis and presence of T.cruzi Ags, indicating a direct participation of the parasite in the genesis of chronic chagasic myocarditis. Different patterns of cytokine production seem to have important role in the outcome of the disease. Participation of the microcirculatory alterations and fibrosis as well as the relationship with the parasite are also emphasized. Finally, the author suggests that the indeterminate form of the disease occurs when the host immunological response against the parasite is more efficient while the chronic cardiopathy occurs in patients with hyperergic and inefficient immune response.
Tissue tropism, the role of reinfection in the development of Chagas' disease, and the selection of subpopulations of Trypanosoma cruzi were evaluated in hamsters inoculated with the VIC strain of T. cruzi. Adult allogeneic male hamsters were inoculated once or reinoculated by the intraperitoneal route up to four times with 2000 blood trypomastigotes. Animals were studied by blood culture, histopathology, immunohistochemistry, and molecular techniques (PCR and low-stringency single specific primer-PCR). Homogeneity of the T. cruzi population observed in different tissues suggests that selective tropism of the VIC strain extends only to various muscle tissues in hamsters and that reinfection is not a factor in the development of the inflammatory processes, although it may aggravate it, possibly due to an increase in tissue parasitism, which might induce autoimmune mechanisms. Reinfection did not induce selection of subpopulations in the tissue or in the blood.
In the present review we have summarized remarkable historical data on Chagas' disease studies putting special emphasis on histopathological findings and pathogenetic theories as well as recent discoveries based on the use of advanced modern technologies in pathology and immunology. A unified theory that links almost all of these findings is proposed. Chronic cardiac Chagas' disease represents the result of a close interaction between the host and the parasite, causing different clinical pictures: patients with an efficient immune response may adequately circumvent the parasitic infection and the individual will develop the indeterminate form. Deficient immune response of the host and/or a high initial parasitemia favor an immune imbalance that might lead to development of a permanent inadequate immunological response against the parasite. The inflammatory response, which is probably recurrent, undergoing periods of more accentuated exacerbation, is most likely responsible for progressive neuronal damage, microcirculatory alterations, heart matrix deformations and consequent organ failure.
Although Chagas' disease esophagopaty and idiopathic (primary) achalasia share several similarities, however, some differences between the two diseases have been noticed. To evaluate if treatment options and their results can be accepted universally, the authors review characteristics of both diseases in the international and Latin American literature. Neuronal denervation, sensitivity to gastrin, patient age, duration of symptoms, lower esophageal sphincter pressure, incidence of vigorous achalasia, and cancer risk are considered points of discrepancy between the maladies. Data with a high level of evidence base are scarce; however, differences between the diseases seem to exist, despite the fact that no influence on response to treatment was noticed.
Various investigators agree that the incidence of cholelithiasis is greater in patients with Chagas disease. The most plausible explanation for this is based on the parasympathetic denervation that occurs over the whole digestive tract due to Chagas disease. In order to analyze the occurrence of this alteration, gallbladder neuron counts were performed on cholelithiasis patients with and without Chagas disease who were being treated at the Department of Digestive Surgery, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil. In the present study, a notable reduction in the number of neurons in the gallbladder wall was observed in Chagas patients, in comparison with non-Chagas subjects.
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