What is Anemia associated with lead poisoning?
When a large amount of lead enters the body, anemia develops, characterized primarily by impaired porphyrin formation. In addition, lead poisoning increases the destruction of red blood cells due to damage to the erythrocyte membrane and the breakdown of the activity of certain enzymes.
Soluble lead salts cause poisoning. More often it is observed in persons who have contact with lead in production. Lead poisoning is often observed in the production of lead ore, lead smelting, battery production, white metal, red lead production, cable production, lead hydrogen hydrogen soldering, shot making, bullets, printing production, paint painting using lead paints, associated with the use of lead-containing insectofungicides. Household lead poisoning is possible with the use of food from handicraft pottery, if it is covered with glaze with lead red lead or lamb. Organic food acids form soluble salts with lead, and lead poisoning develops. Lead poisoning is possible when lead is smelted without taking precautions. Light lead poisoning is described in children who take objects painted in lead paints and newspapers.
Pathogenesis during anemia associated with lead poisoning
Anemia results from impaired porphyrin synthesis. Lead blocks enzymes that are actively involved in the synthesis of heme. As a result, 6-aminolevulinic acid accumulates in urine, and protoporphyrin in erythrocytes. In connection with the violation of heme synthesis, the content of serum iron increases, it is deposited in the organs.
Other mechanisms play a role in the mechanism of development of anemia in lead intoxication. In lead poisoning, the rate of globin biosynthesis is somewhat reduced. It also contributes to the development of hypochromia. In addition, the increased destruction of red blood cells plays a certain role in lead poisoning, since the life of red blood cells is shortened under the influence of this metal.
Symptoms of Anemia Associated with Lead Poisoning
Clinical manifestations of lead poisoning are reduced to lesions of the nervous system, digestive tract and blood.
Mild lead poisoning causes asthenia, headache, dizziness, memory loss, poor sleep, pain in the limbs.
Heavier lead intoxication can lead to pronounced disorders of the nervous system, primarily to the syndrome of motor polyneuritis. Usually, the extensors of the hands and fingers are affected, rarely the flexors. Severe lead intoxication provokes the appearance of paresis of the limbs. Sometimes develop sensitive disorders, pain in the limbs, pain along the nerves. Signs of encephalopathy are possible, nystagmus is noted (involuntary rapid rhythmic movements of the eyeballs), speech disorders, trembling. Occasionally, children have cerebral edema, coma, seizures.
In severe lead poisoning, blood pressure rises, sometimes to high numbers.
Damage to the gastrointestinal tract can occur in the case of lung lead poisoning. It is expressed in a sharp decrease in appetite. With mild intoxication, only accelerated evacuation of barium from the stomach is detected radiologically. With severe lead intoxication, lead colic occurs (sharp cramping in the abdomen), constipation, which is not amenable to any therapy. During this period, there is often a rise in body temperature to subfebrile numbers. X-ray examination in the case of lead colic in some parts of the gastrointestinal tract revealed pronounced spasticity, in others – atony.
The type of patient with lead poisoning is peculiar – an earthen pallor with a grayish tinge, associated with anemia, with a spasm of blood vessels, and also with the deposition of porphyrins in the skin. Often, a lead border is revealed on the gums in the form of a narrow purple band, mainly in the front teeth along the edge of the gum.
Changes in blood in mild lead poisoning consist of mild anemia with a reduced color index (hypochromic anemia). In severe poisoning, pronounced hypochromic anemia is detected. The content of reticulocytes, as a rule, increased to 3-8%, leukocytes – not changed. ESR within normal limits. The content of platelets in patients remains normal, but decreases with very severe lead poisoning. In the bone marrow, the number of erythrocaryocytes increases, while staining for iron there are many granules of iron ringing the nucleus.
Serum iron content in patients with lead poisoning increased.
The most characteristic biochemical sign of lead poisoning is an increase in the urine 6-aminolevulinic acid ten times compared with the norm, it reaches 40-100 mg / g creatinine (at a rate of 0.5-1.5 mg / g). The content of porphobilinogen in lead poisoning increases only 2-3 times, and sometimes remains normal. The level of coproporphyrin is usually increased by 5-10 times compared with the norm. Urine uroporphyrin content is usually normal.
In lead poisoning, the content of free protoporphyrin in erythrocytes is increased, sometimes to 5.13-6.8 µmol / l (300/400 mg%).
Diagnosis of Anemia Associated with Lead Poisoning
The doctor conducts differential diagnosis primarily with iron deficiency anemia. Abdominal pain usually leads to the mistaken idea of blood loss from the gastrointestinal tract due to an ulcer or tumor of the stomach or intestines. Increased serum iron, increased destruction of red blood cells, severe asthenia, or multiple nerve damage, especially in conjunction with anamnesis, help the doctor to establish lead poisoning.
Often it is necessary to differentiate between heterozygous thalassemia and lead intoxication. Heterozygous thalassemia, as well as lead intoxication, are characterized by hypochromic anemia, an increase in the number of reticulocytes, a sharp irritation of the red bone marrow germ, an increase in the content of serum iron. However, the normal content of 6-aminolevulinic acid in thalassemia, the normal size of the spleen in lead poisoning, the presence of sick relatives, changes in the ratios between the different hemoglobin fractions in thalassemia provide considerable assistance in making the correct diagnosis.
Lead intoxication has to be distinguished from various forms of hemolytic anemia, since the lead intoxication increases the content of reticulocytes, irritates the red sprout of the bone marrow, sometimes the level of bilirubin is somewhat elevated. Sometimes, with lead poisoning, a direct Coombs test is positive. Occasionally, in the case of severe lead poisoning, hemosiderin is observed in the urine, which gives grounds for making an erroneous diagnosis of Markiafaw’s disease — Micheli or the hemolysin form of autoimmune hemolytic anemia.
Differential diagnostics is also carried out with acute intermittent porphyria, which is characterized by polyneuritis, sometimes paralysis of four limbs, pain in the abdomen, red urine, an increase in coproporphyrin in the urine. However, unlike lead intoxication with acute intermittent porphyria, there is no hypochromic anemia with a high iron content. In the urine of acute intermittent porphyria, the content of porphobilinogen is primarily increased, to a much lesser extent, 6-aminolevulinic acid, whereas in lead poisoning the content of 6-aminolevulinic acid is increased, and the content of porphobiliogenene is normal or slightly increased. The reaction of Ehrlich with urine to porphobilinogen is always positive in acute intermittent porphyria and negative in lead poisoning.
Treatment of Anemia Associated with Lead Poisoning
Treatment of lead poisoning is to remove lead from tissues with the help of various chelating agents. Thetacin-calcium is most widely used. This medicinal substance is administered intravenously or intravenously. Its dose is 20 ml of a 10% solution per day. After a three-day course of thetacin-calcium, a 3-4-day break is necessary, and then the administration of the drug is repeated. After the first and second course of treatment with complexone, it is desirable to investigate the content of lead and 6-aminolevulinic acid in the urine. If the lead content in the urine remains high, and 6-aminolevulinic acid is elevated, then a 3-day course of treatment with thetacin-calcium is repeated 1 or 2 times.
In most cases, 3 courses of therapy with thetacin-calcium cure lead poisoning in full. Adenosine monophosphate (preparations adenyl, phosphaden) has a certain effect on neurological symptoms. The use of adenosine monophosphate in patients with lead poisoning and polyneuritis accelerates the recovery of movements in the limbs.