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Special Pathology 1 страница






Anaemia

Anaemia is a pathological condition characterized by decreased number of erythrocytes and/or haemoglobin content in a blood unit volume due to their general deficiency (Gk an not, haemia blood, i.e. deficient of blood).

Anaemia should be differentiated from hydraemia (abnormally watery

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blood) in which the erythrocyte and haemoglobin are deficient as well, but not at the expense of their absolute reduction but due to dilution of blood in renal, cardiac and other oedema. Anaemia should also be differentiated from oligohaemia, which is the reduction of the total volume of blood, e.g. immediately after a profuse haemorrhage. The total mass of circulating blood can be normal in anaemia (normovolaemia), increased (hyper-volaemia) or decreased (oligohaemia or hypovolaemia). Thickening of blood in persistent vomiting and profuse diarrhoea can mask anaemia because the total amount of plasma decreases and the number of erythrocytes and haemoglobin in a unit volume of the circulating blood can be normal or even increased.

Anaemia is often characterized not only by quantitative changes in the red blood composition, but also qualitative changes in the structure of erythrocytes and haemoglobin molecules. These changes are important for the transport function of blood and tissue respiration, and can be the cause of additional pathological changes in the body. For example, a congenital defect of erythrocytes in some hereditary haemolytic anaemia may (due to their intense haemolysis) cause haemosiderosis of the internal organs, for­mation of pigment stones in the gall bladder, etc.

Anaemia has a pronounced effect on the vital activity of the body. Anaemization causes oxygen hunger of organs and tissues (hypoxia) and their dystrophy. For example, if the blood haemoglobin content is halved (70—80 g/1), initial symptoms of myocardial dystrophy develop. If the haemoglobin content decreases to 50 g/1, the dystrophic changes become pronounced. Unoxidized products of metabolism (lactic acid, in the first instance) accumulate in the body due to hypoxia. The alkaline reserve of blood decreases. In grave cases, a tendency to acidosis develops which causes further dystrophy of tissues. Severe anaemias attended by marked disorders in tissue metabolism are incompatible with life.

Anaemia of any origin is accompanied by some compensatory pro­cesses, which partly remove or lessen its consequences: (1) blood circula­tion is intensified, i.e. stroke and minute volumes increase, tachycardia develops, and the rate of blood flow increases; (2) blood distribution is altered, blood depots in the liver, spleen, and muscles are activated, and the blood supply to the peripheral tissues becomes limited at the expense of the increased blood supply to the vital organs; (3) oxygen utilization in tissues is intensified and the role of anaerobic processes in tissue respiration increases (anaerobic respiration with glutathione); (4) the erythropoietic function of bone marrow is stimulated. More than 50 types of anaemia are now differentiated.

According to their origin, the following types of anaemia are distinguished.


 

1. Anaemia due to loss of blood (acute and chronic).

2. Anaemia due to disordered haemopoiesis in deficiency of iron
(necessary for the production of haemoglobin), in vitamin B12 deficien­
cy (necessary for normal erythropoiesis), in inhibition of the bone marrow
by endogenous or exogenous toxicosis, radiation, or by some unknown
factors, and also in cases where red bone marrow is replaced by other
tissue, e.g. myeloma or multiple metastases.

3. Anaemia due to excessive haemolysis. This type of anaemia is sub­
divided into: (a) anaemia with prevalent extravascular (intracorpuscular)
haemolysis of erythrocytes in macrophages of the spleen, and, to a lesser
extent, in the bone marrow and liver. These are anaemia caused by
hereditary morphological and functional erythrocyte deficiency
(spherocytic and ovalocytic anaemia), and auto-immune haemolytic
anaemia. They are all characterized by hyperbilirubinaemia and
splenomegaly; (b) anaemia with intravascular, usually acute haemolysis (in
various poisoning, transfusion of incompatible blood, cold and effort
anaemia) attended by release into the plasma of unbound haemoglobin and
by haemoglobinuria; haemosiderosis of the internal organs is observed also
in chronic haemolysis (e.g. in Marchiafava-Micheli disease). This
classification is only conventional because both intracorpuscular and
vascular haemolysis can occur in one and the same form of haemolytic
anaemia.

