Stippled erythrocytes

Heavy lead exposure is associated with reticulocytosis and occurrence of stippled erythrocytes in peripheral blood (US EPA 1986), possible mediated through the effect on P5N. Lead can also shorten the lifespan of circulating erythrocytes, probably by inhibition of the Na, K -ATPase, possibly also affecting the erythrocyte s P5N, and by causing changes in membrane proteins. Anemia may follow of either the nor-mocytic or sideroblastic type. 

NS (occup) Hematological Decreased hemoglobin with or without basophilic stippling of erythrocytes 240 Awad et al. 1986 Baker et al. 1979 Grandjean 1979 Lilis et al. 1978 Pagliuca et al. 1990 Tola et al. 1973 Wada et al. 1973... 

There is no clinical disease state that is pathognomonic for lead exposure. The neurotoxic effects and hematopoietic effects of lead are well recognized. The primary biomarkers of effect for lead are EP, ALAD, basophilic stippling and premature erythrocyte hemolysis, and presence of intranuclear lead inclusion bodies in the kidneys. Of these, activity of ALAD is a sensitive indicator of lead exposure (Hemberg et al. 1970 Morris et al. 1988 Somashekaraiah et al. 1990 Tola et al. 1973), but the assay can not distinguish between moderate and severe exposure (Graziano 1994). Sensitive, reliable, well-established methods exist to monitor for these biomarkers however, they are not specific for lead exposure. Therefore, there is a need to develop more specific biomarkers of effect for lead. Recent data... 

Measuring the child s blood lead level will be very useful in assessing the possibility of lead poisoning. There is evidence that at blood lead levels of about 10 Jig/dL, children are at risk for developmental impairment. Other tests that may be useful include examination for microcytic anemia and erythrocyte stippling and radiographic examination of the long bones for lead lines. 

ALAD depression, 86% anemia basophilic stippling of erythrocytes... 

Blood lead levels provide the best indicators of lead poisoning but do not reflect total body burden (Lee and Moore 1990). The inhibition of erythrocyte 8-aminolevulinic acid indicates lead exposure, but most centers still use blood lead levels for screening (Lee and Moore 1990 Roper et al. 1993 Schaffer and Campbell 1994). Zinc protoporphyrin indicates neurotoxicity from lead but does not have the sensitivity for assessing low levels of exposure (Anger and Johnson 1985 Royce and Needleman 1995). Radiological examination of the abdomen and long bones does not reliably portray exposure. The same holds true for the examination of red blood cells for basophilic stippling and the assay of hair and nail levels for lead (Roper et al. 1993). The Centers for Disease Control and Prevention (CDC) does not recommend use of scarification of the forearm with 25% sodium sulfite solution to assess for black discoloration of skin, a procedure recommended in some sources. Medical centers perform an edetate disodium calcium provocative chelation test with urinalysis and complete blood... 

E. Other tests. Nonspecific laboratory findings that support the diagnosis of lead poisoning include anemia (normocytic or microcytic), and basophilic stippling of erythrocytes, a useful but insensitive clue. Acute high-dose exposure may sometimes be associated with transient azotemia (elevated BUN and serum creatinine) and mild to moderate elevation in serum transaminases. Recently ingested lead paint, glazes, chips, or solid lead objects may be visible on abdominal x-rays. CT or MRI of the brain often reveals cerebral edema in patients with lead encephalopathy. Because iron deficiency increases lead absorption, iron status should be evaluated. 

Hereditary deficiency of erythrocyte pyrimidine 5 nucleotidase results in a chronic haemolytic anaemia. The red cells show basophilic stippling and contain a markedly increased content of nucleotides, 3-6 times greater than normal, and 65 to 80% of nucleotides are pyrimidine in type (Valentine, et al., 1974 Torrance and Whittaker, 1979). Pyrimidine 5 nucleotidase is unique amongst the 5 nucleotidases in its strict substrate specificity for pyrimidine nucleoside 5 monophosphates, its pH profile, and for its cytosolic localisation (Paglia and Valentine, 1975). 

The number of inherited defects of the pyrimidine metabolism described so far is small, compared to that of the purine metabolism. Combined deficiency of orotate phosphoribosyltransferase (OPRT) (EC 2.4.2.10) and orotidine 5 -monophosphate decarboxylase (ODC) (EC 4.1.1.23), designated as type I hereditary orotic aciduria, presents with characteristic clinical features such as hypochromic anemia with a megaloblastic bone marrow and crystalluria. Only six patients have been described and, as far as we know, new cases have not been discovered recently. ODC deficiency with similar clinical phenomena and leading to increased urinary excretion of orotate and orotidine has been detected in only one patient (1). A third defect, a deficiency of pyrimidine 5 -nucleotidase (Py-5NX (EC 3.1.3.5.) in erythrocytes, is associated with chronic hemolytic anemia and prominent basophylic stippling of the erythrocytes due to accumulated pyrimidine nucleotides. An increasing number of patients have been reported, their detection being facilitated by the typical phenomena. We do not know whether the urinary pyrimidine profile in this condition is abnormal. 

Guinea pigs Pb solution, 0.01 mg Pb/cc washed erythrocytes Anemia and stippling of cells in dosed animals Beresina and Engling (1912)... 

CDC, 1978, 1991, 2005 U.S. EPA, 1977, 1986, 2006). The purely lead-associated anemia is taken to be mildly hypochromic or normochromic and nor-mocytic. With severe exposures, one occasionally sees basophilic stippling from deranged erythropoietic activity and accumulation of pyrimidine nucleotides. Reticulocytosis is seen subsequent to reduced erythrocyte survival time. Lead toxicity induces the anemia via the combined effects of reduced hemoglobin production and increased erythrocyte destruction. 

Immature nucleated erythrocytes with basophilic stippling... 

Inhibition of the enzyme 5 -nudeotidase (5 N) allows retention of nuddc acid fragments and riboscNnes, which results in ba hillc stippling and increases the fragility of erythrocytes. 

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