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Biomedical subjects

M Hou

Publications and source records attributed to M Hou.

At least 37 records · Page 2Linked to original sources

Angiotensin II type 1 receptors stimulate protein synthesis in human cardiac fibroblasts via a Ca2+-sensitive PKC-dependent tyrosine kinase pathway.

The aim of the present study was to investigate the proliferative effects of Ang II in human cardiac fibroblasts. The effects of Ang II in human cardiac fibroblasts on the 3H-thymidine incorporation, the cell number, the 3H-leucine incorporation and the total protein content were measured. The expression of receptor mRNA was performed by reverse transcription-polymerase chain reaction (RT-PCR). Ang II increased 3H-leucine incorporation in a concentration-dependent manner but not 3H-thymidine incorporation in primary cultures of human cardiac fibroblasts. The maximum effect (24 +/- 3% over control) was obtained at a concentration of 10 nM. There were no significant alterations of cell number or total protein content, suggesting that Ang II stimulated protein synthesis but did not induce hypertrophy. The accumulation of 3H-leucine was blocked by the AT1 receptor antagonist candesartan but not by the AT2 receptor antagonist PD123319. By using RT-PCR, both AT1 and AT2 receptors mRNA were found to be expressed in human cardiac fibroblasts. The selective MAPKK inhibitor PD098059, the protein kinase C inhibitor K252a or the phospholipase C inhibitor U73122 did not significantly inhibit Ang II augmented 3H-leucine incorporation. However, this was significantly blocked by the Ca2+-dependent protein kinase C inhibitor GO6976, the non-selective protein kinase inhibitor staurosporine and the tyrosine kinase inhibitor tyrphostin 25. The effects of Ang II were unaffected by the Gi-protein blocker pertussis toxin, indicating a Gi-protein-independent pathway. Ang II was synergistic with insulin but showed no significant increase on 3H-leucine incorporation when combined with PDGF or EGF. In summary, Ang II stimulates protein synthesis through AT1 receptors in human cardiac fibroblasts, but has no hypertrophic or hyperplastic effect. The response is mediated by a MAPKK-independent and Ca2+-sensitive PKC-dependent pathway.

Angiotensin II↗

Stage-specific inhibition of deoxyribonucleic acid synthesis and induction of apoptosis by antracyclines in cultured rat spermatogenic cells.

A rapid in vitro method has been developed to detect early effects of cytostatic drugs on rat spermatogenesis. The induction of programmed cell death (apoptosis) and changes in DNA synthesis induced by doxorubicin and idarubicin were measured in specific stages of the cycle of seminiferous epithelium including mitotic (stage V) and meiotic (stage VIII-IX) S-phase cells. The model was used to investigate the protective effect of an organic thiophosphate, amifostine, against the toxicity of antracyclines. Premitotic DNA synthesis was found to be more sensitive than premeiotic DNA synthesis to antracyclines. Idarubicin was more toxic than doxorubicin to germ cells in inducing apoptosis and suppressing DNA synthesis. Amifostine had no protective effect against doxorubicin- or idarubicin-induced inhibition of DNA synthesis. In contrast, a significant stimulation of DNA synthesis in premitotic cells by amifostine was found, suggesting that this compound may have a stimulative effect on spermatogenic stem cells. These data show that stage-specific dissection of the seminiferous tubules and their in vitro exposure to predetermined doses of drugs may give us a unique possibility to detect drug action and protection against the cytotoxicity of antineoplastic agents at the cellular level of the spermatogenic cycle.

Animals↗

Cytokines induce upregulation of vascular P2Y(2) receptors and increased mitogenic responses to UTP and ATP.

