Anemia fetus

Exposure to excessive amounts of lead over a long period of time (chronic exposure) increases the risk of developing certain diseases. The parts of the body which may be affected include the blood, nervous system, digestive system, reproductive system, and kidneys. These effects include anemia, muscular weakness, kidney damage, and reproductive effects, such as reduced fertiHty in both men and women, and damage to the fetus of exposed pregnant women. 

Attention to iron metabolism is particularly important in women for the reason mentioned above. Additionally, in pregnancy, allowances must be made for the growing fetus. Older people with poor dietary habits ( tea and toasters ) may develop iron deficiency. Iron deficiency anemia due to inadequate intake, inadequate utilization, or excessive loss of iron is one of the most prevalent conditions seen in medical practice. 

In the U.S., the central nervous system syndrome is usually more common among children, and the gastrointestinal syndrome is more prevalent in adults. Exposure to lead is also linked to decreased fertility in men. Lead is a probable human carcinogen, based on sufficient animal evidence. Populations at increased risk of toxicity from exposure to lead include developing fetuses and young children, individuals with decreased kidney function, and children with sickle-cell anemia. 

A couple is expecting their first child and have consulted a genetic coun or because the woman had a brother who died of sickle cell anemia. There is also a history of disease in the man s family. Fetal cells are obtained by amniocentesis. Which test would best determine whether the fetus would be born with the disease ... 

Risk factors for deficiency Pregnancy (neural tube defects in fetus may result) Alcoholism Severe malnutrition Risk fiictors for deficiency Pernicious anemia Gastric resection Chronic pancreatitis Severe malnutrition Vegan Infection with D. latum... 

Tablets/Capsules/Oral solution Ribavirin may cause birth defects or death of the exposed fetus. Ribavirin is contraindicated in women who are pregnant or in men whose female partners are pregnant (see Warnings), in patients with a history of hypersensitivity to ribavirin or any component of the drug, and in patients with hemoglobinopathies (eg, thalassemia major, sickle-cell anemia).

Use with ribavirin Ribavirin may cause birth defects and/or death of the fetus. Extreme care must be taken to avoid pregnancy in female patients and in female partners of male patients. Ribavirin causes hemolytic anemia. The anemia associated with ribavirin therapy may result in a worsening of cardiac disease. Ribavirin is genotoxic and mutagenic and should be considered a potential carcinogen. 

Clark and colleagues (27) found evidence of maternal toxicity influencing fetal findings in studies with diflunisal in rabbits, in which fetal axial skeletal defects were observed. Diflunisal was found to produce severe maternal hemolytic anemia and greatly decreased erythrocyte ATP levels. The authors were able to demonstrate that the skeletal malformations resulted from maternal hypoxia secondary to anemia, rather than from a direct effect of the drug on the embryo or fetus. In addition, it was demonstrated that diflunisal had no effects on rat erythrocyte ATP levels, and the compound was categorized as not teratogenic in rats or mice. 

Hematopoietic development of blood cells begins mainly in the spleen and liver of the fetus during early pregnancy. By the seventh month, however, the marrow of a fetus becomes the primary site of blood cell formation [1]. During childhood, the marrow of the central axial skeleton such as the pelvis, spinal cord, and ribs, and of the extremities, such as the wrist and ankle, provides the key site of hematopoiesis. Hematopoiesis at the periphery (also known as extramedullary hematopoiesis) slowly decreases with age. Chronic administration of hematopoietic growth factors can reverse this decline. Severe hemolytic anemia and hematopoietic malignancies can also reverse the process. 

The occurrence of aplastic anemia in chronic benzene toxicity may be accelerated in individuals with viral hepatitis (Aksoy 1989). Furthermore, children and fetuses may be at increased risk because their hematopoietic cell populations are expanding and dividing cells are at a greater risk than quiescent cells. 

The homozygous state of a-thalassemia type-1 (a-Thi) leads to a form of erythroblastosis fetalis and intrauterine death [ (K2, L18, L20, L21, L22, L23, L24, L26, P4, T6, T7, T8) and others]. This form of hydrops fetalis is found in Chinese from various countries, in Filippinos, and in Thais. All children are either stillborn or die within hours after birth. The hematological observations usually include anemia with reticulo-cytosis, hypochromia with macrocytosis, aniso- and poikilocytosis, and many erythroblasts. The red cells sickle rather easily. Most fetuses are hydropic (but not all). 

Folale deficiency occurs in pregnancy on a wide scale. The increased utilization of the vitamin by die fetus and related tissues, as well as the secretion in milk during lactation, can place an increased demand on the dietary folates consumed by the mother. Sea ere folate deficiency leads to megaloblastic anemia. This disease, in which the synthesis of red blood cells is impaired, tends to occur with pregnancy in underdeveloped countries, but usually not in North America or Europe, Goat s milk is a poor source of folate and vitamin Bjj. Ovcrrchancc on goal s milk as a source of food for infants can result in a deficiency in these vitamins and in anemia. 

Lead is one of the systemic poisons, in that once absorbed into the circulation, it is distributed throughout the body where it causes serious health effects. Manifested effects of Pb poisoning include nausea, anorexia, and severe abdominal cramps, weight loss, anemia, renal tubular dysfunction, muscle aches, and joint pains. Lead can pass the placental barrier and may reach the fetus, resulting in miscarriages, abortions, and stillbirths. 

Kanno H, Murakami K, Hariyama Y, Ishikawa K, Miwa S, Fujii H. Homozygous intragenic deletion of type I hexokinase gene causes lethal hemolytic anemia of the affected fetus [letter]. Blood... 

Bart s (y ). Mothers carrying a fetus with Hb Bart s usually present clinically between 20 and 26 weeks gestation with pregnancy-induced hypertension and polyhydramnios. Ultrasound of the fetus shows hydrops. Severe anemia (Hb usually <80g/L) is noted on a fetal blood sample obtained by cordocentesis. It is important to rule out other causes for the hydropic fetus by performing TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex) testing. 

Hb Bart s hydrops fetalis is almost invariably fatal,with some fetuses dying in utero and others surviving a few hours after birth. Treatment using intrauterine transfusion has had very limited success, with potential complications in the children of growth retardation and severe brain damage, which may possibly be related to long-standing intrauterine anemia. 

For sensitized mothers with an at-risk fetus, serial titers are performed on maternal serum every month until 24 weeks gestation, then every 2 weeks thereafter. If a critical titer anti-D is detected, then ultrasound Doppler measurements are used to determine the peak velocity of blood flow in the fetal middle cerebral artery. Higher velocity is a strong indicator of fetal anemia. In addition, amniocentesis is performed to assess the bilirubin concentration in amniotic fluid. 

Depression may be more prevalent than in the general population, especially in patients with unstable disease. Delay in growth and sexual development are seen in patients with SCD. Adults with SCD have decreased fertility. Finally, pregnancy inhoduces an increased risk for the mother with SCD and for the fetus. The anemia of SCD may lead to intrauterine growth retardation. Preterm labor and premature delivery are common occurrences in mothers with SCD,... 

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