Cases reported "Anemia"

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1/8. flour contamination as a source of lead intoxication.

    CASE REPORT: A 43-year-old man was hospitalized because of severe anemia and recurrent bouts of abdominal pain over 20 days. There was no known occupational exposure to toxins. Concomitantly, the patient's father complained of having the same symptoms. Familial lead poisoning was diagnosed when all 6 family members tested had high blood leads (31-64 micrograms/dL). RESULTS: Following detailed examination of the potential sources common to all members of the household, the cause of poisoning was determined to be corn flour containing 38.7 mg/g lead. physicians are reminded to consider lead poisoning in the differential diagnosis of individuals with unexplained symptoms, particularly those of abdominal discomfort and anemia.
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2/8. Lead induced anaemia due to traditional Indian medicine: a case report.

    Lead intoxication in adults without occupational exposure is a rare and unexpected event. The case of a western European is reported who had severe anaemia after ingestion of several ayurvedic drugs, obtained during a trip to india. Laboratory findings showed high blood lead concentrations, an increased urinary lead concentration, and an increased urinary excretion of delta-aminolaevulinic acid. Also, slightly increased urinary concentrations of arsenic and silver were found. physicians should be aware that with growing international travel and rising self medication with drugs from uncontrolled sources the risk of drug induced poisoning could increase in the future.
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3/8. infant hypervitaminosis a causes severe anemia and thrombocytopenia: evidence of a retinol-dependent bone marrow cell growth inhibition.

    vitamin a is a pivotal biochemical factor required for normal proliferation and differentiation as well as for specialized functions, such as vision. The dietary intake of 1500 IU/day is recommended in the first year of life. Here, we report the case of an infant who had been given 62 000 IU/day for 80 days. The infant showed several clinical signs of retinol intoxication, including severe anemia and thrombocytopenia. bone marrow showed a remarkably reduced number of erythroid and megakaryocytic cells. The interruption of vitamin a treatment was immediately followed by clinical and biochemical recovery. To clarify whether the effects of retinol are due to a direct action on bone marrow cell proliferation, we investigated the activity of retinol (both the drug and the pure molecule) on the growth of K-562, a multipotent hematopoietic cell line, and on bone marrow mesenchymal stem cells. We observed that vitamin a strongly inhibited the proliferation of the cells at concentrations similar to those reached in vivo. Subsequent biochemical analyses of the cell cycle suggested that the effect was mediated by the up-regulation of cyclin-dependent kinase inhibitors, p21(Cip1) and p27(Kip1). These are the first findings to demonstrate that infant hypervitaminosis a causes a severe anemia and thrombocytopenia and that this is probably due to the direct effect of the molecule on the growth of all bone marrow cellular components. Our data also suggest potential bone marrow functional alterations after excessive vitamin a intake because of emerging social habits.
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4/8. Morphologic findings in bone marrow precursor cells in zinc-induced copper deficiency anemia.

    Damage to the bone marrow elements, as shown by cytoplasmic vacuolization, has been reported in patients with acute alcohol intoxication, drug reactions, nutritional deficiencies, myeloproliferative syndromes, malignant hematologic conditions, some metabolic conditions, and in those treated with chemotherapeutic agents. A case of zinc toxicity with anemia, leukopenia, and cytoplasmic vacuolization of both myeloid and erythroid precursors is described. The patient described was a 30-year-old quadriplegic man who was receiving oral zinc to promote the healing of and prevention of decubitus ulcers. In the gut, dietary zinc interacts with copper in a competitive manner, and high levels of zinc can lead to copper deficiency. zinc-induced copper deficiency anemia can be morphologically identified in the bone marrow preparations by cytoplasmic vacuolization of both myeloid and erythroid precursor elements.
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5/8. Radiological diagnosis of inorganic lead poisoning.

    A 43-year-old woman had abdominal pain and anemia due to inorganic lead poisoning. Plain abdominal x-ray films showed metallic densities within the lumen of the large bowel. The patient admitted that she used to chew the sheets of metallic lead enclosing wine bottle necks regularly. We report the case because of both the unusual radiographic findings and the exceptional source of lead intoxication.
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6/8. Prenatal and early postnatal intoxication by inorganic mercury resulting from the maternal use of mercury containing soap.

    A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3-month-old black boy in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal, ocular and haematological defects may have resulted from exposure to mercury during foetal life and the 1-month lactation period due to the extensive use of inorganic mercury containing cosmetics by the mother.
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7/8. lead poisoning in an art conservator.

    A case of lead poisoning in a female art conservator is reported. The patient had experienced excessive lead exposure while restoring an antique Peruvian tapestry from the Chancay period (1000 to 1500 AD) using a powdered pigment (cinnabar), which had been recovered from the same tomb in which the tapestry was found. Over two months, prominent neurological, gastrointestinal, and diffuse muscular symptoms developed. Severe anemia accompanied by basophilic stippling of RBCs led to the diagnosis of lead poisoning, which was confirmed by markedly elevated blood lead levels (up to 130 micrograms/dL) and impairment of heme synthetic enzymes. The severity of the intoxication necessitated chelation therapy. Chemical analysis of the antique powdered pigment showed it to be the source of lead exposure, in that it contained about 1% lead.
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8/8. herbal medicine-associated lead intoxication.

    A female patient visited our hospital with abdominal pain and anemia. Examination for a gastrointestinal disease gave no diagnostic information. Laboratory studies of the parameters of heme biosynthesis revealed an enzymatic inhibition by lead. The diagnosis of lead poisoning was confirmed by detection of an elevated blood lead level. Excessive lead ingestion was thought to be caused by herbal medicines and/or by an earthen teapot.
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