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Because of the widespread use of dichlorvos (DDVP) for domestic applications, evaluation of their toxic effects is of major concern to public health. Lycopene may lower oxidative stress by a mechanism that is not fully elucidated. The present study was undertaken to evaluate the protective efficacy of lycopene in terms of normalization of altered biochemical parameters following DDVP treatment in rats. Animals were divided into four groups. The first group was used as control, while groups 2, 3, and 4 were orally treated with lycopene (10 mg kg(-1) body weight (b.w.)), DDVP (1.6 mg kg(-1) b.w.), and DDVP plus lycopene, respectively. Results showed that oral administration of DDVP for 30 days increased the levels of lipid peroxidation markers such as malondialdehyde, 4-hydroxynonanal, and protein carbonyl content in liver. Also, a decrease in levels of vitamin C, vitamin E, and reduced glutathione was detected due to DDVP administration. These were accompanied by a decrease in the activities of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase in the liver tissue. Moreover, DDVP increased the activities of serum transaminases, alkaline phosphatase, lactate dehydrogenase, and lipoxygenase, and the levels of bilirubin, total cholesterol, low-density lipoprotein cholesterol, triglyceride and DNA-protein crosslinks, and 8-hydroxy-2-deoxyguanosine, while decreased the level of high-density lipoprotein cholesterol. Our results provide new insights into the biochemical studies of relation between DDVP hepatotoxicity and lycopene treatment. Administration of lycopene to DDVP-treated rats reverted the status of hepatic markers to near-normal levels. These data suggest that lycopene can protect against the liver damage induced by DDVP.

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BACKGROUND/AIMS: Idiopathic (autoimmune) thrombocytopenic purpura has been previously reported as a rare complication in children following parvovirus B19 infection. In the immunocompromised host who is unable to produce neutralizing antibody, an infection with parvovirus B19 can persist and cause chronic bone marrow failure. METHODS: We describe a child who had undergone liver transplantation and who had idiopathic thrombocytopenic purpura, whose history and laboratory findings suggested parvovirus B19 infection. The infection disappeared without persistent viremia, and the thrombocytopenia responded completely to the administration of gamma globulin while the patient was undergoing chronic immunosuppression therapy. RESULTS/CONCLUSION: Transplant physicians need to be aware of this complication, and parvovirus B19 infection should be included in the differential diagnosis of liver recipients presenting with severe thrombocytopenia.

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UNLABELLED: Two siblings, a 12-year-old girl and a 7-year-old boy, had recurrent episodes of haemolytic-uraemic syndrome/thrombotic thrombocytopenic purpura, manifested mainly by thrombocytopenia and micro-angiopathic haemolytic anaemia. During 11 years of follow up the girl responded only to steroids, whereas many other therapeutic modalities were ineffective. Following treatment with low dose danazol relapses became fewer and of diminished severity and completely subsided after 6 months. The boy started his illness with signs of haemolytic uraemic syndrome and later developed neurological manifestations. During a 6 year follow up he responded only to plasma exchange. Although chronic thrombocytopenia persisted during the past 3 years, the boy's clinical condition improved. CONCLUSION: A family with two children with recurrent episodes of thrombotic thrombocytopenic purpura is described. In one child danazol could have had a beneficial effect.

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The prevalence, clinical manifestations and serological markers of hepatitis C virus (HCV), hepatitis B virus (HBV) and human immunodeficiency virus (HIV) infections were studied in 112 multiply transfused patients (49 hemophiliacs receiving either nonheat-treated factor concentrates or cryoprecipitate, 33 thalassemic, 20 refractory anemia and 10 leukemia patients). Positive serological markers for HCV, HBV and HIV were found to correlate with number of donors and duration of disease (logistic regression P = 0.0001 and 0.01 respectively). Viral infectivity was significantly correlated with type of blood product. HCV seropositivity was more common in hemophiliacs treated with nonheat-treated factor concentrates (93%) compared to those receiving cryoprecipitate (37%) or nonhemophiliacs receiving red packed cells (20%) (P < 0.001). Likewise, HBV seropositivity in patients receiving the above blood products was 83%, 61% and 26% respectively (P < 0.001), and HIV seropositivity was 35%, 6% and 0% respectively (P < 0.001). Acute or chronic liver disease was documented in 4 of 14 (28%) HCV-positive patients. Increased liver enzymes were recorded in sera of 43% HCV-positive patients and 18% HBV-positive patients compared to 22% of HBV and 20% HCV-seronegative patients (P = 0.076). Of 47 HCV-positive patients 24 were coinfected by HBV and 9 had triple infection (HCV, HBV and HIV). No solitary HIV infection was found. HIV seropositivity was always accompanied by serologic evidence for HBV with or without HCV infection.

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A newborn with congenital juvenile chronic myelogenous leukemia (JCML) is described. The diagnosis was suggested by the characteristic clinical and hematologic presentation, and was confirmed by the results of in-vitro cultures of the hematopoietic progenitors, which showed excessive proliferation of monocytic colonies, with and without the addition of exogenous granulocyte-macrophage colony stimulating factor (GM-CSF). Based on published in-vitro response of JCML cells to alpha interferon-2 (alpha IFN 2), we treated this child for 17 weeks with subcutaneous alpha interferon, 1,000,000 units per day. In contrast to previous in vitro results, treatment of this patient affected neither the clinical course of the disease, nor the in vitro growth of the peripheral blood-derived monocytic colonies.

