Autoimmune Gastritis

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amikhchi

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So autoimmune gastritis (type A chronic) is related to auto-antibodies to parietal cells, but in pathoma it says the pathogenesis is mediated by t-cells (referring to it as Type 4 HSR), leading to auto-antibody formation; in first aid immuno section pernicious anemia is a type 2 HSR (makes sense)...

is first aid just referring to pernicious anemia alone is a type 2, but chronic gastritis is a type 4 HSR that leads to pernicious anemia (type 2)?

am i just looking at this all wrong?😕
 
So autoimmune gastritis (type A chronic) is related to auto-antibodies to parietal cells, but in pathoma it says the pathogenesis is mediated by t-cells (referring to it as Type 4 HSR), leading to auto-antibody formation; in first aid immuno section pernicious anemia is a type 2 HSR (makes sense)...

is first aid just referring to pernicious anemia alone is a type 2, but chronic gastritis is a type 4 HSR that leads to pernicious anemia (type 2)?

am i just looking at this all wrong?😕

Interesting question I don't know the answer to but I hope someone responds.
 
From Robbins:

"It was initially thought that the autoantibodies to parietal cell components, most prominently the H+,K+-ATPase, or proton pump, and intrinsic factor were involved in the pathogenesis of autoimmune gastritis. However, this is unlikely because neither secreted intrinsic factor nor the luminally oriented proton pump are accessible to circulating antibodies, and passive transfer of these antibodies does not produce gastritis in experimental animals. It is more likely that CD4+ T cells directed against parietal cell components, including the H+,K+-ATPase, are the principal agents of injury. This is supported by the observation that transfer of H+,K+-ATPase-reactive CD4+ T cells into naive mice results in gastritis and production of H+,K+-ATPase autoantibodies. There is no evidence of an autoimmune reaction to chief cells, suggesting that these are lost through gastric gland destruction during autoimmune attack on parietal cells. If autoimmune destruction is controlled by immunosuppression, the glands can repopulate, demonstrating that gastric stem cells survive and are able to differentiate into parietal and chief cells."
 
From Robbins:

"It was initially thought that the autoantibodies to parietal cell components, most prominently the H+,K+-ATPase, or proton pump, and intrinsic factor were involved in the pathogenesis of autoimmune gastritis. However, this is unlikely because neither secreted intrinsic factor nor the luminally oriented proton pump are accessible to circulating antibodies, and passive transfer of these antibodies does not produce gastritis in experimental animals. It is more likely that CD4+ T cells directed against parietal cell components, including the H+,K+-ATPase, are the principal agents of injury. This is supported by the observation that transfer of H+,K+-ATPase-reactive CD4+ T cells into naive mice results in gastritis and production of H+,K+-ATPase autoantibodies. There is no evidence of an autoimmune reaction to chief cells, suggesting that these are lost through gastric gland destruction during autoimmune attack on parietal cells. If autoimmune destruction is controlled by immunosuppression, the glands can repopulate, demonstrating that gastric stem cells survive and are able to differentiate into parietal and chief cells."

So basically its like hashimoto's thyroiditis. Autoantibodies are present, but the real damage is mediated by T-cells.

Hopefully they won't ask questions about a contested topic like this though. Another one is whether RA is type4 or type3. Most recent evidence says its more type4, but First aid says 3.
 
So basically its like hashimoto's thyroiditis. Autoantibodies are present, but the real damage is mediated by T-cells.

Hopefully they won't ask questions about a contested topic like this though. Another one is whether RA is type4 or type3. Most recent evidence says its more type4, but First aid says 3.

Yeah I saw this about RA somewhere as well (UWorld I think). It totally blew me away because I had no idea.
 
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