Páncreas anular: a propósito de un caso / Annular pancreas: report of a case

El Páncreas Anular es una de las malformaciones congénitas extrínsecas más frecuentes de durante el desarrollo del intestino cefálico, quecausa una obstrucción parcial o completa en la segunda porción del duodeno. Presentamos el caso de una lactante de cuatro semanas deedad, transferida de la ciudad de Oruro al Hospital del Niño de la ciudad de La Paz, por emesis incoercible y bajo peso; estudios radiológicossugieren cuadro duodenal obstructivo, evidenciándose el mismo en el acto quirúrgico, originado por páncreas anular...

The annular pancreas is one of the most frequent congenital malformations that occur during the development of the intestine causing a partial or complete obstruction of the second portion of the duodenum. We present the case of a four weeks old baby girl who was transferred from the city of Oruro to the Hospital del Niño (Children’s Hospital) in La Paz due to incontrollable vomiting and low weight. The abdominal x-ray suggested duodenal obstruction that was evident on surgery, caused by annular pancreas.

Páncreas divisum / Pancreas divisum

El páncreas divisum es la malformación congénita más frecuente del páncreas. Se produce por una alteración en la migración de los esbozos pancreáticos en el embrión. La mayoría de los pacientes son asintomáticos y su principal síntoma es el dolor abdominal. Se ha asociado como etiología de pancreatitis aguda y/o crónica, para lo cual el estudio diagnóstico con una colangiopancreatografía ha sido fundamental. El tratamiento inicial en los pacientes sintomáticos es médico y endoscópico. La cirugía sólo se utiliza como tratamiento de última línea y en casos seleccionados.

Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes?

Despite extensive genetic and immunological research, the complex etiology and pathogenesis of type I diabetes remains unresolved. During the last few years, our attention has been focused on factors such as abnormalities of islet function and/or microenvironment, that could interact with immune partners in the spontaneous model of the disease, the non-obese diabetic (NOD) mouse. Intriguingly, the first anomalies that we noted in NOD mice, compared to control strains, are already present at birth and consist of 1) higher numbers of paradoxically hyperactive ß cells, assessed by in situ preproinsulin II expression; 2) high percentages of immature islets, representing islet neogenesis related to neonatal BETA-cell hyperactivity and suggestive of in utero BETA-cell stimulation; 3) elevated levels of some types of antigen-presenting cells and FasL+ cells, and 4) abnormalities of extracellular matrix (ECM) protein expression. However, the colocalization in all control mouse strains studied of fibroblast-like cells (anti-TR-7 labeling), some ECM proteins (particularly, fibronectin and collagen I), antigen-presenting cells and a few FasL+ cells at the periphery of islets undergoing neogenesis suggests that remodeling phenomena that normally take place during postnatal pancreas development could be disturbed in NOD mice. These data show that from birth onwards there is an intricate relationship between endocrine and immune events in the NOD mouse. They also suggest that tissue-specific autoimmune reactions could arise from developmental phenomena taking place during fetal life in which ECM-immune cell interaction(s) may play a key role

Study of the evolution of the placenta and fetal pancreas in the pathophysiology of growth retardation intrauterine due to restricted maternal diet

Intrauterine growth retard (IUGR) continues to be a significant perinatology problem at the end of this century. The nature of the etiologic agent, the time when the attack occurred during pregnancy and its duration affect the type of IUGR. Objective: To study the evolution of fetal pancreas and placenta between the 18th and 2 1st day of pregnancy in rats submitted to maternal protein-calorie restriction. Design: Randomized controlled trial on laboratory animal. Sample: Forty-one normoglycemic pregnant Wistar rats. Intervention: Rats were divided into six experimental groups according to their access to food and date of cesarean section (18th or 21 st day): control with free access to food; diet restricted to 25 per cent introduced on 1 st day of pregnancy; and diet restricted to 25 per cent after the 3rd day of pregnancy. Main measurements: Newborn weight, placenta weight, histopathological study (morphological histochemistry). Results: Maternal protein-calorie malnutrition caused intrauterine growth retard (IUGR) after the 18 th day of pregnancy. Dietary restriction did not interfere with the morphology of the fetal pancreas and theimmunohistochemical study of the placenta showed that glycogen stores were decreased between the 18 th and 21 st day in the control group and in a diet restricted to 25 per cent from the first day of pregnancy. Dietary restriction after the 3rd day of pregnancy led to low placental glycogen concentrations on the 18 th day and disappearance on the 21 st day. Conclusion: The pathophysiology of IUGR due to maternal protein-calorie restriction in rats is related to lower placental weight and low placental glycogen stores.

Morphogenic development of the pancreas in the staged human embryo

The Carnegie stage is widely applied in the field of human embryology, and it is more logical to analyze the embryos by this stage than CR length or menstrual age. In this study, the early development of the pancreas is studied by tissue observation and reconstruction using serial sections of 33 human embryo ranging from Carnegie stages 11 to 23. The dorsal pancreas develops from the dorsal wall of the duodenum in stage 12, and the ventral pancreas from the proximal part of the cystic primordium in stage 13 or 14 as a single epithelial thickening, but in one case, as a bilateral thickening which contains some isolated spaces. The rotation of the ventral pancreas starts in stage 15, and completes in stage 17. Surrounding connective tissue differentiates in stage 18.