scholarly journals Chronic Atrophic Gastritis with Negative Intrinsic Factor and Parietal Cell Antibody Presenting as a Severe Hemolytic Anemia

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
G. F. Cittolin-Santos ◽  
S. Khalil ◽  
J. K. Bakos ◽  
K. Baker

A 28-year-old Caucasian male with Hashimoto’s disease and vitiligo presented with two weeks of dizziness on exertion following pharyngitis which was treated with prednisone 40 mg by mouth once a day for five days. Initial workup revealed anemia, elevated lactate dehydrogenase (LDH), and low haptoglobin. He underwent workup for causes of hemolytic anemia which was remarkable for a peripheral blood smear with hypersegmented neutrophils and low vitamin B12 levels concerning for pernicious anemia. Parietal cell and intrinsic factor antibodies were negative, and he then underwent an esophagogastroduodenoscopy with biopsy. The biopsy was negative for Helicobacter pylori, and the immunohistochemical stains were suggestive of chronic atrophic gastritis. He was started on vitamin B12 1,000 mcg intramuscular injections daily. His hemoglobin, LDH, and haptoglobin normalized. Given the absence of the parietal cell antibody and intrinsic factor antibody, this is a rare case of seronegative pernicious anemia.

1968 ◽  
Vol 55 (5) ◽  
pp. 575-583 ◽  
Author(s):  
I. Michael Samloff ◽  
Martin S. Kleinman ◽  
Michael D. Turner ◽  
Michael V. Sobel ◽  
Graham H. Jeffries

Blood ◽  
1972 ◽  
Vol 39 (6) ◽  
pp. 862-865 ◽  
Author(s):  
Leonard S. Goldberg ◽  
Jo Ellen Cunningham ◽  
Paul I. Terasaki

Abstract Sera from 60 patients with pernicious anemia were studied for the presence of lymphocytotoxins (LCT), blocking and binding autoantibodies to intrinsic factor, and gastric parietal cell autoantibody. LCT were found in 21 sera. Cytotoxic activity was detected at 15°C but not at 24°C and did not appear to have HL-A specificity. Autocytotoxins were present in four of eight patients tested. Blocking antibody to intrinsic factor was found in 34 sera, binding antibody in 14 sera, and parietal cell antibody in 48 sera. Sera from 14 patients contained all three types of autoantibodies, and 12 sera were void of these autoantibodies. Of the 14 sera with three types of autoantibodies, LCT were detected in ten; none of the 12 sera without autoantibodies showed cytotoxic activity. These studies suggest that LCT may reflect the degree of autoimmune derangement in pernicious anemia; alternatively, LCT may represent naturally occurring immunosuppressants.


2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Amanda M. Woodford ◽  
Rabhea Chaudhry ◽  
Gabriella A. Conte ◽  
Varsha Gupta ◽  
Madhurima Anne

Vitamin B12 is an essential nutrient which plays an important role in neurological function, hematopoiesis, and DNA synthesis. Low levels usually stem from either poor intake or a malabsorptive process. Presently, the most common cause of vitamin B12 deficiency is food-bound cobalamin malabsorption, which occurs when there is impaired release of vitamin B12 from ingested food due to an outstanding factor preventing the release of the nutrient from its transport protein. Such causes include achlorhydria, gastritis, gastrectomy, or the use of PPIs or antacids. A rarer cause is autoimmune chronic atrophic gastritis, resulting in pernicious anemia. In this disease process, there is destruction of parietal cells and thus a reduction in intrinsic factor, which is essential to the absorption of vitamin B12. Deficiency will result in a variety of abnormalities including but not limited to pancytopenia, paresthesias, and neuropsychiatric symptoms. A rare manifestation of vitamin B12 deficiency is hemolytic anemia, which occurs due to intramedullary and extramedullary dysfunction. This case describes a 46-year-old male with no past medical history who presented with chest pain, fatigue, and progressive weakness, found to have hemolytic anemia, ultimately attributed to vitamin B12 deficiency. Antiparietal cell antibodies and intrinsic factor antibodies (IFA) were both negative. Still, the patient underwent an endoscopy with biopsies of the stomach; pathology was consistent with chronic metaplastic atrophic gastritis. The patient improved with intramuscular vitamin B12 supplementation. This case highlights both a rare cause and presentation of vitamin B12 deficiency. Patients with autoimmune chronic atrophic gastritis should have antiparietal cell or intrinsic factor antibodies. Still, seronegative patients have been reported, like this patient. Additionally, hemolytic anemia secondary to vitamin B12 deficiency is uncommon. The presentation will usually mirror that of a thrombotic microangiopathy (TMA), including hemolytic anemia with schistocytes on peripheral blood smear and thrombocytopenia, as it did in this patient. This clinical entity is described as pseudothrombotic microangiopathy and is crucial to identify in order to prevent the initiation of invasive treatment strategies such as plasmapheresis.


2000 ◽  
Vol 118 (4) ◽  
pp. A1251
Author(s):  
Masanori Ito ◽  
Ken Haruma ◽  
Tomoari Kamada ◽  
Yasuhiko Kitadai ◽  
Mitsu-hiro Mihara ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A709
Author(s):  
Masanori Ito ◽  
Ken Haruma ◽  
Shunji Kaya ◽  
Kazuya Taniguchi ◽  
Maki Miyamoto ◽  
...  

Blood ◽  
1966 ◽  
Vol 27 (5) ◽  
pp. 599-610 ◽  
Author(s):  
S. ARDEMAN ◽  
I. CHANARIN ◽  
A. JACOBS ◽  
LORRAINE GRIFFITHS

Abstract Addisonian pernicious anemia was present in 6 of 9 siblings (Generation II). All 9 siblings had evidence of gastric pathology as judged by the presence of antibodies against parietal cells, abnormalities in the gastric biopsy, and diminution of secretion of acid and intrinsic factor. Parietal cell antibodies were present in 10 of 17 offspring of these 9 siblings who were available for study. Gastric biopsy in the older members of this generation (III) showed atrophic gastritis; some of the younger members showed superficial gastritis. Loss of intrinsic factor was always accompanied by loss of gastric secreting cells and there was no evidence that decline of intrinsic factor secretion occurred independently of hydrochloric acid.


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