CÁNCER GÁSTRICOJesús A. Custodio MarroquínEstudiante de Medicina IX diferentes factores asociados con la aparición del cáncer gástrico, Anemia perniciosa (20 veces más frecuente que en sujetos normales). La anemia perniciosa es la causa más frecuente de déficit de vitamina B12 en adultos. Esta entidad se ha asociado con la gastritis crónica atrófica. y negatividad para anticuerpos anticélula parietal gástrica en una her-mana no trilliza. . recent retrospective study found a low incidence of gastric cancers or dysplasia in a. endocrinas, y de algunas no endocrinas (células parietales gástricas, melanocitos, etc.); . Puede también asociarse a vitiligo y anemia perniciosa, es más En el Addison de naturaleza autoinmune, asociado a SPA II puede haber anemia macrocítica por anticuerpos frente a . Cancer ; 54;
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Pernicious anaemia PA is the most common cause of vitamin B 12 deficiency in adults. PA is associated with type A chronic atrophic gastritis, autoantibodies to gastric parietal cells and to intrinsic factor, achlorhydria, low serum pepsinogen concentrations and high serum gastrin levels. Histological changes chronic atrophic gastritis may be detected years before the anaemia is manifested, and the progression of chronic atrophic gastritis to clinical anaemia is likely to years 1.
PA usually remains silent until end-stage, and some studies consider that up to 2 percent of the general population older than 60 years-old have undiagnosticated PA 1. However, macrocytic anaemia is not the only haematological presentation of atro-phic gastritis. In developed countries, cobalamin deficiency in children and young adults is more often secondary to ileal diseases, and diagnosis of PA is rare. Some authors have described a familial disease aggregation in PA, but systematic familial screening has not been recommended as a rule.
We report a case of familial PA in 3 young adult triplets. A year-old woman with a history of psoriasis complicated with psoriatic arthritis was referred to our hospital for the study of a normocytic anaemia. At that moment, physical examination was normal, and blood analysis revealed haemoglobin 9. The remaining hematologic parameters, hepatic biology, and renal function were within the normal range.
Screening serology for celiac disease atTG, antiendomisial was also negative. Endoscopic gastric biopsies showed chronic gastritis without inflammatory infiltrate but with a marked focal reduction in the number of gastric glands, and without Helicobacter pylori infection.
A screening study of pernicious anemia was carried out in two monozygotic triplets of the patient. Increased gastrinemia and low seric pepsinogen were also found. The gastric biopsy demonstrated a chronic atrophic gastritis, and duodenal biopsy ruled out celiac disease.
In the remaining triplet, a mild normocytic anemia with vitamin B 12 deficiency, positive aPCA, increased gastrinemia and low seric pepsinogen levels, was also shown. Gastric biopsies were diagnostic of chronic atrophic gastritis. After PA diagnosis in all three triplets, an older sister was likewise evaluated. Although a mild normocytic anemia with low seric cobalamin levels was observed, negative aPCA and aIFA, normal seric concentration of gastrin and pepsinogen, and normal gastric histology ruled out PA.
Ileal disease was ruled out by means of ileocolonoscopy and ileal biopsies, as well as an intestinal barium-meal follow-through. Fecal elastase show a normal exocrine pancreatic function. Cobalamin levels returned to normal range after parenteral administration for a few months, and remained stable thereafter.
There are two main mechanisms responsible of cobalamin malabsorption in PA. First, there is a progressive loss of parietal cells from the gastric mucosa that lead to the failure of intrinsic factor production. Second, the autoantibodies present in the gastric juice can bind to the vitamin B 12 -binding site of intrinsic factor, and block the formation of the vitamin B 12 -intrinsic factor complex.
The damage of parietal cells also abolishes acid secretion, that leads to achlorhydria. Likewise, gastric acid secretion, is necessary for the solubilization and reduction of food iron permitting normal iron absorption.
In turn, iron deficiency is a known complication of pernicious anemia at disease presentation or following cobalamin treatment 4. In contrast to the adult onset of the disease, childhood PA, is not associated with achlorhydria or chronic atrophic gastritis.
Some authors suggested that this pediatric presentation of PA might be the result of a genetically determined failure to secrete intrinsic factor or even the secretion of a defective intrinsic factor A genetic predisposition to PA has been suggested 7,8. In fact, several authors have reported familial aggregability of PA 6and up to 20 percent of the relatives mainly first-degree female relatives of PA patients are also affected 1,9, Furthermore, a cluster of PA and gastric autoantibodies with autoimmune endocrinopaties has been also reported 4.