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The growth retardation of children with thalassemia major is multifactorial. Along the endocrine axis of growth hormone (GH), serum somatomedin has been shown to be deficient and GH response to GH-releasing hormone impaired, while GH response to provocative stimuli is normal. We studied the spontaneous secretion of GH in seven patients with thalassemia major and growth retardation. Three of the patients were hypothyroid, and the other four were euthyroid. Spontaneous secretion of GH in all seven patients was subnormal: the number of pulses, the mean pulse amplitude, and the integrated concentration of GH were all lower than in 14 age- and sex-matched (10 pubertal and 4 prepubertal) control subjects. GH response to provocative stimuli was normal in the euthyroid patients. This pattern of response corresponds with the definition of neurosecretory dysfunction of GH secretion. It is concluded that the growth retardation of patients with thalassemia major is partly due to neurosecretory dysfunction of GH secretion.

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An 11-year-old boy was hospitalized with sudden blindness and sagittal sinus vein thrombosis, which were the presenting signs of acute promyelocytic leukemia (APL). The association of disseminated intravascular clotting (DIC) with APL is well-known, and DIC usually affects the smaller blood vessels. The obliteration of a large blood vessel, as in our case, is an uncommon manifestation of DIC. This presentation of acute childhood leukemia is unusual and, to the best of our knowledge, has not been previously reported.

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A patient with acute hyperleukocytotic myelogenous leukemia who presented with acute respiratory distress is reported. Clinical manifestations included dyspnea, tachypnea, hyperventilation, and cyanosis. Blood gas analysis revealed hypoxemia, hypocapnia, and metabolic acidosis. Chest X-ray and perfusion lung scanning were normal. Pulmonary leukostasis syndrome (PLS) was later confirmed at autopsy. In a patient with hyperleukocytosic from acute nonlymphocytic leukemia and respiratory distress, a normal perfusion lung scintigraph should make one consider the PLS.

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A 5-year-old girl with refractory anaemia with excess of blasts in transformation (RAEBT) terminating in acute nonlymphocytic leukemia is reported. The patient's serum had an inhibitory effect on normal hemopoiesis. T cell subsets defined by monoclonal antibodies revealed a decrease in helper/inducer T cell population (OKT4-positive cells) and inversion of the T4/T8 ratio. It is suggested that imbalance in immunoregulatory T cells, which has a crucial role in the control of hemopoiesis, may be a primary event in the pathogenesis of myelodysplastic syndrome which eventually develops into an overt leukemia.

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An asymptomatic hypercalcemic IgG-Kappa myeloma patient is presented. A calcium-IgG complex was isolated and purified from the serum by column chromatography. Following further purification on a Sepharose protein A column, the IgG-Kappa molecule did not contain any detectable amount of calcium, indicating that calcium is loosely bound to IgG. The monoclonal IgG demonstrated a strong calcium binding capacity in vitro. The calcium-IgG complex in the serum was shown not to be saturated and thus could absorb more ionized calcium. In view of the presence of an abnormal monoclonal IgG capable of binding excess calcium, and the fact that the asymptomatic patient did not respond to the antihypercalcemic drugs, the treatment was stopped.

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A 6-month-old full-term infant had severe anemia and neutropenia. The patient was being fed cow's milk and a diet of corn flour. Thorough investigation revealed low serum iron concentration, severe hypocupremia, low ceruloplasmin, retardation of bone age, and metaphysial irregularities and spurring. Bone marrow aspirate revealed cytoplasmic vacuolization in precursors of the erythroid and myeloid series and ringed sideroblasts. Therapy with oral iron, folic acid, and vitamin C was futile. Administration of copper sulfate resulted in brisk increase in neutrophils and reticulocytes. The child maintained normal levels of hemoglobin, neutrophils, serum copper and ceruloplasmin, and serum iron one year after copper therapy was discontinued. The probable role of unrecognized copper deficiency in causing anemia in infants more than 6 months of age is discussed, and the importance of serum copper examination in refractory iron deficiency anemia and neutropenia is stressed. To the best of our knowledge, no such case has previously been described in the literature.

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A calcium binding IgG was isolated and purified by column chromatography from serum of a myeloma patient with asymptomatic hypercalcaemia. The myeloma IgG, characterized as an IgG kappa, revealed a normal sized heavy chain (56 000 dalton), and a light chain of 31 000 dalton. Another population of IgG separated and purified from the same patient's serum did not bind calcium and had a normal 26 000 dalton light chain. Calcium binding activity in vitro is optimal at pH 8.0, and reaches its maximum after 3 h of 45Ca myeloma IgG incubation. Cleavage of the purified IgG by trypsin yielded peptides which were further isolated by column chromatography and characterized as Fab and Fc fragments. Light and heavy chains were obtained by reacting the immunoglobulin with dithiothreitol and iodoacetamide followed by Sephadex G-100 chromatography. Calcium binding activity was proved to be associated with Fab IgG fragment. Preparates containing Fc, heavy or light chains did not bind calcium in vitro.

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A patient with polycythemia vera (PV) received successive treatment by phlebotomies, radioactive phosphorus, myleran and cyclophosphamide. Sixteen years after the diagnosis, he developed acute myeloblastic leukemia. A complete remission was achieved following two courses of COAP (cyclophosphamide, vincristine, Cytosine Arabinoside, and prednisone) therapy. Four months later, while still in leukemic remission, he became mildly polycythemic again and the treatment with phlebotomies and cyclophosphamide was resume. The patient has subsequently been in complete remission of leukemia for over three years and his polycythemia is controlled by small doses of cyclophosphamide. This appears to be a unique case of such a prolonged remission of leukemia in the course of PV, with a return to a mild polycythemia state.

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