Sangrado digestivo alto secundario a tumor del estroma gastrointestinal (GIST) asociado a linfoma MALT: caso clínico

Marcelo Castillo Paucar; Gabriela Fernanda Quingalombo Cargua; Tania Paulina Garcés García

doi:10.51597/rmicg.v2i2.52

Sangrado digestivo alto secundario a tumor del estroma gastrointestinal (GIST) asociado a linfoma MALT: caso clínico

Revista Medicina e Investigación Clínica Guayaquil ◽

10.51597/rmicg.v2i2.52 ◽

2021 ◽

Vol 2 (2) ◽

pp. 41-45

Author(s):

Marcelo Castillo Paucar ◽

Gabriela Fernanda Quingalombo Cargua ◽

Tania Paulina Garcés García

Keyword(s):

Linfoma No Hodgkin ◽

S 100 ◽

H Pylori ◽

Marcadores Tumorales

Los tumores del estroma gastrointestinal (GIST) son neoplasias raras que se localizan predominantemente en el estómago; sus síntomas son sangrado gastrointestinal, anemia y dolor abdominal. Se diagnostica en presencia de positividad del proto oncogén KIT o CD34, desmina, S-100, DOG1, entre otros. El tratamiento es la resección en cuña o imatinib según el estadio. El linfoma MALT es un linfoma no Hodgkin extra nodal de estirpe B que se localiza en el estómago frecuentemente. Su sintomatología suele ser inespecífica: náuseas, vómitos, anorexia, pérdida de peso y sangrado. Su diagnóstico requiere la presencia de células plasmáticas, folículos reactivos y células tipo centrocitos que invaden la mucosa y forman lesiones linfoepitaliales; son positivos para CD20, CD10, CD5 y ciclina D1. Las neoplasias sincrónicas gástricas son pocos frecuentes, el diagnóstico generalmente ocurre de forma incidental durante el estudio histopatológico de una pieza quirúrgica. Estos tumores representan un reto clínico para su tratamiento, ya que cada uno debe ser estadificado por separado. Se presenta el caso clínico de un paciente de 31 años, quien consulta por hematemesis y melenas, con antecedentes de lesión subcardial subepitelial en endoscopía previa, con marcadores tumorales negativos y estudio histopatológico que demostró un tumor del estroma gastrointestinal tipo de células fusiformes asociado a linfoma no Hodgkin; quien recibió tratamiento erradicador para H. pylori e Imatinib con adecuada respuesta.

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The rod-to-coccoid body transformation in cultures of Helicobacter pylori

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100160686 ◽

1990 ◽

Vol 48 (3) ◽

pp. 626-627

Author(s):

A. R. Crooker ◽

W. G. Kraft ◽

T. L. Beard ◽

M. C. Myers

Keyword(s):

Helicobacter Pylori ◽

Growth Cycle ◽

Negative Bacterium ◽

Body Formation ◽

Coccoid Form ◽

Spiral Form ◽

Prolonged Culture ◽

H Pylori ◽

Upper Gastrointestinal

Helicobacter pylori is a microaerophilic, gram-negative bacterium found in the upper gastrointestinal tract of humans. There is strong evidence that H. pylori is important in the etiology of gastritis; the bacterium may also be a major predisposing cause of peptic ulceration. On the gastric mucosa, the organism exists as a spiral form with one to seven sheathed flagella at one (usually) or both poles. Short spirals were seen in the first successful culture of the organism in 1983. In 1984, Marshall and Warren reported a coccoid form in older cultures. Since that time, other workers have observed rod and coccal forms in vitro; coccoid forms predominate in cultures 3-7 days old. We sought to examine the growth cycle of H. pylori in prolonged culture and the mode of coccoid body formation.

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Vacuoles Induced in Mammalian Cells by Helicobacter Cytotoxin are Acidic Organelles

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158388 ◽

1990 ◽

Vol 48 (3) ◽

pp. 168-169

Author(s):

M. H. Chestnut ◽

C. E. Catrenich

Keyword(s):

Acridine Orange ◽

Mammalian Cells ◽

Laser Scanning ◽

Laser Scanning Microscopy ◽

Confocal Laser ◽

Ulcer Disease ◽

Gastroduodenal Disease ◽

H Pylori

Helicobacter pylori is a non-invasive, Gram-negative spiral bacterium first identified in 1983, and subsequently implicated in the pathogenesis of gastroduodenal disease including gastritis and peptic ulcer disease. Cytotoxic activity, manifested by intracytoplasmic vacuolation of mammalian cells in vitro, was identified in 55% of H. pylori strains examined. The vacuoles increase in number and size during extended incubation, resulting in vacuolar and cellular degeneration after 24 h to 48 h. Vacuolation of gastric epithelial cells is also observed in vivo during infection by H. pylori. A high molecular weight, heat labile protein is believed to be responsible for vacuolation and to significantly contribute to the development of gastroduodenal disease in humans. The mechanism by which the cytotoxin exerts its effect is unknown, as is the intracellular origin of the vacuolar membrane and contents. Acridine orange is a membrane-permeant weak base that initially accumulates in low-pH compartments. We have used acridine orange accumulation in conjunction with confocal laser scanning microscopy of toxin-treated cells to begin probing the nature and origin of these vacuoles.

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