Haemolytic anaemia is also often subdivided as follows: (a) hereditary (congenital) anaemia, which includes membranopathy of erythrocytes (associated with abnormality of protein or lipid complexes of erythrocyte envelope, causing changes in their shape and premature decomposition; microspherocytic anaemia, ovalocytic anaemia, etc.); enzymopenic anaemia (due to deficiency of various enzyme systems of erythrocytes, which promotes their accelerated decomposition) and haemoglobinopathy in which the structure of haemoglobin or its synthesis are disturbed (sickle-cell anaemia, thalassaemia); (b) acquired anaemia (auto-immune haemolytic and iso-immune anaemia, and also anaemia caused by mechanical injury to erythrocytes, acquired membranopathies, toxic anaemia, etc.).

Apart from the pathogenetic classification, there are classifications based on other principles. Three groups of anaemia, for example, are distinguished in accordance with haemoglobin saturation of erythrocytes (by the colour index): normochromic (0.8-1.0), hypochromic (less than 0.8) and hyperchromic anaemia (more than 1.0). The group of hypochromic anaemia includes iron-deficiency anaemia: chronic (less acute) posthaemorrhagic anaemia, gastrogenic iron-deficiency anaemia, and juvenile chlorosis. Hyperchromic anaemia is caused by the deficiency



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of vitamin B12. This is Addison-Biermer anaemia, bothriocephalus anaemia, and also achrestic anaemia (due to defective utilization of vitamin B12). Other anaemias proceed without considerable changes in the colour index of blood and are therefore normochromic.

It is very important to assess the regenerative capacity of the bone mar­row upon which (to a certain degree) depend treatment and prognosis of the diseases. Distinguished are regenerative anaemia, i.e. anaemia in which the bone marrow preserves its capacity to produce new erythrocytes; hyporegenerative anaemia, in which this capacity is impaired; and aregenerative or aplastic anaemia, in which bone marrow function is com­pletely or almost completely lost. The regenerative function of the bone marrow is assessed by the rate at which the quantity of reticulocytes in­creases in the peripheral blood and by the proportion of the erythro- and leucoblastic elements in the sternal punctate. Their normal ratio is 1: 3 or 1: 4, while in regenerative anaemia, in which erythropoiesis dominates in the compensatory function of the bone marrow, this ratio becomes 1: 1, 2: 1 and even higher. This shift is absent in hypo- or aregenerative anaemia, while the reticulocyte content of the peripheral blood is low.

ACUTE POSTHAEMORRHAGIC ANAEMIA

Anaemia caused by an acute blood loss (acute posthaemorrhagic anaemia) occurs mostly in various injuries associated with traumatized large vessels (extrauterine pregnancy, delayed placental detachment during labour, etc.). Acute posthaemorrhagic anaemia occurs in diseases that can be attended by profuse bleeding, e.g. in gastric and duodenal ulcer, degrading tumour of the stomach, kidneys, or the lung, in tuberculosis and abscess of the lung, bronchiectasis, varicose dilation of the oesophageal veins in liver cirrhosis, haemor-rhagic diathesis, and especially in haemophilia.

Clinical picture. In cases with external haemorrhage, the physician can often locate the source of bleeding at first sight (e.g. in injury). The patient's grave condition can in these cases be directly attributed to profuse blood loss. Haemorrhage from the internal organs can be manifested by blood vomiting (unaltered blood originates from the oesophagus; brown blood from the stomach), by expectoration of blood (scarlet foaming liquid), by the presence of blood in faeces (melaena in haemorrhage from the stomach or the small intestine; dark or scarlet blood originates from the large intestine, especially from its terminal part) and by blood presence in the urine (haematuria). It should be remembered that in gastro-intestinal haemorrhage, the blood can only be discharged into the environment in a.certain lapse of time (with the vomit or excretions). Moreover, haemorrhage caused by the rupture of the spleen, liver, or by the internal injury to the chest can be difficult to establish because blood will ac­cumulate in the abdominal or pleural cavity.

