Biomedical subjects

P Butthep

Publications and source records attributed to P Butthep.

26 records · Page 2Linked to original sources

PubMed1992

Interaction between endothelial cells and thalassemic red cells in vitro.

Erythrocytes from 45 patients with thalassemia and/or hemoglobinopathies were studied for their cytoadherence property to the vascular endothelial cells in vitro. In plasma free medium, erythrocytes from patients with beta-thal/Hb E both splenectomized and nonsplenectomized, HbH diseases (alpha-thal 1/alpha-thal 2 and alpha-thal 1/Hb Constant Spring genotypes) and homozygous Hb E subjects bind to endothelial cells at a greater number as compared to the binding cell number of normal erythrocytes (p-value < 0.05 in all types). Addition of autologous platelet-rich plasma or whole blood to the culture system causes further increase in the number of adhering beta-thalassemia red cells. Platelet-rich plasma had more enhancement effect than the whole blood. However, no such enhancement of both platelet-rich plasma and whole blood was demonstrated in the culture of normal or alpha-thalassemia erythrocytes. Increased binding between red cells and endothelial cells may contribute to the greater risk of vascular occlusion in thalassemic patients.

Blood Platelets↗

PubMed1992

Thalassemic serum impairs endothelial cell growth in vitro.

Endothelial cells cultured for 3 days in the presence of hemoglobin H pooled sera had significantly decreased cell proliferation compared to those in normal serum. Inhibition was demonstrated at a concentration of 20% pooled serum in the cultured medium. Further decrease was shown in the presence of 30% pooled hemoglobin H sera. Sera from two genotypes of Hb H disease (alpha-thal 1/alpha-thal 2 and alpha-thal 1/Hb Constant Spring) had the same degree of inhibitory effect. Pooled sera from beta-thal/Hb E patients (both splenectomized or nonsplenectomized cases) had no such inhibitory effect. However, at day 4 and 5, the growth pattern relatively declined. Bilirubin at a concentration greater than 4.0 mg% in the medium 199 also caused significant decrease in cell proliferation. Since the diluted Hb H serum had bilirubin less than 4.0 mg%, the inhibitory effect of the pooled HbH serum is thus not due to effect of bilirubin. The difference between HbH and beta-thal/HbE sera in terms of inhibition of endothelial cell proliferation is the new finding that needs further investigation to explain vascularization and hemostasis in the patients of these two genotypes.

Bilirubin↗

PubMed1992

An unusual adhesion between red-cells and platelets in falciparum malaria.

A Thai female patient infected with P. falciparum had 80 per cent P. falciparum infected red cells at ring stage in the peripheral blood smear. The complications included anemia, thrombocytopenia, acute renal failure and pulmonary edema. A marked decrease in platelets number, low hemoglobin, low hematocrit and decreased red blood cell count were detected. More than 70 per cent of total platelets detected in the blood smear were binding to parasitized red blood cells. The number of binding platelets declined with decreasing per cent parasitized red cells. It was also noted that some platelets (10-20%) adhered to nonparasitized red cells. An increased number of large lymphocytes was shown by increased numbers of large unstained cells (LUC) by H* 1 automated analyzer. The peripheral blood smear showed abnormal binding of platelets to the infected red cells more frequently than to non infected red cells and free platelets on the day of high parasitemia. This abnormal phenomena was related to the number of platelets in the circulation. When the parasitized red cells were not detected in the blood smear, the number of platelets in the circulation had returned to normal.

Acute Kidney Injury↗

PubMed1992

Cytometric analysis of paroxysmal nocturnal hemoglobinuria erythrocytes.