P2Y(2) receptors, which mediate contractile and mitogenic effects of extracellular nucleotides in vascular smooth muscle cells (VSMCs), are upregulated in the synthetic phenotype of VSMCs and in the neointima after balloon angioplasty, suggesting a role in the development of atherosclerosis. Because released cytokines in atherosclerotic lesions mediate multiple effects on gene transcription in VSMCs, we speculated that cytokines could be involved in the regulation of P2Y(2) receptor expression. Using a competitive reverse transcription-polymerase chain reaction, we detected that interleukin (IL)-1beta induced a time- and dose-dependent upregulation of P2Y(2) receptor mRNA, which was dramatically enhanced when combined with interferon-gamma or tumor necrosis factor-alpha. Lipopolysaccharide also significantly increased the expression of P2Y(2) receptor mRNA. The upregulation of P2Y(2) receptor mRNA was paralleled at the functional level because IL-1beta significantly increased the UTP-stimulated DNA synthesis and the release of intracellular Ca(2+). Actinomycin D completely blocked the upregulation of P2Y(2) receptor mRNA expression by IL-1beta, indicating de novo mRNA synthesis. There was no cAMP accumulation in the cells stimulated with IL-1beta. The cyclooxygenase inhibitor indomethacin and the protein kinase C inhibitor RO-31-8220 inhibited IL-1beta-induced upregulation of P2Y(2) receptor mRNA expression, whereas rapamycin and PD098059 had no effects. Furthermore, neither P38 mitogen-activated protein kinase inhibitor SB20358 alone nor its combination with PD098059 blocked the effect of IL-1beta on the expression of P2Y(2) receptor mRNA. Our results demonstrate that inflammatory mediators upregulate vascular P2Y(2) receptors at the transcriptional and at the functional level through protein kinase C and cyclooxygenase but not cAMP, extracellular signal-regulated kinases 1 and 2, or P38-dependent pathways. This may result in increased growth-stimulatory or contractile effects of extracellular UTP and ATP, which may be of importance in the development of vascular disease.

Adenosine Triphosphate↗

Characterization of contractile P2 receptors in human coronary arteries by use of the stable pyrimidines uridine 5'-O-thiodiphosphate and uridine 5'-O-3-thiotriphosphate.

The present study was designed to evaluate the relative contribution of the different contractile P2 receptors in endothelium-denuded human coronary arteries by use of extracellular nucleotides, including the stable pyrimidines uridine 5'-O-3-thiotriphosphate (UTPgammaS) and uridine 5'-O-thiodiphosphate (UDPbetaS). The isometric tension of isolated vessel segments was recorded in vitro, and P2 receptor mRNA expression was examined by reverse transcription-polymerase chain reaction. alphabeta-Methylene-adenosine triphosphate (alphabeta-MeATP) elicited contractions at a low concentration (pEC(50) = 5.2), indicating the presence of contractile P2X receptors. The P2Y responses were analyzed after P2X receptor desensitization with 10 microM alphabeta-MeATP. The stable nucleotides UTPgammaS and adenosine 5'-O-3-thiotriphosphate (ATPgammaS), which are agonists of P2Y(2) or P2Y(4) receptors, were approximately 2 log units more potent than the endogenous UTP and ATP (pEC(50) = 4.6 and 3.8 for UTPgammaS and ATPgammaS). The efficacy of these responses were approximately double that of the P2X agonist alphabeta-MeATP (E(max) = 125% for UTPgammaS, 126% for ATPgammaS, and 68% for alphabeta-MeATP), suggesting a primary role for contractile P2Y(2/4) receptors. The P2Y(2) receptor agonist diadenosine tetraphosphate also stimulated contraction, whereas the selective P2Y(1) agonist adenosine 5'-O-thiodiphosphate and the selective P2Y(6) agonist UDPbetaS had no effect. Reverse transcription-polymerase chain reaction analysis of mRNA from endothelium-denuded human coronary arteries demonstrated strong bands for P2Y(2) and P2X(1), although bands for P2Y(1), P2Y(4), and P2Y(6) receptor mRNA could also be detected. In conclusion, the stable pyrimidines UDPbetaS and UTPgammaS are important tools for P2 receptor subtype characterization in intact tissues with ectonucleotidase activity. Extracellular nucleotides elicit contraction of human coronary arteries primarily by activation of P2Y(2) and P2X receptors, whereas a role for P2Y(1) and P2Y(6) receptors can be excluded. Antagonists of P2Y(2) and P2X receptors may be useful in the treatment of coronary vasospastic disorders.

Adenosine Triphosphate↗

DNA methylation and expression of p16(INK4A) gene in pulmonary adenocarcinoma and anthracosis in background lung.