The first sign of a sudden haemorrhage is the feeling of weakness, dizziness, noise in the ears, palpitation of the heart, nausea, and in rare cases vomiturition. In severe cases with pro­fuse blood loss, the patient is in the state of shock (if the bleeding is caused by an injury) or collapse (if haemorrhage is due to affection of the internal organs). The patient's condition depends not only on the amount of blood loss, but also on the rate at which blood is lost. In­spection reveals pronounced and in some cases deadly pallidness; the skin is covered with


sticky cold sweat, the skin temperature is subnormal. Respiration is superficial and ac­celerated. The pulse is fast, small, and (in severe cases) thready. Arterial pressure (both systolic and diastolic) is low. Auscultation of the heart reveals marked tachycardia.

The pathological and compensatory changes in acute blood loss with benign outcome can be divided into three stages (or phases). First oligohaemia develops. It causes a reflex spasm of the vessels to decrease the volume of the vascular system and to recover blood from its reserves (depots). For this reason, the blood haemoglobin and erythrocyte content may re­main normal within the first hours (or even within 1 or 1.5 days) following the blood loss. Tissue fluids are drawn into the vessels to cause hydraemia in 2 or 3 days: the erythrocyte and haemoglobin content in unit volume decreases. Signs of marked activation of erythropoiesis appear on the third to seventh day. Anaemia becomes hypochromic in the loss of considerable amount of blood due to exhaustion of the iron store.

Treatment. Bleeding should be arrested as soon as possible by placing a tourniquet or by a tamponade of the external haemorrhages in wounds. Surgical intervention is indicated in con­tinuing haemorrhage from the internal organs. Measures to prevent shock or collapse should also be taken. Blood loss should be compensated for by infusion of whole blood or its substitutes; cardiac and vascular medicinal preparations should be administered. Iron preparations should be given to patients with profuse blood loss in several days after the haemorrhage has been arrested.

IRON DEFICIENCY ANAEMIA

Iron deficiency anaemia (anaemia sideropriva gastroenterogenica) arises in the deficit of iron which is necessary for the production of haemoglobin in erythrocytes. This type of anaemia develops in patients with decreased iron absorption due to resection of the stomach (" agastric anaemia"), removal of a considerable part of the small intestine, especially of its proximal part, in intestinal diseases attended by abnormal absorp­tion, and in the iron deficit in food. The latter occurs mostly in children with prolonged milk diet and copper deficit. Increased iron demands occur during intense growth of the body. During establishment of the menstrual cycle in young girls (menstrual loss of blood and ironions) juvenile iron deficiency anaemia (juvenile chlorosis) may develop. Chronic haemorrhage also causes iron deficiency anaemia.

Repeated (not profuse) loss of blood cause anaemization due to exhaustion of the iron store which is necessary for the production of haemoglobin in erythrocytes. Daily intake of iron with food is small, about 11-28 mg, and one fourth of this quantity is only absorbed. This is equivalent to the iron content of 15 ml of blood. Daily loss of 15 ml (or even smaller amount) of blood therefore inevitably exhausts the iron store to cause iron deficiency anaemia.

Chronic blood loss and chronic posthaemorrhagic anaemiaattends manydiseases of the internal organs, and in the first instance, ofthe gastro-intestinal tract. In mostcases these are gastric or duodenal ulcer, cancer, polyposis of the stomach and intestine, haemorrhoids, and certain types of helminthiasis. Chronic posthaemorrhagic anaemia often occurs in



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tumours of the kidneys, cavernous tuberculosis of the lungs, and in uterine haemorrhage.

Some other factors promote anaemia. These are mainly those factors which can decrease the iron stores of the body. For example, patients with secondary gastric hyposecretion and enteritis develop anaemia sooner and it runs a more severe course in the presence of even insignificant chronic haemorrhage. Gravity of chronic posthaemorrhagic anaemia arising in pa­tients with degrading tumours of the gastro-intestinal tract, kidney, or the uterus, is intensified by the toxic effect of the tumour on the haemopoiesis and by multiple metastases into the bone marrow, etc. Hydrochloric acid of the gastric juice promotes reduction of trivalent iron to its divalent form, which is easier assimilated. But recent studies show that hydrochloric acid does not play a decisive role in activation of iron absorption.

In the absence of adequate iron supply to the body or its utilization from the store, the synthesis of haemoglobin, myoglobin, and iron-containing enzymes of various cells involved in the oxidation processes is upset. This impairs nutrition of tissues and accounts for the development of many symptoms of the disease. The clinical picture of iron deficiency anaemia is explained by insufficient oxygen transport to tissues due to anaemia on the one hand, and by disordered cell respiration on the other.

