Microangiopathic haemolytic anaemia with thrombocytopenia induced by vitamin B12 deficiency long term after gastrectomy

Harada, Yukinori; Komori, Itsumi; Morinaga, Kouhei; Shimizu, Taro

doi:10.1136/bcr-2018-225915

Cited by 9 publications

(8 citation statements)

References 22 publications

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“…Although rare, reports of this disease process exist in the literature. However, in a majority of these cases, the diagnosis of pernicious anemia is demonstrated through histological exam in addition to laboratory studies, or evidence of prior gastrectomy or ileum resection [9][10][11]. Historically, these laboratory studies included surveilling for intrinsic factor deficiency using the Schilling test [12].…”

Section: Discussionmentioning

confidence: 99%

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Woodford

Chaudhry

Conte

et al. 2021

Case Reports in Hematology

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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.

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Section: Discussionmentioning

confidence: 99%

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Woodford

Chaudhry

Conte

et al. 2021

Case Reports in Hematology

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“…Other than in congenital abnormal cobalamin metabolism due to a functional loss of the MMACHC gene, acquired VB 12 deficiency rarely causes pseudo-TMA. Pernicious anemia and gastrectomy have been reported to be associated with pseudo-TMA due to VB 12 deficiency in the elderly ( 6 , 9 ). Although a case of pseudo-TMA due to acquired VB 12 deficiency associated with neglect has been reported in pediatric patients ( 10 , 11 ) we believe that this adult case offers an important clinical lesson because the patient developed pseudo-TMA because of a lack of VB 12 due to insufficient dietary care.…”

Section: Discussionmentioning

confidence: 99%

Pseudo-thrombotic Microangiopathy Caused by Acquired Cobalamin Deficiency Due to Unintentional Neglect

et al. 2021

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Acquired vitamin B12 (VB12) deficiency is a rare cause of thrombotic microangiopathy (TMA). We experienced an 86-year-old Japanese woman who presented with coma, renal dysfunction, and microangiopathic hemolytic anemia. Although we initially considered thrombotic thrombocytopenic purpura, we eventually diagnosed her to have VB12 deficiency due to inappropriate dietary care based on her low serum VB12 level, social history, and negative parietal cell finding and the presence of intrinsic factor antibody. Because similar cases are expected to increase in today's aging society, our experience underscores the importance of including acquired VB12 deficiency in the differential diagnosis of TMA, even in elderly patients without a history of gastrectomy.

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“…She was suspected to have TTP but her ADAMTS13 was reported as normal. Investigations showed very low vitamin B12 and she responded very well to vitamin B12 supplementation alone [40]. Tran et al published a series of 41 patients with acquired vitamin B12 deficiency presenting with TMA features.…”

Section: Acquired Vitamin B12 Deficiency and Pseudo-tmamentioning

confidence: 99%

Vitamin B12 deficiency and metabolism-mediated thrombotic microangiopathy (MM-TMA)

Sabry

Elemary

Burnouf

et al. 2020

Transfusion and Apheresis Science

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Thrombotic microangiopathies (TMA) are characterized by microangiopathic hemolytic anemia, thrombocytopenia and organ damage resulting from mechanical factors, accumulation of the ultra-large von Willebrand factor multimers or complement-mediated abnormalities. Severe acquired vitamin B12 (Cobalamin-Cbl) deficiency or congenital defective Cbl metabolism could lead to a picture that mimics TMA. The later has been termed metabolism-mediated TMA (MM-TMA). This confusing picture is mediated partly by the large red cell fragmentation coupled with reduced platelet production in the absence of vitamin B12 and partly by the accumulated byproducts and metabolites that induce endothelial injury and hence organ damage. Expensive and complicated treatment for TMA is often initiated on an empiric basis, pending the results of confirmatory tests. In contrast, vitamin B12 Pseudo-TMA and MM-TMA could be treated with proper vitamin B12 supplementation. It is therefore important to identify these disorders promptly. The recent availability of a validated scoring system such as the PLASMIC score uses simple clinical and laboratory parameters. As it incorporates the mean corpuscular volume in its laboratory parameters, this helps in the identification of pseudo and MM-TMA. Perhaps some minor modification of this scoring system by changing the parameters of hemolysis to include reticulocytosis and rather than and/or other hemolytic parameters could even help refine this identification.

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Microangiopathic haemolytic anaemia with thrombocytopenia induced by vitamin B12 deficiency long term after gastrectomy

Cited by 9 publications

References 22 publications

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Pseudo-thrombotic Microangiopathy Caused by Acquired Cobalamin Deficiency Due to Unintentional Neglect

Vitamin B12 deficiency and metabolism-mediated thrombotic microangiopathy (MM-TMA)

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