Case Report: Simultaneously diagnosed gastric adenocarcinoma and pernicious anemia – a classic association

Primary gastric cancer remains one of the most prevalent malignancies worldwide. Often patients remain asymptomatic until it is detected at an advanced stage with a poor prognosis. Thus, it’s characteristically difficult to initially diagnose until it becomes late stage, at which point prognosis becomes poor. Pernicious anemia is a classic risk factor for the development of primary gastric cancer, but is uncommonly seen in clinical practice. Over time, patients who produce the autoantibodies to intrinsic factor that cause pernicious anemia typically will present initially with clinically significant megaloblastic anemia and peripheral neuropathy. However, patients can also present with more nonspecific signs and symptoms. Thus, clinicians should remain vigilant as circulating anti-intrinsic factor antibodies only worsen the disease over time and increase the risk of developing primary gastric cancer. This report not only presents the rare concurrent diagnosis of pernicious anemia and gastric cancer, but also aims to increase clinical awareness of these two conditions’ classic association because early diagnosis and treatment significantly impacts morbidity and mortality.

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CONGENITAL PERNICIOUS ANEMIA: EFFECTS ON GROWTH, BRAIN, AND ABSORPTION OF B12

PEDIATRICS ◽

10.1542/peds.42.1.149 ◽

1968 ◽

Vol 42 (1) ◽

pp. 149-156

Author(s):

Brian McNicholl ◽

Bridget Egan

Keyword(s):

Gastric Mucosa ◽

Early Diagnosis ◽

Pernicious Anemia ◽

Autosomal Recessive ◽

Megaloblastic Anemia ◽

Intrinsic Factor ◽

Normal Gastric Mucosa ◽

Adult Type ◽

B12 Deficiency ◽

One Year

Three Irish children, two of them siblings, developed megaloblastic anemia around one year; deficiency of intrinsic factor (I.F.), presumably congenital, was shown by Schilling tests and assay of gastric juice. Congenital pernicious anemia (P.A.), in contrast to adult P.A., shows normal gastric mucosa and acidity and no antibodies to gastric mucosa or I.F. Adult type P.A., with gastric atrophy and achlorhydria, if occurring in childhood, can be called "juvenile P.A.," "congenital P.A." being reserved for the type described here. P.A. associated with polyendocrinopathy and the type described by Imerslund due to specific B12 malabsorption should be named accordingly. Congenital P.A.'s inheritance is thought to be autosomal recessive. Growth retardation and acceleration appeared to be related to B12 deficiency and treatment. I.Q.'s of around 70 in each child may represent the effects of B12 deficiency on cerebral growth. An initial malabsorption of B12 was shown to improve markedly with B12 treatment. In diagnosis of megaloblastic anemia, only that due to B12 deficiency will respond to dosage of 2 to 5 µg B12 (intramuscular) daily. Early diagnosis and treatment may prevent brain damage.

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PERNICIOUS ANEMIA, NUTRITIONAL MACROCYTIC ANEMIA, AND TROPICAL SPRUE

Blood ◽

10.1182/blood.v3.1.36.36 ◽

1948 ◽

Vol 3 (1) ◽

pp. 36-56 ◽

Cited By ~ 16

Author(s):

LUCY WILLS

Keyword(s):

Gastric Mucosa ◽

Pernicious Anemia ◽

Megaloblastic Anemia ◽

Genetic Defect ◽

Macrocytic Anemia ◽

Intrinsic Factor ◽

High Protein Diet ◽

Tropical Sprue ◽

Blood Levels ◽

Intracellular Enzyme

Abstract The following tentative conclusions as to the relationship of pernicious anemia, nutritional macrocytic anemia and tropical sprue to one another and their pathogenesis are drawn from a study of the literature and from unpublished work: 1. That these three clinical conditions are three distinct entities possessing a common characteristic in the presence of a panhemopoietic dystrophy characterized by a megaloblastic erythropoiesis and corresponding changes in the myeloid cells and platelets. 2. That this panhemopoietic dystrophy possibly results from the breakdown of an intracellular enzyme system but that the deficiencies causing the breakdown differ; in pernicious anemia the liver principle is apparently at fault, in endemic nutritional macrocytic anemia another unidentified factor is missing, in sprue either or both may be at fault. 3. Folic acid is active therapeutically in all three diseases, but in all it generally fails to restore completely normal blood levels. 4. Pernicious anemia is probably due to a genetic defect which produces an atrophy of the gastric mucosa. As a consequence of this interference with gastric function there is a failure in the formation or absorption of the liver factor and possibly of another neurotrophic factor, which failure results in the development of a macrocytic megaloblastic anemia and the characteristic changes in the nervous system. Indefinite replacement therapy is necessary as the changes in the gastric mucosa are irreversible. The cause of the increased hemolysis is unknown. 5. Endemic nutritional macrocytic anemia is an unconditioned food deficiency, the deficiency being in a factor other than the liver principle, possibly a co-enzyme present in or associated with good biologic protein and the vitamin B2 complex. There are no characteristic pathologic changes except those of the hemopoietic organs which are not specific to the disease. A hemolytic type of the disease occurs in areas of high malarial incidence. After successful treatment the disease does not relapse if the diet is satisfactory. Pregnant women are particularly liable to develop the disease. 6. Tropical sprue is due to a functional disorder of the intestine, possibly primarily a failure in phosphorylation of fatty acids, glycerol and glucose. Diarrhea with characteristic stools and a macrocytic anemia are characteristic findings. The macrocytic anemia may be due to a failure in absorption of one or more essential hemopoietic factors or to a lack of Castle’s intrinsic factor. The cause of the functional breakdown is unknown. Treatment is with a high protein diet and liver extracts. Relapses are common. My thanks are due to my colleagues for carrying on my work while I wrote this paper.

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Studies on Intrinsic Factor and Pernicious Anemia: III. Intrinsic Factor Activity and B12-Binding Power of Electrophoretic Fractions of Intrinsic Factor Concentrates

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.3109/00365516109137275 ◽

1961 ◽

Vol 13 (2) ◽

pp. 245-248 ◽

Cited By ~ 1

Author(s):

H. Berlin ◽

R. Berlin ◽

G. Brante ◽

S-G. Sjöberg

Keyword(s):

Pernicious Anemia ◽

Intrinsic Factor ◽

Factor Activity ◽

Binding Power

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A case report on Subacute Combined Degeneration of spinal cord in children – A rare neurological manifestation in Vitamin B12 deficiencies

International Journal of Bioassays ◽

10.21746/ijbio.2017.6.12.2 ◽

2017 ◽

Vol 6 (12) ◽

pp. 5562

Author(s):

Tiana Mary Alexander ◽

Vineeta Pande ◽

Sharad Agarkhedkar ◽

Dnyaneshwar Upase

Keyword(s):

Spinal Cord ◽

Case Report ◽

Vitamin B12 ◽

Pernicious Anemia ◽

Chronic Diarrhea ◽

Megaloblastic Anemia ◽

Vegetarian Diet ◽

Malabsorption Syndrome ◽

Subacute Combined Degeneration ◽

B12 Deficiency

Megaloblastic anemia is a common feature between 6 months – 2 years and rarely occurs after 5 years of age, especially in a child consuming non-vegetarian diet. B12 deficiency may occur after 5 years of age because of chronic diarrhea, malabsorption syndrome, or intestinal surgical causes. Pernicious anemia causes B12 deficiency, but nutritional B12 deficiency with subacute combined degeneration causing ataxia is rare.

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