Oral Treatment of Megaloblastic Anaemia with Small Amounts of Vitamin B12 and Intrinsic Factor

1955 ◽  
Vol 13 (4) ◽  
pp. 193-206 ◽  
Author(s):  
Poul Bastrup-Madsen ◽  
Leif Paulsen
Keyword(s):  
Oral Treatment ◽  
Intrinsic Factor ◽  
Megaloblastic Anaemia ◽  
Vitamin B

Megaloblastic anaemia and miscellaneous deficiency anaemias

2020 ◽  
pp. 5407-5426
Author(s):  
A.V. Hoffbrand
Keyword(s):  
Dna Synthesis ◽  
Intrinsic Factor ◽  
Pernicious Anaemia ◽  
Megaloblastic Anaemia ◽  
Folate Metabolism ◽  
Vitamin B ◽  
High Dose ◽  
Dietary Folate ◽  
Treatment And Prevention ◽  
Dose Oral

Megaloblastic anaemias are characterized by red blood cell macrocytosis. They arise because of inhibition of DNA synthesis in the bone marrow, usually due to deficiency of one or other of vitamin B12 (cobalamin) or folate, but sometimes as a consequence of a drug or a congenital or acquired biochemical defect that disturbs vitamin B12 or folate metabolism, or affects DNA synthesis independent of vitamin B12 or folate. Acquired pernicious anaemia—antibodies in serum and gastric juice directed against parietal cells (85–90% of cases) and intrinsic factor (50%), and raised serum gastrin are associated with autoimmune gastritis and failure of absorption of vitamin B12. Treatment and prevention of megaloblastic anaemia—vitamin B12 deficiency—may be treated with intramuscular hydroxocobalamin (1-mg doses, six given in the first 2–3 weeks, then every 3 months). Oral therapy is practised by a minority and is unlikely to be useful in pernicious anaemia. Neurological complications are irreversible unless treated early. Folate deficiency—high-dose oral folic acid (5 mg daily) overcomes folate malabsorption, but this should not be given alone where vitamin B12 deficiency coexists because neurological disease may be precipitated or exacerbated (although the haematological abnormalities improve). Where folate metabolism is disturbed by methotrexate, oral or parenteral folinic acid is given to restore DNA synthesis. Prevention—dietary folate fortification is an accepted and highly effective public health measure in many countries (none in Europe) for reducing the incidence of neural tube birth defects.

scholarly journals Oral Treatment of Pernicious Anaemia with a Combined Vitamin B12 and Intrinsic Factor Preparation

BMJ ◽  
1955 ◽  
Vol 2 (4937) ◽  
pp. 461-463 ◽  
Author(s):  
E. K. Blackburn ◽  
H. Cohen ◽  
G. M. Wilson
Keyword(s):  
Vitamin B12 ◽  
Oral Treatment ◽  
Intrinsic Factor ◽  
Pernicious Anaemia

Ileocaecal tuberculosis: an under-recognised cause of vitamin B12 deficiency

2018 ◽  
Vol 49 (2) ◽  
pp. 143-144
Author(s):  
Ashok Kumar Pannu ◽  
Dinesh Raja Palanisamy
Keyword(s):  
Terminal Ileum ◽  
Vitamin B12 Deficiency ◽  
Abdominal Tuberculosis ◽  
Megaloblastic Anaemia ◽  
Vitamin B ◽  
Lower Quadrant ◽  
Abdominal Tenderness ◽  
B12 Deficiency ◽  
Clinical Triad ◽  
Right Lower Quadrant

A combination of anaemia and knuckle pigmentation should always raise concern for megaloblastic anaemia. As the terminal ileum is the site of vitamin B12 absorption and also the commonest site of abdominal tuberculosis, a clinical triad of prolonged fever, knuckle pigmentation and right lower quadrant abdominal tenderness should suggest ileocaecal tuberculosis in endemic areas.

Megaloblastic anaemia and miscellaneous deficiency anaemias

2010 ◽  
pp. 4402-4420 ◽  
Author(s):  
A.V. Hoffbrand ◽  
Drew Provan
Keyword(s):  
Bone Marrow ◽  
Blood Cell ◽  
Dna Synthesis ◽  
Red Blood Cell ◽  
Megaloblastic Anaemia ◽  
Vitamin B ◽  
Inhibition Of Dna Synthesis

Megaloblastic anaemias are characterized by red blood cell macrocytosis. They arise because of inhibition of DNA synthesis in the bone marrow, usually due to deficiency of one or other of vitamin B12 (cobalamin) or folate, but sometimes as a consequence of a drug or a congenital or acquired biochemical defect that disturbs their metabolism, or affects DNA synthesis independent of vitamin B...

