People with megaloblastic anemia may suffer from atrophic gastritis due to loss of the intrinsic factor normally present in the gastric juice. Patients with megaloblastic anemia may also suffer from neuritis involving the nerves of the spine. There may not be any pain, but such people may have difficulty walking in the dark. All cases of neuritis should be thoroughly investigated to be sure the patient does not have diabetes or some other underlying disease.
What are the causes of megaloblastic anemia?
In every case of megaloblastic anemia there is inadequate secretion of intrinsic factor by the stomach. This is essential for the absorption of the extrinsic factor, vitamin B12 or cyanocoblamin, which is responsible for the maturation of red blood corpuscles: the deficiency causes megaloblastic degeneration of the bone marrow and of the posterolateral column of the spinal cord and peripheral nerves. Due to inadequacy of vitamin B 12 erythropoiesis takes the abnormal megaloblastic pathway, producing pathological erythrocytes, which get into the general circulation and are readily destroyed by the reticuloendothelial cells. The result is progressive megaloblastic anemia.
Folic acid has also been found to effect maturation of the red blood corpuscles. Achlorhydria is always present. Any disturbance of fat metabolism are not so obvious even in advanced cases, fat loss is not marked. But blood cholesterol may be slightly lowered.
What are the signs and symptoms of megaloblastic anemia?
The skin is lemon yellow in color, the body is found fairly well nourished with yellowish fat and reddish brown muscles. The serous membranes and retina have petechial hemorrhages. The viscera appear anemic.
Heart is flabby, pale yellow, dilated and the myocardium and especially the subendocardial tissues show fatty degeneration.
Mucous membranes of the tongue, stomach and sometimes of intestines are often enlarged. In the stomach, the changes are more marked in the fundus with atrophy of the glands and disappearance of the peptic and oxyntic cells.
In a small number of cases, the spinal cord shows degeneration of the posterior and lateral columns.
Liver is slightly enlarged and shows fatty degeneration. In liver, in the kidneys and in other tissues, iron is deposited. Spleen is slightly enlarged and more so during exacerbations showing marked reticulo-endothelial cellular activity.
Achlorhydria is always present and this is often associated with loss of appetite, flatulence, nausea, vomiting and diarrhoea; severe paroxysmal epigastric pain is present in some cases and also glossitis causing smooth glazed tongue in an advanced case.
Complexion becomes progressively pale and in an advanced case, lemon yellow and waxy. The skin, conjunctiva and the mucous membrane of the mouth and tongue look markedly bloodless.
Later on, the ankles become oedematous; occasionally anasarca and hydrothorax may appear.
Moderate degrees of fever of irregular type are usually present especially during relapses.
Weakness progressively increases, afterwards even slight exertion causes marked dsypnoea, palpitation, giddiness and faintness.
Gastric contents show absence of hydrochloric acid and pepsin. The urine and stool contain an excess of bile pigments.
What are the complications?
Complications are comparatively few. Carcinoma of the stomach, gall bladder diseases, gout, venous thrombosis, rarely retinal hemorrhages and many intercurrent diseases are occasionally associated.
The specific treatment is to supply the haemopoietic principle in adequate doses. Vitamin B12 is so effective that it has nearly replaced liver extract injections. It must be remembered that given alone it may precipitate or aggravate spinal lesion.
Oral administration of dilute hydrochloric acid after food is useful in some cases.