However in recent reviews, Helicobacter pylori has been involved in the development of atrophic gastritis, and it is well established that H.
In addition, two-thirds of patients with atrophic gastritis and a large proportion of PA patients, have co-existing H. By now, familial screening is not advised among new-diagnosed PA relatives. Patients with PA are at a greater risk for the development of gastric neoplasms both carcinoid and adenocarcinoma. Intestinal metaplasia and atrophic gastritis associated with achlorhydria have been postulated as potencial pathogenic factors for the development of gastric cancer in patients with PA.
Although they have to be considered as a high risk group, guidelines for cancer screening in these patients are still lacking.
In clinical practice, gastroscopy is performed periodically in most of PA patients. There is no agreement in the appropiateness of routine endoscopic screening in patients with PA In these sense, a recent retrospective study found a gastrixo incidence of gastric cancers or dysplasia in a series of 68 PA patients followed-up with biannual endoscopies The authors suggested that a biannual endoscopic follow-up is not necessary and that, gastroscopic surveillance must be performed in longer periodicity.
The present case-report underlines the existence of familiar aggregation and, in turn, genetic factors in PA. Two out of the three patients were diagnosed while being clinically asymptomatic, although they had a significant cobalamin deficiency. Taking into account that PA is a known risk factor for gastric neoplasms, familial screening might be of relevance in case of twins, but systematic familial screening in all PA patients has to be accurately evaluated in the setting anemai prospective studies.
A case report an literature review. Askciado anaemia in triplets. Pernicious anemia is the most common cause of vitamin B12 deficiency in adults. This entity is associated with chronic atrophic gastritis. We report a case of pernicious anaemia in triplets. We also report a fourth gasrico of cobalamin deficiency with antibodies against intrinsic factor and anti parietal cell antigen negative antibodies in a sibling.
The present article reviews the pediatric presentation of pernicious anemia and highlights the possible existence of familial aggregation. Furthermore, the need for systematic familial screening and the usefulness of an endoscopic follow-up program in patients pernicisoa pernicious anemia are evaluated.
En este trabajo se describe la existencia de anemia perniciosa en 3 hermanas trillizas. In developed countries, cobalamin deficiency in children and young adults is more often secondary to ileal diseases, and diagnosis of PA is rare.
We report a case of familial PA in 3 young adult triplets. Gastric biopsies were diagnostic of chronic atrophic gastritis. Cobalamin levels returned to normal range after parenteral administration for a few months, and remained stable thereafter. Some authors suggested that this pediatric presentation of PA might be the result of a genetically determined failure to secrete intrinsic factor or even the secretion of a defective intrinsic factor 6.
By now, familial screening is not advised among new-diagnosed PA relatives. Taking into account that PA is a known risk factor for gastric neoplasms, familial screening might be of relevance in case of twins, but systematic familial screening in all PA patients has to be accurately evaluated in the setting of prospective studies.
N Engl J Med,pp.
Lack of specific association between gastric autoimmunity hallmarks and clinical presentations of atrophic body gastritis. W J Gastroenterol, 11pp. Ggastrico Rev, 31pp. American Society of Znemia published online Iron deficiency occurs frequently in patients with pernicious anaemia. JAMA,pp. Familial autoimmune haemolytic anaemia associated with rheumatoid arthritis and pernicious anaemia. Br J Haemat, 18pp. Familial juvenile pernicious anaemia: Br J Haemat, 3pp.
Familial selective malabsorption of vitamin B Megaloblastic anemia occurring simultaneously in white female monozygotic twins. Can Med Assoc J, 92pp.
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Immunogenetics of autoimmune diseases. Helicobacter pylori infection induces antibodies cross-reacting with human gastric mucosa. Gastroenterology,pp. The risk of gastric carcinoma and carcinoid anemai in patientswith pernicious anaemia.
A prospective follow-up study. Scan J Gastroenterol, 33pp. Gastroscopic screening in 80 patients with pernicious anaemia. Gut, 24pp. Gastroscopic screening for gastric carcinoids in pernicious anemia.
Endsocopy, 20pp. Gastroscopic follow-up of pernicious anaemia patients. Gut, 34pp. Endoscopic findings in a biennal follow-up program in patients with pernicious anemia. Hepatogastroenterol, 50pp. Therapeutic requirements in active ulcerative proctitis: Si continua navegando, consideramos que acepta su uso. To improve our services and products, we use “cookies” own or third parties authorized to show advertising related to client preferences through the analyses of navigation customer behavior.
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Anemia perniciosa by Luis Gonzalez on Prezi
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