The p16 (CDKN2/MTS-1/INK4A) tumor-suppressor gene is frequently inactivated by DNA methylation in lung carcinomas. To clarify whether background anthracosis may play a role in DNA methylation and inactivation of the p16 gene, we examined DNA methylation of the p16-promoter region by methylation-specific polymerase chain reaction, and p16 expression immunohistochemically, and compared the results with the level of background anthracosis which was measured by an original quantitative method. At autopsy, DNA methylation of the p16 gene was observed in 6/19 tumors (32%) from patients who had died of pulmonary adenocarcinoma. The degree of background anthracosis (the effect of extrinsic carcinogenic factors) (mean absorbance value, A = 0.715) of the cases with p16-gene methylation was significantly higher than that without methylation (mean A value = 0.298). p16 expression was inactivated in all tumors with p16-gene methylation. The mean A value of black dust matter deposition in cases with normal expression of p16 (A = 0.151) was significantly lower than cases with abnormal expression of p16 (A = 0.531). These results indicate that the level of background anthracosis is closely associated with inactivation of p16 expression and also DNA methylation of the p16-gene promoter region in pulmonary adenocarcinogenesis. Int. J. Cancer (Pred. Oncol.) 84:609-613, 1999.

Adenocarcinoma↗

MAPKK-dependent growth factor-induced upregulation of P2Y2 receptors in vascular smooth muscle cells.

The ATP- and UTP-sensitive P2Y2 receptor which mediates both contractile and mitogenic effects has recently been shown to be upregulated in the synthetic phenotype of the vascular smooth muscle cell (VSMC). Using a competitive RT-PCR we demonstrate that the P2Y2 receptor mRNA is increased by fetal calf serum and other growth factors in a MAPKK-dependent way. This was confirmed at the functional level by examining UTP-stimulated release of intracellular Ca2+. Furthermore, the P2Y2 receptor mRNA is positively autoregulated by ATP and the mRNA is rapidly degraded with only 26% remaining after 1 h in the presence of actinomycin D. Our results indicate growth factor regulation and rapid turnover of the P2Y2 receptor mRNA, which may be of importance in atherosclerosis and neointima formation after balloon angioplasty.

Animals↗

Increase in cardiac P2X1-and P2Y2-receptor mRNA levels in congestive heart failure.

We wanted to study the expression of P2-receptors at the mRNA-level in the heart and if it is affected by congestive heart failure (CHF). To quantify the P2 receptor mRNA-expression we used a competitive RT-PCR protocol which is based on an internal RNA standard. The P2 receptor mRNA-expression was quantified in hearts from CHF rats and compared to sham-operated rats. Furthermore, the presence of receptor mRNA was studied in the myocardium from patients with heart failure. In the sham operated rats the G-protein coupled P2Y-receptors were expressed at a higher level than the ligand gated ion-channel receptor (P2X1). Among the P2Y-receptors the P2Y6-receptor was most abundantly expressed (P2Y6 > P2Y1 > P2Y2 = P2Y4 > P2X1). A prominent change was seen for the P2X1- and P2Y2-receptor mRNA levels which were increased 2.7-fold and 4.7-fold respectively in the myocardium from the left ventricle of CHF-rats. In contrast, the P2Y1-, P2Y4- and P2Y6-receptor mRNA levels were not significantly altered in CHF rats. In human myocard the P2X1-, P2Y1-, P2Y2-, P2Y6- and P2Y11-receptors were detected by RT-PCR in both right and left atria and ventricles, while the P2Y4-receptor band was weak or absent. In conclusion, most of the studied P2-receptors were expressed in both rat and human hearts. Furthermore, the P2X1- and P2Y2-receptor mRNA were upregulated in CHF, suggesting a pathophysiological role for these receptors in the development of heart failure.

Adolescent↗

[The expression of bombesin receptor in gastric cancer].

OBJECTIVE: To observe the expression of receptor mRNA and its protein in SGC 7901 cells. METHODS: (1) RT-PCR and Southern blot hybridization were performed for detection of gastrin releasing peptide GRP-R mRNA; (2) Covalent cross-linking study with biotinyl-bombesin and enhanced chemoluminescence (ECL) was performed to identify GRP-R at protein levels in SGC 7901 cells. RESULTS: (1) It is shown that the molecular weight of the cDNA was consistent with that of expected. Southern blot was then used to further prove that specific GRP-R mRNA was expressed by SGC 7901. (2) GRP-R protein was shown by covalent cross-linking in SGC 7901 and the molecular weight of bombesin/GRP-R in SGC 7901 cells was about 75000. CONCLUSION: By using RT-PCR, Southern blot and covalent cross-linking techniques, it was demonstrated that SGC 7901 cells can express bombesin receptor mRNA and protein. The results of this study provides a basis for further researches on bombesin intracellular signal transmission pathway and the role of bombesin and bombesin receptor antagonists in oncological research.