Some species differences in the intrinsic factor stimulation of B12 uptake by small intestine in vitro

1959 ◽  
Vol 197 (4) ◽  
pp. 926-928 ◽  
Author(s):  
T. Hastings Wilson ◽  
Elliott W. Strauss
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Species Differences ◽  
Intrinsic Factor ◽  
Vitamin B ◽  
Guinea Pig Ileum ◽  
Rat Intestine ◽  
Intrinsic Factors ◽  
Stimulation Of

Sacs of everted small intestine from a variety of animals were incubated in bicarbonate-saline containing vitamin B12 with and without intrinsic factor (IF). B12 uptake by rat intestine was stimulated only by its own intrinsic factor. Guinea pig ileum responded to all intrinsic factors tested (guinea pig, rat, hog, hamster, human being and rabbit). The intestines of hamster and rabbit were intermediate in specificity, responding to some, but not all, of the IF preparations. Species differences occur in both the intestine and intrinsic factor preparations. The guinea pig ileum was suggested as a possible assay for both hog and human IF.

scholarly journals Demyelinating lesions as a presenting feature of pernicious anaemia: Case report and literature review

2017 ◽  
Vol 4 (3) ◽  
pp. 7
Author(s):  
Rahul Daimari ◽  
Anthony A Oyekunle ◽  
Cassandra A Ocampo ◽  
Lawrence Kwape
Keyword(s):  
Clinical Features ◽  
Clinical Laboratory ◽  
Intrinsic Factor ◽  
Pernicious Anaemia ◽  
Neurological Impairment ◽  
Megaloblastic Anaemia ◽  
Cobalamin Deficiency ◽  
Female Population ◽  
Radiologic Findings ◽  
Demyelinating Lesions

Background: Pernicious anaemia (PA) describes megaloblastic anaemia resulting from cobalamin deficiency that is due to the absence of intrinsic factor (IF). Most cases are autoimmune in origin, with antibodies to parietal cells, IF or the cobalamin – IF complex.Methods: We report the clinical features, investigation and treatment of a patient in whom the first presentation of PA was demyelinating brain lesions. She presented with clinical features initially of neurological impairment and subsequently anaemia. Imaging studies were consistent with demyelinating lesions extending from the cortex to the midbrain. Peripheral blood and bone marrow findings were consistent with megaloblastic anaemia, which were confirmed by subnormal serum cobalamin levels. The patient was treated with parenteral cobalamin and oral folic acid.Results: She responded with complete resolution of anaemia and complete clinical neurological response.Conclusion: Clinical, laboratory and radiologic findings are important in the screening of patients presenting with demyelinating lesions, as these may help in the diagnosis of rare cases of PA. These tests are just as relevant even in the young African female population.

Progressive Imbalance and Visual Impairment in a Patient With Diabetes

2021 ◽  
pp. 248-250
Author(s):  
Neeraj Kumar
Keyword(s):  
Lower Limb ◽  
Peripheral Blood ◽  
Blood Smear ◽  
Serum Gastrin ◽  
Methylmalonic Acid ◽  
Intrinsic Factor ◽  
Peripheral Blood Smear ◽  
Vitamin B ◽  
Neurologic Manifestations ◽  
History Of

A 72-year-old man with hypothyroidism and type 2 diabetes sought care for a 3-year history of slowly progressive, ascending lower limb paresthesias and imbalance. Three months earlier, he noted subacute onset of finger numbness and substantial worsening of imbalance with infrequent falls. He also had a 1-year history of progressive visual decline that persisted despite cataract surgery. Additional symptoms included intermittent light-headedness and confusion. Laboratory evaluations showed a decreased hemoglobin value and an increased mean corpuscular volume. Macrocytic red blood cells were noted on a peripheral blood smear. Serum vitamin B12 level was less than 70 ng/L. Levels of plasma homocysteine and serum methylmalonic acid were markedly increased to 375 µmol/L and 143 nmol/L, respectively. Serum copper level was normal. Serum parietal cell antibodies were increased to 46 U, and intrinsic factor antibodies were absent. Serum gastrin was markedly increased. The clinical presentation in this patient suggested a myeloneuropathy. His vitamin B12 level was undetectable and accompanied by a macrocytic anemia and increased methylmalonic acid and homocysteine levels. Even though intrinsic factor antibodies were negative, the clinical picture was supportive of subacute combined degeneration in the setting of pernicious anemia. The patient was started on vitamin B12 replacement. At 6-month follow-up he had striking improvement in gait and vision. The light-headedness and confusion were no longer present. His examination was remarkable only for mild impairment, with tandem gait and a slightly positive Romberg sign. The lower limb reflexes were reduced. Impaired position perception at the toes persisted, but vibration perception in the lower limbs improved. Laboratory investigations showed normalization of the hemoglobin, vitamin B12, methylmalonic acid, and homocysteine levels. The serum gastrin level had improved but was still increased at 742 pg/mL. The best-characterized neurologic manifestations of vitamin B12 deficiency include myelopathy and myeloneuropathy. Autonomic neuropathy, optic neuropathy, and neuropsychiatric manifestations have also been reported. Neurologic manifestations may occur without evidence of the characteristic hematologic derangement, megaloblastic anemia. Macrocytosis or hypersegmented neutrophils on peripheral blood smear may be clues.

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