scholarly journals A Case of Pernicious Anaemia with Psoriasis

2020 ◽  
Vol 15 (2) ◽  
pp. 243-245
Author(s):  
Md Anisur Rahman ◽  
Most Umme Habiba Begum ◽  
Md Abdur Razzak ◽  
Jesmin Khandker

Pernicious anaemia often poses diagnostic and therapeutic challenges to the clinician. Herein, we representing a 55 years old lady who presented with anaemia along with its classical symptoms and features of peripheral neuropathy due to Pernicious anaemia associated with Psoriasis and Arthropathy without any association of other autoimmune disorder. She had all objective evidences of autoimmune atrophic gastritis in gastric fundic biopsy and positive anti-intrinsic factor antibody. Treatment with injection vitamin B12 improved the condition rapidly. JAFMC Bangladesh. Vol 15, No 2 (December) 2019: 243-245

2019 ◽  
Vol 8 (11) ◽  
pp. 1992 ◽  
Author(s):  
Marco Vincenzo Lenti ◽  
Edith Lahner ◽  
Gaetano Bergamaschi ◽  
Emanuela Miceli ◽  
Laura Conti ◽  
...  

Background: Autoimmune atrophic gastritis (AAG) leads to iron and/or vitamin B12 malabsorption, with subsequent haematological alterations which could represent the sole clinical manifestation. We aimed to assess patterns of anaemia and micronutrient deficiencies in patients with AAG at the time of diagnosis. Methods: Observational, multicentre, cross-sectional study including consecutive adult patients diagnosed with AAG within the last ten years. Cell blood count, red cell distribution width, serum vitamin B12, and ferritin were collected. Multivariate analysis for predictive factors of anaemia was computed. Results: 654 AAG patients (mean age 59.2 ± 13.8 years, female (F): male (M) ratio = 2.3:1) were included. Anaemia was present in 316 patients (48.3%; mean age 60.1 ± 15.8 years, F:M ratio = 2.3:1). Pernicious anaemia (132/316 cases, 41.7%) was more common in males (27.1% versus 12.4%; p = 0.001) and in older patients (63.0 ± 14.6 versus 58.9 ± 14.9 years; p = 0.014), while iron deficiency anaemia (112/316 cases, 35.4%) was more common in females (16.9% versus 10.0%; p = 0.039) and in younger patients (56.8 ± 16.6 versus 60.2 ± 14.6 years; p = 0.043). The prevalence of iron deficiency was equally distributed between anaemic and non-anaemic patients (p = 0.9). Anisocytosis (odds ratio: 10.65, 95% confidence interval: 6.13–18.50, p < 0.0001) was independently associated with anaemia. Conclusions: Anaemia is a common manifestation in AAG patients, mostly due to micronutrient deficiencies. Scant haematologic alterations and micronutrient deficiencies may precede overt anaemia.


Author(s):  
Chris Bunch

This chapter addresses the diagnosis, investigation, and management of anaemia due to a deficiency in iron, vitamin B12, or folate. Erythropoiesis requires an adequate supply of iron for haem formation, as well as vitamin B12 and folic acid (folate) to support high levels of DNA synthesis, and a lack of any of these will result in anaemia. Iron-deficient anaemias are typically microcytic, while a deficiency in vitamin B12 or folate results in megaloblastic haemopoiesis and a macrocytic anaemia. Iron deficiency results from poor dietary iron intake, poor absorption, increased demands, blood loss, or combinations of these. The usual cause of severe vitamin B12 deficiency in Western countries is an autoimmune atrophic gastritis, in which there is a loss of gastric parietal cell numbers and an absence of intrinsic factor production, which effectively prevents vitamin B12 absorption. This is the classical pernicious anaemia, and it is often seen in association with other autoimmune disorders. Folate deficiency may result from poor diet, malabsorption, or when demand for folate is increased, for example, during pregnancy, or with increased haemopoiesis in haemolytic anaemias or myeloproliferative disorders.


BMJ ◽  
1955 ◽  
Vol 2 (4937) ◽  
pp. 461-463 ◽  
Author(s):  
E. K. Blackburn ◽  
H. Cohen ◽  
G. M. Wilson

Gut ◽  
1973 ◽  
Vol 14 (1) ◽  
pp. 13-19 ◽  
Author(s):  
R. G. Strickland ◽  
J. M. Fisher ◽  
K. Lewin ◽  
K. B. Taylor

The Lancet ◽  
1976 ◽  
Vol 307 (7954) ◽  
pp. 310-311 ◽  
Author(s):  
R.A. Thompson

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.


Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 747-753 ◽  
Author(s):  
H. G. Desai ◽  
F. P. Antia

Abstract Sixteen patients (from Bombay) with severe vitamin B12 malabsorption due to intrinsic factor deficiency, presenting as subacute combined degeneration of the cord (7), tropical sprue (3), anemia (2), thyrotoxicosis (2), diabetes mellitus (1), and pain in the abdomen (1), are reported. The difficulties of establishing a definite diagnosis of pernicious anemia in Indian population are described. The lower incidence of circulating intrinsic factor antibody (IFA) in Indian patients with histamine-fast achlorhydria and poor vitamin B12 absorption is emphasized. The necessity of separating atrophic gastritis, with severely impaired vitamm B12 absorption, from pernicious anemia on the basis of absence or presence of IFA in serum and/or gastric juice cannot be overemphasized.


The Lancet ◽  
1967 ◽  
Vol 289 (7488) ◽  
pp. 501-502
Author(s):  
Harriet Dige-Petersen ◽  
Paul Rødbro ◽  
Jette Howitz

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