Blotting, Southern↗

[The establishment of a human pancreatic mixed ductal-endocrine carcinoma cell line].

OBJECTIVE: Establishment of a human pancreatic mixed ductal-endocrine carcinoma cell line. METHODS: A specimen of this type of cancer was obtained from a male patient at the head of pancreas. The tumor tissue was minced into pieces and inoculated subcutaneously in nude mice. With two successive subcutaneous implants, a piece of tumor tissue taken from the 2(nd) implanted neoplasm of a nude mouse was minced into minute tissue masses and inoculated in a media containing 10% fetal bovine serum. RESULTS: Currently, it has been passed to the 55(th) passage. Cells of this cell line (PC-EN) kept simultaneously the morphologic patterns of a pancreatic ductal and endocrine tumor which were verified by histochemistry and immunohistochemistry assays. Some of the PC-EN cells showed presence of neuroendocrine granules by electron microscopy. The growth rate of this cell line was relatively low. Kakryotype analysis showed two cell populations with its major mode of chromosomes numbers as 48 in one, and 56 in the other. Study on K-ras gene demonstrated that PC-EN harbored a mutated codon 12. Several gastrointestinal hormones and CEA were detected in PC-EN cells and in the supra-cultured medium using radioimmunoassay. CONCLUSIONS: The cellular and molecular biologic characteristics of PC-EN cells illustrated that this cell line preserved the morphology of a pancreatic ductal and endocrine tumor and possessed a special growth property, chromosome karyotype, and mutation of Ki-ras gene, but also showed a biologic exocrine and endocrine functions of the pancreas. The establishment of PC-EN cell line will provide a useful model in vitro for further investigating the cellular and molecular biology of exocrine and endocrine tumors of the pancreas.

Aneuploidy↗

[Analysis of the causes of necrosis of retained flap on tibial side after transplantation of the great toe nail flap].

OBJECTIVE: In order to investigate the causes of necrosis of the retained flap after transplantation of the great nail flap, according to the principle of plastic surgery, the following operation was designed. METHODS: A tongue-shaped great toe flap was made with its base on the tibial side of the great toe and the width of the base was 1 cm to 1.5 cm. The flap contained the supporting vessels and nerves and the periosteum was also preserved. RESULTS: From June 1982 to November 1997, the flap was used to repair 267 case, 277 fingers defects. After operation, the retained flap on the tibial side developed necrosis in 13 sides, an incidence of 4.69%, and in 78 sides, there was necrosis on the grafted skin on the donor site, an incidence of 28.7%. Most of the wounds healed after changing dressing, while 37 wounds healed from another skin graft. Of these cases, 178 cases had been followed up for 5 months to 16 years. It was found that the retained tibial tongue-shaped flap showed hyperplasia which extended to the weightbearing area of metatarso-phalangeal of great toe. It showed that the taking off of great toe nail flap according to first dorsal metatarsal artery (FDMA) I, II or III type, the incidence of development of necrosis of retained flap on tibial side showed no significant difference (P > 0.05). CONCLUSION: It was believed that the necrosis of the retained flap was not related to the FDMA classification but had relation with the design, operative technique and presence of infection.

Adolescent↗

Phenotype changes of the vascular smooth muscle cell regulate P2 receptor expression as measured by quantitative RT-PCR.

Studies using selective agonists have suggested that the contractile effect of extracellular nucleotides, such as ATP and UTP, in blood vessels is mediated mainly by P2X1 receptors with a smaller contribution of P2Y receptors while the mitogenic effect is mediated by P2Y (P2Y1, P2Y2, P2Y4, and P2Y6) receptors with no effect of P2X1 receptors. This indicates a difference in P2 receptor expression between the contractile and the synthetic phenotype of the SMC. To measure the expression of mRNA for these receptors a competitive RT-PCR assay was developed that utilised synthetic RNA-competitors allowing determination of the number of mRNA copies for each receptor in the samples. In the synthetic phenotype the mitogenic P2Y1 and P2Y2 receptor transcripts were upregulated by 342- and 8-fold, respectively, while the contractile P2X1 receptor is totally downregulated and the P2Y4 and P2Y6 receptors were unchanged. This plasticity of the receptor expression may be important in the transition from the contractile to the synthetic SMC phenotype.