Clinical picture. Slow development (within months and years) of iron deficiency anaemia accounts for actuation of the compensatory mechanisms. Most patients therefore are well adapted to the disease and can satisfactorily stand even significant anaemia.

We shall not discuss patient's complaints associated with the main disease, to which anaemia is secondary (e.g. the cause of chronic haemor­rhage). The specific complaints of anaemic patients will only be empha­sized: weakness, dizziness, dyspnoea (especially exertional), increased fatigue, noise in the ears, and fainting. Many patients develop various dyspeptic symptoms: decreased appetite, perverted taste, slight nausea, heaviness in the epigastrium after meals, and regurgitation. Diarrhoea is also frequent. Slight paraesthesia (tingling and pricking) is possible. Ex­cruciating dysphagia sometimes develops during swallowing dry or solid food in especially severe cases. This sideropenic dysphagia was first described by Rossolimo and Bekhterev in 1900-1901. Later this syndrome was described by Plummer and Vinson. The dysphagia is explained by ex­tension of the atrophic process from the stomach onto the oesophageal mucosa, and sometimes by its development in the proximal part of the soft connective-tissue membranes and bridges.

Inspection of the patient reveals pallor. Certain trophic changes in the skin, its appendages, and mucosa can be due to the general iron deficit. The skin is dry and sometimes slightly scaling. The hair is brittle, early


grey, and showing the tendency to falling. The nails become flat, sometimes spoon-like, opaque, marked by transverse folds, and brittle (koilonychia). The mouth angles often have fissures (angular stomatitis), the papillae of the tongue are levelled (atrophic glossitis). The teeth lose their luster and quickly decompose despite a thorough care. If iron preparations are taken for a long time, the teeth may blacken due to forma­tion of black iron sulphite (by the reaction of iron with hydrogen sulphide which is liberated by the carious teeth). Purulent inflammation of the gum mucosa around the tooth necks develops (alveolar pyorrhoea).

Physical examination can reveal a slight indistinct enlargement of the left ventricle, systolic murmur at the heart apex, and nun's murmur over the jugular vein (mostly on the right). Lymph nodes, liver and spleen are not enlarged.

Study of the blood reveals decreased erythrocyte and even more decreased haemoglobin content of the blood. The colour index is less than 0.85; in grave cases it is 0.6—0.5, and even lower. Microscopy of blood (Plate 30) reveals pallid erythrocytes (hypochromia), anisocytosis, and poikilocytosis. The average diameter of erythrocytes is less than normal (microcytosis). The number of reticulocytes is small. Anaemia is usually at­tended by thrombocytoleukopenia, sometimes relative monocytosis, lym-phocytosis, and eosinopenia. The iron content of the serum is decreased (1.5—2.5 times and more). The percentage of transferrin saturation also decreases (below 15).

Decreased activity of the iron-containing enzymes of tissue respiration provokes (or intensifies) atrophy of the gastro-intestinal mucosa. The study of gastric juice reveals in most cases achlorhydria or even achylia; the total amount of the excreted juice is much decreased. X-rays reveal levelled folds of the oesophageal and gastric mucosa. Oesophagoscopy and gastroscopy confirm atrophy of the oesophageal and gastric mucosa.

Course. The course of the disease is chronic and gradually progressive if the iron deficit in the body increases.

Treatment. Iron preparations (haemostimulin, etc.) are given. If the pa­tient has gastritis or peptic ulcer, the iron preparations should better be given intramuscularly or intravenously (ferbitol, fercoven, etc.). The therapy gives a comparatively rapid and permanent effect: work capacity is rapidly restored, erythrocyte and haemoglobin of blood normalize in 3—5 weeks. The patient should however be regularly (several times a year) given prophylactic courses of therapy with iron preparations in order to prevent possible relapses of the disease. The diet of patients with iron deficiency anaemia should be rich in iron salts, e.g. liver, meat, eggs, apples, dried fruits.. Efficacy of treatment of anaemia caused by chronic loss of blood depends on removal of the source of blood loss.


