Blood anemia

Neuropathy Acute nephropathy Neuropathy Vitamin D metabolism Blood pressure Blood anemia U-aminolevulinic acid B-EPP... 

Blood Anemia, post-malarial Bertholletia excelsa H.B.K. (Lecythidaceae) outer fruit case... 

In man, folate affects pi imarily the composition of blood (anemia, thrombocytopenia). A common cause of deficiency symptoms is a disturbance in the utilization of folate rather than inadequate dietary intake. Vitamin B12 acts synergistically with folate. 

Electrospray mass spectra of globins from the blood of (a) a child diagnosed as having the sickle-cell anemia trait and (b) of its mother. As well as the usual p-globin sickle-cell variant at m/z 15,837.2, a new variant (P-Montreal-Chori) appears at m/z 15,879.3 and is observed in both the child and the mother. 

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. 

Lead-induced anemia results from impairment of heme biosynthesis and acceleration of red blood cell destmction (10,13). Lead-induced inhibition of heme biosynthesis is caused by inhibition of S-aminolevulinic acid dehydratase and ferrochelatase which starts to occur at blood lead levels of 10 to 20 pu gjdL and 25 to 30 //g/dL, respectively (10,13). Anemia, however, is not manifested until higher levels are reached. 

Deficiency or Toxicity in Humans. Molybdenum deficiency in humans results in deranged metaboHsm of sulfur and purines and symptoms of mental disturbances (130). Toxic levels produce elevated uric acid in blood, gout, anemia, and growth depression. Faulty utiH2ation results in sulfite oxidase deficiency, a lethal inborn error. 

Fohc acid is a precursor of several important enzyme cofactors required for the synthesis of nucleic acids (qv) and the metaboHsm of certain amino acids. Fohc acid deficiency results in an inabiUty to produce deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and certain proteins (qv). Megaloblastic anemia is a common symptom of folate deficiency owing to rapid red blood cell turnover and the high metaboHc requirement of hematopoietic tissue. One of the clinical signs of acute folate deficiency includes a red and painhil tongue. Vitamin B 2 folate share a common metaboHc pathway, the methionine synthase reaction. Therefore a differential diagnosis is required to measure foHc acid deficiency because both foHc acid and vitamin B 2 deficiency cause... 

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. 

The filariform larva found in moist soils may be either ingested or penetrate the skin of its host. It is then carried through the circulatory system to the lungs and migrates up the respiratory tree into the digestive tract. The worms feed on intestinal tissue and blood. Some worms may persist in humans as long as nine years. Infestations cause cutaneous reactions, pulmonary lesions, intestinal ulcerations, and anemia. 

Plasmodium vivax, responsible for the most prevalent form of malaria (benign tertian), has an incubation period of 8—27 days (14 average). A variety seen in northern and northeastern Europe has an incubation period as long as 8—10 months. The disease can cause splenic mpture and anemia. Relapses (renewed manifestations of erythrocytic infection) can occur with this type of malaria. Overall, P. vivax is stiU susceptible to chloroquine however, resistant strains have been reported from Papua New Guinea and parts of Indonesia. Plasmodium malariae the cause of quartan malaria, has an incubation period of 15—30 days and its asexual cycle is 72 hours. This mildest form of malaria can cause nephritis in addition to the usual symptoms. It is a nonrelapsing type of malaria but the ted blood ceU infection can last for many years. No resistance to chloroquine by this plasmodium has been reported. Plasmodium ovale responsible for ovale tertian malaria, has an incubation period of 9—17 days (15 average). Relapses can occur in people infected with this plasmodium. No chloroquine resistance has been reported for this parasite. 

Ribavirin is not incorporated into the DNA or RNA of either mammalian or viral systems. It has been shown (123), however, that a high dosage of ribavirin given over a prolonged period to Rhesus monkeys results in anemia of red blood cells. This effect is dose related and reversible upon cessation of treatment. Guanosine partially reverses the antiviral effect of ribavirin against certain vimses. 

Aplastic anemia and leukemia are not the only health effects ascribed to benzene exposure. A number of recent studies have associated benzene exposure with chromosomal changes (aberrations) (118). Other studies have shown abnormalities in porphyrin metabolism and decrease in leucocyte alkaline phosphatase activity in apparendy healthy workers exposed to 10—20 ppm benzene (119,120). Increases in leukoagglutinins, as well as increases in blood fibrinolytic activity, have also been reported and are believed to be responsible for the persistent hemorrhages in chronic benzene poisoning (121,122). 

Several nonoccupational health problems have been traced to cobalt compounds. Cobalt compounds were used as foam stabilizers in many breweries throughout the world in the mid to late 1960s, and over 100 cases of cardiomyopathy, several followed by death, occurred in heavy beer drinkers (38,39). Those affected consumed as much as 6 L/d of beer (qv) and chronic alcoholism and poor diet may well have contributed to this disease. Some patients treated with cobalt(II) chloride for anemia have developed goiters and polycythemia (40). The impact of cobalt on the thyroid gland and blood has been observed (41). 

Benzene zero 0.005 Anemia decrease in blood platelets increased risk of cancer Discharge from factories leaching from gas storage tanks and landfills... 

There are undifferentiated stem cells of the blood elements in the bone marrow that differentiate and mature into erythrocytes, (red blood cells), thrombocytes (platelets), and white blood cells (leukocytes and lymphocytes). The production of erythrocytes is regulated by a hormone, erythropoietin (see the section on kidney toxicity), that is synthetized and excreted by the kidney. An increase in the number of premature erythrocytes is an indication of stimulation of erythropoiesis, i.e., increased production of erythrocytes in anemia due to continuous bleeding. 

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