Adenosine Triphosphate↗

Biotinylated platelets have an impaired response to agonists as evidenced by in vitro platelet aggregation tests.

Biotinylation of platelets, using a water soluble biotin analogue which reacts with primary amines, has been proposed to be a reliable technique for study of in vivo survival of platelets and their subpopulations. The information about the influence of this technique on platelet function has been limited. In the present work we studied the effect of in vitro biotinylation on platelet function and activation. Washed human platelets, at a concentration of 1 x 10(9)/L, were biotinylated with five different concentrations of sulfo-NHS-biotin or NHS-LC-biotin, ranging from 0 to 5 mM. The degree of platelet activation during and after biotinylation was monitored by measuring the externalization of P-selectin, and the platelet function was evaluated by aggregometry. It was observed that biotinylated platelets, in a dose dependent manner, displayed an impaired aggregation response. A slight increase in platelet membrane P-selectin occurred during the labelling procedure.

Adenosine Diphosphate↗

Immediate results and dilatation effect of the vein-covered Palmaz-Schatz stent assessed by intravascular ultrasound.

To evaluate the clinical results of stenting using the vein-covered Palmaz-Schatz (PS) stent by intravascular ultrasound (IVUS). Twenty-eight patients with angina pectoris or confirmed ischemia were entered into this study. Thirteen were allocated to the vein-covered PS stent group and 15 to the normal Palmaz-Schatz stent group. The immediate clinical results in these groups and changes in lumen dimension as assessed by IVUS, were investigated. Acute success was 100% in both groups. There were no immediate complications. Subacute thrombosis occurred in one patient in the vein-covered PS group. In the vein-covered PS group, percent diameter stenosis of the involved coronary artery changed from 70.2% before stenting to 8.8% immediately after and 42.2% at 5 months follow-up. The respective values were 84.5%, 13.4%, and 36.5% in the normal Palmaz-Schatz group. Restenosis in the vein-covered group was 23.1% and in the Palmaz-Schatz group was 20%, showing no significant differences between the two groups. The luminal area in the vein-covered group as assessed by IVUS increased from 3.2 mm2 to 7.4 mm2 (pre to post) and from 3.2 mm2 to 8.2 mm2 in the normal Palmaz-Schatz group. The plaque area decreased from 13.6 mm2 to 10 mm2 (pre to post) in the vein-covered group and from 13.0 mm2 to 9.2 mm2 in the Palmaz-Schatz group. In this study, conducted in a limited number of cases, it is possible to use vein-covered stent like as usual Palmaz-Schatz stent. The vein-covered stent had less dilative effect compared with the Palmaz-Schatz stent. This was probably because of its increased profile but there was no difference in the occurrence of subacute thrombosis or in restenosis rate.

Aged↗

Adjustable forming of thermoplastic composites for orthopaedic applications.

The present study was focused on the development of a special thermoforming technique for manufacturing of continuous fibre reinforced thermoplastic composite parts with complex surface contours. In particular, a stamp forming process was modified to investigate the potential manufacturing advantages of thermoplastic composites in orthopaedic applications. An apparatus was designed which allowed the thermoforming procedure to be fully automatic, i.e. a cold pre-consolidated laminate panel, as the feed material, was heated up in an infrared heating zone and then transferred into a cold mould system, where it was stamp formed. Both halves of the mould were made of many tiny round metal sticks in a metal frame. This needle-bed mould allowed one to copy any contour by pushing it slightly on spring fixed sticks. The desired position of these sticks could then be adjusted by forcing the side plates of the metal frame together. To prevent any press mark of stick-tops on the composite, i.e. to achieve smooth surfaces of the themoformed composite parts, flexible rubber pads were needed to cover the mould surfaces. Experimental results showed that the surface profile of CF/PP and GF/PP composites formed by the needle-bed mould reproduced fairly well the contour of a saddle shaped, complex model sample. Unique properties of this needle-bed mould are that it can be repeatedly used, and that it can copy any complex surface contours, for example a bone surface, by simply adjusting the stick positions according to the special surface requirements.

