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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An adult presenting with anemia and seizures was found to have lead poisoning. Chelation therapy undertaken before the source of exposure was known was accompanied by clinical improvement. Recurrence of an excessive body lead burden despite chelation led to the discovery of pica for lead-contaminated garden soil. Lead nephropathy progressed when the geophagia was resumed.
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PMID:Geophagic lead nephropathy: case report. 31 27

Lead has a wide range of applications, and its production and use result in contamination of the environment, including food and drinking water. Geochemical studies indicate that the majority of lead in ecosystems originated from industrial operations, and that human lead intake has increased 100-fold above the "natural" level. Prehistoric human skeletons contain about two orders of magnitude less lead than present-day samples. Biochemical interference with heme biosynthesis can be detected as a result of current lead exposures, inhibition of aminolevulinate dehydratase and accumulation of zinc protoporphyrin in erythrocytes being the earliest effects. Anemia is uncommon except for cases of lead poisoning, but even slightly increased lead absorption results in a decrease in hemoglobin concentrations. Modern neurobehavioral test methods have disclosed increased prevalence of psychological dysfunction associated with augmented lead absorption. Biochemical and behavioral changes occur below the recommended limit for blood lead concentration of 60 micrograms/100 ml. Several diagnostic tests for lead toxicity are available. The protoporphyrin concentration in the blood seems to be the best risk indicator. The highest occupational lead exposures occur in lead smelters and storage battery plants, but several other industrial operations may result in high lead levels. As much as 1% of the working population may have a significantly increased lead absorption with possible adverse effects.
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PMID:Widening perspectives of lead toxicity. A review of health effects of lead exposure in adults. 40 Sep 72

The activity of the enzyme delta-aminolevulinic acid dehydratase (ALA-D) was strongly depressed in erythrocytes, spleen and renal tissue of rainbow trouts (Salmo gairdnerii) exposed to sublethal levels of inorganic lead (10, 75 and 300 microgram Pb2+/L) for 30 days. The fish exposed to the highest lead concentration also showed an anemic response and basophilic stippling of erythrocytes. The lead exposure did not cause any alteration of the white blood cell picture. The ALA-D inhibition, the anemia and basophilic stippling seemed to persist in the lead-exposed fish even after a recovery period of seven weeks in lead-free water.
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PMID:Effects of inorganic lead on delta-aminolevulinic acid dehydratase activity and hematological variables in the rainbow trout, Salmo gairdnerii. 48 10

Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.
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PMID:Lead toxicity and nutritional deficiencies. 51 Feb 31

Lead-containing paints were administered orally to 27 rhesus monkeys for periods of 18-667 days. Lead acetate was fed to nine monkeys of three different species for 9-156 days. Excretion of one week's dose of lead in six primates ranged from 35 to 94%. The animals incurred moderate to extreme elevations of lead in blood, most lost weight, or had depressed weight gains, and developed Burtonian lines, some died suddenly and unexpectedly, and many terminated in a moribund state with profound anemia. Only one neonate had obvious signs of lead encephalopathy. The monkeys' ages, dose and source of lead, and possibly other factors, affected their response to lead.
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PMID:Experimental lead paint poisoning in nonhuman primates. I. Clinical signs and course. 81 84

A retired teamster with abdominal pain and anemia was found to have lead intoxication presumably due to and old bullet in his ankle. Most lead particles within the body need not be removed. Lead solubility characteristics exemplified by this case cuase us to recommend that bullets and lead particles facing synovial spaces should be removed.
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PMID:Bullets, joints, And lead intoxication. A remarkable and instructive case. 82 11

Lead-induced anemia in rats, which is of a microcytic, hypochromic type, has been shown to be a result of an interference with the metabolism of copper and iron. In this complex interaction, copper may be the target upon which ingested lead has its antagonistic effect on hematopoiesis. The depressions in hematocrit and hemoglobin levels resulting from exposure to lead may occur secondarily to the effects of a lead-induced copper deficiency on iron mobilization and utilization. The metabolic fault induced by lead is seen in a reduction of serum iron, elevation of serum iron binding capacity, and increase in liver iron, all manifestations of systemic effects related to an interference with copper metabolism. These results relate many of the characteristics of the lead-induced anemia to those found in the copper-deficiency anemia.
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PMID:Anemia of lead intoxication: a role for copper. 90 22

Two cases of lead arsenate polyneuropathy are described in two farmers from the same rural area; the etiology of the neurologic al disorder was ascertained only after repeated hospital admissions. It was a neuropathy of the radial nerve associated with signs of peripheral impairment of the lower limbs with pains and paresthesias. Abdominal colies, arterial hipertension, anaemia and signs of renal impairment were also present. Specific therapy was undertaken which was soon followed by nearly full recovery. Lead and arsenic toxicology are discussed with particular focusing on the necessity emphasis on commun occupational hazards both in terms of diagnostic and therapeutic procedures. The differential diagnosis is considered between the observed clinical picture and other polyneuropathies of different etiology i.e. dysmetabolic (porphyria) or toxic (insecticides, T.O.C.P., etc).
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PMID:[Lead arsenate as an underestimated cause of polyneuropathy in rural environment: description of two cases]. 102 47

The toxicity of dietary lead in Japanese quail was investigated. The data indicated that dietary lead, in the form of lead acetate, was toxic to young quail at the level of 500 p.p.m. and this toxicity was evidenced by an inhibition of normal growth and by anemia. The anemic state in the lead toxic quail was more readily detected by reduced blood hemoglobin concentrations than by packed cell volumes. In addition, the data suggested that lead interfered with normal sexual development in the males. Lead at levels as high as 1000 p.p.m. did not prevent normal primary antibody responses to sheep erythrocytes.
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PMID:Toxicity of dietary lead in Japanese quail. 118 20

Toxic effect of lead is related, among others, to metabolic interactions with essential trace elements i.e. iron, zinc and copper. Lead stimulates urinary excretion of these elements interfering with their reabsorption in kidney as well as inhibits ceruloplasmin activity in plasma, ferrochelatase activity in reticulocytes and copper- and zinc-dependent superoxide dismutase activity in tissues--with all functional consequences for organism. Iron, zinc and copper deficiency results in increased lead toxicity through considerable enhancement of lead absorption from intestinal tract, producing greater degree of anemia as well as decreasing of metalloenzymes activity. Increasing dietary zinc and probably copper suppresses intestinal absorption of lead. The addition of iron, zinc and copper to the diet prevents lead accumulation within the tissues and subsequent toxicity of this element. It seems that increasing intake of food products containing a lot of essential trace elements can diminish risk of lead toxicity for human.
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PMID:[Effects of harmful trace elements on iron, zinc and copper: their interactions in animals and humans. II. Lead]. 180 38


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