Intrinsic Factor Within Parietal Cells Patients With Juvenile Pernicious Anemia

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.

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Blocking and Binding Antibodies to Intrinsic Factor and Parietal Cell Antibody in Pernicious Anemia

Gastroenterology ◽

10.1016/s0016-5085(19)34006-5 ◽

1968 ◽

Vol 55 (5) ◽

pp. 575-583 ◽

Cited By ~ 50

Author(s):

I. Michael Samloff ◽

Martin S. Kleinman ◽

Michael D. Turner ◽

Michael V. Sobel ◽

Graham H. Jeffries

Keyword(s):

Pernicious Anemia ◽

Parietal Cell ◽

Intrinsic Factor ◽

Cell Antibody ◽

Parietal Cell Antibody

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Absorption of Liver-bound Vitamin B12 in Relation to Intrinsic Factor

Blood ◽

10.1182/blood.v32.2.313.313 ◽

1968 ◽

Vol 32 (2) ◽

pp. 313-323 ◽

Cited By ~ 9

Author(s):

KUNIO OKUDA ◽

ISAO TAKARA ◽

TERUMI FUJII

Keyword(s):

Vitamin B12 ◽

Pernicious Anemia ◽

Rat Liver ◽

Intrinsic Factor ◽

In Vitro Digestion ◽

Enhanced Absorption ◽

Biochemical Studies ◽

Peptide Complexes ◽

Liver Powder

Abstract Rat liver containing radioactive native B12 was prepared by repeated injections of 57Co-OH-B12, and absorption of liver B12 was measured in patients with pernicious anemia and in subjects without stomach, using physiologic doses. It was found that absorption of liver B12 was very poor, not superior to that of free OH-B12, and coadministration of IFC markedly enhanced absorption. In vitro digestion of rat liver with several enzymes, as determined from liberation of dialyzable radioactivity, suggested its easy digestibility. Biochemical studies of the dialyzable products of liver containing 57Co-B12 failed to demonstrate any detectable quantities of radioactivity other than free 57Co-OH-B12. A study in which cow liver powder mixed with a small quantity of 57Co-CN-B12 was fed to humans and digestion of liver was estimated from the reduction in absorption of radioactivity, indicated that most of the extractable liver B12 was liberated free in the intestine. Thus, no evidence has been obtained for the production of B12-peptide complexes from liver by digestion that require no IF for absorption.

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Vitamin B12 Malabsorption Due to Intrinsic Factor Deficiency in Indian Subjects

Blood ◽

10.1182/blood.v40.5.747.747 ◽

1972 ◽

Vol 40 (5) ◽

pp. 747-753 ◽

Cited By ~ 3

Author(s):

H. G. Desai ◽

F. P. Antia

Keyword(s):

Vitamin B12 ◽

Pernicious Anemia ◽

Indian Population ◽

Intrinsic Factor ◽

Subacute Combined Degeneration ◽

Factor Deficiency ◽

Vitamin B12 Absorption ◽

Intrinsic Factor Deficiency ◽

Intrinsic Factor Antibody ◽

Vitamin B12 Malabsorption

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.

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Effect of Histamine H2-Receptor Antagonists on Vitamin B12 Absorption

Annals of Pharmacotherapy ◽

10.1177/106002809202601018 ◽

1992 ◽

Vol 26 (10) ◽

pp. 1283-1286 ◽

Cited By ~ 29

Author(s):

Rex W. Force ◽

Milap C. Nahata

Keyword(s):

Acid Secretion ◽

Healthcare Providers ◽

Intrinsic Factor ◽

Parietal Cells ◽

Data Sources ◽

Vitamin B ◽

Receptor Antagonists ◽

Histamine H2 Receptor ◽

Medline Search ◽

Gastric Parietal Cells

OBJECTIVE: To discuss the potential of histamine H2-receptor antagonists (H2RAs) to cause malabsorption of vitamin B12 (cyanocobalamin). DATA SOURCES: Pertinent literature was identified via a MEDLINE search. Journals and references cited in published articles also were used as data sources. STUDY SELECTION: Studies evaluating the effect of H2RAs on vitamin B12 absorption were reviewed. DATA SYNTHESIS: H2RAs decrease acid secretion by the gastric parietal cells. Gastric acid and pepsin produced by these cells are required for the cleavage of vitamin B12 from dietary sources. Intrinsic factor (IF), also produced by gastric parietal cells, is required for vitamin B12 absorption from the gastrointestinal tract. Although H2RAs have not conclusively been shown to decrease IF secretion, studies have demonstrated a significant reduction in food-bound vitamin B12 absorption secondary to decreased acid secretion in patients taking these drugs. CONCLUSIONS: H2RAs have the potential to cause vitamin B12 deficiency. This may be important in patients with inadequate stores of vitamin B12 (e.g., poor diet), particularly those receiving H2RA therapy continuously for more than two years. Healthcare providers should be aware of this potential adverse effect.

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Time Pattern of Vitamin B12Co60 Urinary Excretion in Man After Oral Administration and Parenteral "Flushing"

Blood ◽

10.1182/blood.v11.4.352.352 ◽

1956 ◽

Vol 11 (4) ◽

pp. 352-356 ◽

Cited By ~ 3

Author(s):

WILLIAM R. BEST ◽

WENDELL A. LANDMANN ◽

LOUIS R. LIMARZI

Keyword(s):

Oral Dose ◽

Oral Administration ◽

Urinary Excretion ◽

Pernicious Anemia ◽

Intrinsic Factor ◽

Time Pattern ◽

Number Of Patients ◽

Excretion Rates ◽

The Individual ◽

Factor Concentrate

Abstract Serial urine collections in a number of patients with pernicious anemia given 2 µg B12Co60 orally followed in two hours by 1000 µg nonradioactive vitamin B12 showed little urinary radioactivity at any time. When these tests were repeated together with a potent oral dose of intrinsic factor concentrate, there was little activity during the first four hours. Peak excretion rates occurred most commonly between 6 and 12 hours after ingestion of radioactive B12, sometimes even later. The time of peak excretion was fairly characteristic for the individual. Secondary peaks occasionally occurred, and only slight radioactivity usually remained after 24 hours. It is postulated that the delayed peak is related to the time it takes for B12 to be transported in the intestine to the point of absorption or to the duration of the intracellular metabolic processes of absorption. For most purposes the use of fractional urinary collections is not necessary.

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