Erythrocytes from six cases of paroxysmal nocturnal hemoglobinuria (PNH) were analysed by the H*1 hematology analyser using laser inspection for each individual red cell. The computer program categorized the red cells into 9 groups based on the data of red cell volume and intracellular hemoglobin concentration. The only 46.3 +/- 10.9 per cent (Mean +/- SD) of PNH red cells were normochromic normocytic. Hypochromia (hemoglobin concentration less than 28 g/dL) with normal red cell volume (between 60 to 120 fL) were found in 22.8 +/- 19.7 per cent and with large cell volume (greater than 120 fL) = 14.9 +/- 4.5 per cent of total red cells. Large cells with normal hemoglobin concentration were found in 12.9 +/- 13.2 per cent. The red cells had increased heterogeneity in red cell volume measured as red cell distribution width (RDW), Mean +/- SD = 23.6 +/- 2.3 per cent and increased heterogeneity in their hemoglobin concentration distribution with (HDW) (3.4 +/- 0.5 g/dL). The high RDW was resulted from increased number of varying size of macrocytes and the high HDW was caused by the increased number of hypochromic red cells. Heterogeneity in PNH red cell population described in this study has been postulated to relate with the clonal abnormality of the PNH red cells.

Adult↗

PubMed1989

Decreased sensitivity of artesunate and chloroquine of Plasmodium falciparum infecting hemoglobin H and/or hemoglobin constant spring erythrocytes.

Plasmodium falciparum infecting hemoglobin (Hb) H and/or Hb Constant Spring erythrocytes in vitro was relatively more resistant than that infecting normal erythrocytes to artesunate and chloroquine, while the sensitivity to pyrimethamine was unchanged. The 50% inhibitory concentrations (IC50) for artesunate in HbH (alpha-thal 1/alpha-thal 2), HbH (alpha-thal 1/Hb Constant Spring), and homozygous Hb Constant Spring erythrocytes were 4.5 +/- 2.8, 8.5 +/- 3.2, and 2.6 +/- 1.6 nM compared with 0.82 +/- 0.35 nM in normal erythrocytes (P less than 0.002 for all three cases). The IC50 for chloroquine were 97 +/- 46, 162 +/- 67, and 93 +/- 36 nM, respectively, in the variant erythrocytes, compared with 48 +/- 13 nM in normal erythrocytes (P less than 0.002, 0.002, and 0.02, respectively). The differences in sensitivity to artesunate and chloroquine of the parasite infecting HbH erythrocytes are probably related to their oxidative mode of action and relatively high amounts of antioxidant enzymes in the host erythrocytes. This novel example of dependence on the host of the malarial parasite drug sensitivity may have implications for chemotherapy of malaria in patients with genetically variant erythrocytes.

Animals↗

PubMed1988

Impaired parasite growth and increased susceptibility to phagocytosis of Plasmodium falciparum infected alpha-thalassemia or hemoglobin Constant Spring red blood cells.

In vitro multiplication of Plasmodium falciparum in hemoglobin H or hemoglobin Constant Spring red blood cells (from homozygotes or double heterozygotes) was significantly reduced as compared with that in normal erythrocytes. The parasitized genetically abnormal red blood cells showed furthermore a high propensity for being phagocytosed by peripheral blood monocytes. Both impaired parasite growth and increased susceptibility to phagocytosis may be related to mechanisms for protection of the variants from P. falciparum infection.

Animals↗

PubMed1987

Inhibitory effect of beta zero-thalassaemia/haemoglobin E erythrocytes on Plasmodium falciparum growth in vitro.

The growth of Plasmodium falciparum in erythrocytes from individuals with beta zero-thalassaemia or haemoglobin (Hb) E, or both, was assessed in vitro. A significant inhibitory effect on the growth of the parasite was found only with erythrocytes from individuals doubly heterozygous for beta zeros-thalassaemia and HbE. The inhibitory effect was particularly marked with erythrocytes from splenectomized beta zeros-thalassaemia/HbE patients. The protective effect was related to HbF, Hb levels and shape abnormalities of the variant erythrocytes.

Animals↗

PubMed1986

Increased phagocytosis of Plasmodium falciparum-infected erythrocytes with haemoglobin E by peripheral blood monocytes.

Erythrocytes from subjects with homozygous and heterozygous haemoglobin E (HbE) infected with Plasmodium falciparum in vitro were phagocytosed to a greater extent by normal human monocytes than infected erythrocytes from normal subjects. Susceptibility to phagocytosis was maximal when the parasites developed to trophozoite and schizont stages in both normal and patients' erythrocytes. The increased susceptibility of P. falciparum-infected HbE erythrocytes to phagocytosis by monocytes may play a role in protection against malaria.

Cells, Cultured↗