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•'■ *'■ VITAMIN B12 (FOLIC ACID) DEFICIENCY ANAEMIA

Aetiology and pathogenesis. Vitamin B12 (folic acid) deficiency anaemia was first described by Addison in 1855. One of its forms was later given the name of Addison-Biermer anaemia. In 1868, Biermer published a more detailed description of the disease, which he called pernicious or malignant anaemia, because its prognosis was then grave and patients usually died in a few months or years after the appearance of the first symptoms.

The disease was effectively treated for the first time by Minot and Mur­phy (1926). The patients were given raw calf liver in large amounts every day. Minot and Murphy noted that distinct remissions followed in patients who were given this diet and conjectured that raw liver contained a certain substance which is necessary for normal haemopoiesis, and whose absence or deficit causes pernicious anaemia. The next stage in the study of this disease is connected with experiments carried out by Castle (1929). He noted that meat treated with gastric juice (containing various amounts of hydrochloric acid) produces an anti-anaemic effect when administered into the stomach of patients with the Addison-Biermer anaemia. Gastric juice alone, untreated meat, or meat treated with gastric juice of patients with the Addison-Biermer anaemia have no anti-anaemic effect. Castle sug­gested that a special substance, haemopoietin, was necessary for normal maturation of erythrocytes. Haemopoietin is produced by combination of a certain extrinsic factor supplied with food and the intrinsic factor con­tained in normal gastric juice.

At the present time, Castle's conjecture concerning the pathogenesis of Addison-Biermer anaemia has been proved experimentally and clinically. The extrinsic and intrinsic factors and their biological role have been studied sufficiently well. The factor is vitamin B12 (cyanocobalamin) discovered by Smith in 1948 which is contained in calf liver, kidneys, meat, eggs, and gastromucoprotein produced by the accessory cells of the glands found in the fundus of the stomach. In healthy subjects, vitamin B12 com­bines with gastromucoprotein in the stomach to give a sufficiently stable complex which protects vitamin B12 from intestinal microflora to ensure adequate absorption of vitamin B12 (mainly in the ileum). Gastromucopro­tein is absent from the gastric juice of patients with the Addison-Biermer anaemia due to pronounced atrophic gastritis. In the absence of gastromucoprotein, vitamin B12 delivered with food is decomposed by in­testinal flora and is not assimilated by the body to cause vitamin B12 deficit. In other cases, vitamin B12 (folic acid) deficiency anaemia is the result of vast resection of the stomach, severe enteritis, increased demands for vitamin B12 in pregnancy, its consumption by helminths (bothrioce-


phaliasis), and in disordered assimilation of this vitamin by the bone marrow (achrestic anaemia).

An important biological effect of vitamin B12 is activation of folic acid. Like vitamin B12, folic acid belongs to substances included in the group of vitamin B. It is contained in leaves of various plants, fresh vegetables, beans, liver, and kidneys of animals. Folic acid is deposited in the human body mainly in the liver, where it is present in inactive state. Vitamin B12 pro­motes formation of folic acid derivatives, folates, which are probably the factor necessary for haemopoiesis in the bone marrow. In conditions associated with vitamin B12 and folate defi­ciency, the synthesis of DNA is disordered; this in turn causes disorders in cell division; the cells become large and qualitatively inadequate. Erythroblasts are affected most severely: large cells of embryonal haemopoiesis, megaloblasts, are found in the bone marrow instead of erythroblasts. They are not only larger than erythroblasts; they also differ in the structure of their nuclei and protoplasm, earlier and more intense saturation with haemoglobin during their differentiation (at the stage of reticular structure of the nucleus), retarded mitotic divi­sion, and mainly in their inability to grow to normal erythrocytes. Most megaloblasts are decomposed in the bone marrow before they reach the stage of a nucleated cell. Only a small quantity of megaloblasts are differentiated to anuclear cells (megalocytes) and enter the blood vessels. Megalocytes are larger and more saturated with haemoglobin than erythrocytes and differ from them by morphological and functional inadequacy. Megalocytes have no such high oxygen-transport capacity as the erythrocytes and are quickly decomposed by reticuloen-dothelial cells: the average life of megalocytes is about three times shorter than of eryth­rocytes.

The absence of gastromucoprotein in gastric juice (like achlorhydria which usually attends this disease) is due to atrophy of the gastric mucosa. Some investigators believe that atrophy of gastric mucosa is not inflammatory in its origin as it was believed earlier (atrophic gastritis) but is a result of congenital insufficiency of its glandular apparatus which is manifested with time. In the opinion of other authors, the atrophy of gastric mucosa is caused by antibodies produced by the patient's body to the gastric glandular cells, which can however be slightly altered by toxic effects or inflammation (auto-immune mechanism).

If the second coenzyme of vitamin B12, desoxyadenosylcobalamin, is deficient, fat metabolism becomes upset with accumulation of methylmalonic acid, which is toxic for the nervous system (provokes funicular myelosis).

The Addison-Biermer anaemia attacks commonly the aged; the in­cidence among women is higher than in men.

Pathological anatomy. The skin and the organs are pallid. Small haemorrhages are possi­ble. Haemosiderosis of the liver, kidneys, bone marrow and dystrophic changes in them are characteristic. These changes are observed also in the myocardium, the brain, and the spinal cord (mostly in the lateral cord). Bone marrow is affected by hyperplasia; it is bright-red, the foci of extramedullar haemopoiesis are seen in the spleen and the lymph nodes. Histological studies show prevalence of red blood cells; many young forms, myeloblasts are seen. Megaloblasts, the large cells of perverted erythropoiesis, are especially numerous.

Clinical picture. The onset of the disease is insidious. The patient grows weaker, he complains of heart palpitation, dizziness, and dyspnoea, especially during exercise or brisk movements; the work capacity is im­paired, the appetite becomes poor; slight nausea is possible. The first com­plaint is often the burning sensation in the tongue. This is explained by the



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development of atrophic glossitis (see below) which usually attends this disease. The patient often develops achylic diarrhoea or, on the contrary, persistent constipations. Dystrophic changes in the nervous system cause skin anaesthesia and paraesthesia; the gait is often affected in grave cases: spastic paresis develops (incomplete spastic paralysis of the lower ex­tremities); the knee reflex disappears, the function of the urinary bladder and the rectum can also be affected. All these symptoms are known as the funicular myelosis which develops due to the predominant affection of the lateral spinal columns. Symptoms of the disordered activity of the central nervous system (deranged sleep, emotional lability, etc.) become apparent.

Inspection of the patient reveals pallor of the skin and mucosa, usually with a yellowish tint due to increased decomposition of megalocytes and formation of bilirubin from the released haemoglobin, and a slight swelling of the face. The patient is not thin. Quite the reverse: most patients are well fed. The bright-red smooth and glossy tongue (because of the pronounced atrophy of the papillae) is quite characteristic of the Addison-Biermer anaemia. This symptom is known as Hunter's glossitis (W. Hunter was the first to describe this symptom). The mouth mucosa and the posterior wall of the throat are also atrophied. The tip and edges of the tongue, and also the mouth mucosa can be ulcerated. The tendency to caries is often seen in the teeth.

Pressing or tapping on the flat and some tubular bones (especially the tibia) is often painful. This is the sign of bone marrow hyperplasia. Palpa­tion can reveal a slight enlargement of the liver and the spleen.

The cardiovascular system is usually involved as well. The left border of the heart is displaced to the left, tachycardia develops, " anaemic" systolic murmur is heard at the heart apex in 75 per cent of cases; the nun's mur­mur is often heard over the jugular veins. The pulse is soft and accelerated. Most patients develop hypotension. ECG shows a certain decrease in the general voltage, the decreased T wave and the S-T interval.

Changes in the gastro-intestinal tract are pronounced. Especially characteristic is atrophy of gastric mucosa which can be revealed by X-ray examination, and more distinctly by gastroscopy. The atrophy is often focal, and the affected sites (mostly in the fundus of the stomach) can be seen as iridescent spots. Atrophy can combine with polyps in the folds of gastric mucosa and its polypous thickening. It should be remembered that anaemia, including pernicious anaemia, can be a symptom of a malignant tumour in the stomach. Cancer of the stomach occurs in patients with the Addison-Biermer anaemia 8 times more frequently than in healthy persons. Patients with this disease should therefore be systematically inspected by X-rays (by gastroscopy whenever possible). Almost all patients develop achlorhydria. In 98 per cent of cases it has the histamine-resistant






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