Journal Article↗

Plasma thrombopoietin levels in thrombocytopenic states: implication for a regulatory role of bone marrow megakaryocytes.

To evaluate the diagnostic value of thrombopoietin (TPO, c-mpl ligand) measurements, and clarify the regulatory mechanisms of TPO in normal and in thrombocytopenic conditions, the plasma TPO concentration was determined in normal individuals (n = 20), umbilical cord blood (n = 40), chronic idiopathic thrombocytopenic purpura (ITP; n = 16), in severe aplastic anaemia (SAA; n = 3), chemotherapy-induced bone marrow hypoplasia (n = 10), myelodysplastic syndrome (MDS; n = 11), and sequentially during peripheral blood progenitor cell transplantation (n = 7). A commercially available ELISA and EDTA-plasma samples were used for the analysis. The plasma TPO concentration in the normals and umbilical cord blood were 52 +/- 12 pg/ml and 66 +/- 12 pg/ml, respectively. The corresponding values in patients with SAA and chemotherapy-induced bone marrow hypoplasia were 1514 +/- 336 pg/ml and 1950 +/- 1684 pg/ml, respectively, and the TPO concentration, measured sequentially after myeloablative chemotherapy and peripheral blood progenitor cell transplantation, was inversely related to the platelet count. In contrast, the plasma TPO recorded in patients with ITP (64 +/- 20 pg/ml) and MDS (68 +/- 23 pg/ml) were only slightly higher than normal levels. In conclusion, TPO levels were significantly elevated in patients in which bone marrow megakaryocytes and platelets in circulation were markedly reduced, whereas TPO levels were normal in ITP patients, and only slightly increased in the MDS patients. These latter patients displayed a preserved number of megakaryocytes in bone marrow biopsies. Our data support the suggestion that megakaryocyte mass affects the plasma TPO concentration. In thrombocytopenic patients a substantially increased plasma TPO implies deficient megakaryocyte numbers. However, TPO measurements do not distinguish between ITP and thrombocytopenia due to dysmegakaryopoiesis, as seen in MDS patients.

Adolescent↗

The implication of anthracosis in the development of pulmonary adenocarcinoma.

The relationship between anthracosis, which is the deposition of black dust matter in the lung parenchyma, and the development of pulmonary adenocarcinoma has not been fully characterized. In order to clarify whether background black dust matter deposition could be implicated in the development of pulmonary adenocarcinoma, we measured the level of anthracosis at autopsy in 47 patients who had died of pulmonary adenocarcinoma. Both lungs of all 47 cadavers were examined. Twenty-micrometer sections were cut from formalin-fixed, paraffin-embedded blocks of the largest cut surface of each lung. Black dust matter was extracted from the sections and blotted onto a nitrocellulose membrane. The density of the blotted black dust matter was then analyzed using an imaging densitometer. There were no significant differences in the density of black dust matter deposition between lungs affected by pulmonary adenocarcinoma and control lungs. However, well differentiated adenocarcinomas tended to develop more frequently than poorly differentiated ones in lungs showing less deposition. We found a very strong correlation between the degree of black dust matter deposition and smoking history. Patients with severe anthracosis tended to have a poorer prognosis than those with mild anthracosis.

Adenocarcinoma↗

Impact of endogenous thrombopoietin levels on the differential diagnosis of essential thrombocythaemia and reactive thrombocytosis.

By using the newly commercialized Quantikine human TPO immunoassay, plasma thrombopoietin (TPO) concentrations were measured in 12 patients with essential thrombocythaemia (ET), 13 patients with reactive thrombocytosis (RT) and 11 healthy volunteers. For the healthy volunteers the mean plasma TPO concentration was 21.1+/-11.0 pg/ml. The mean plasma TPO concentration in the group of RT was slightly lower (16.4+/-8.6 pg/ml) but did not differ significantly from the control group. The mean plasma TPO concentration in ET patients (44.1+/-45.2 pg/ml) was significantly (p<0.05) higher than the mean for RT patients, but did not differ statistically from the mean of healthy volunteers. These data suggest a defective clearance of plasma TPO in patients with ET.

Adult↗

Platelet proteins as autoantibody targets in idiopathic thrombocytopenic purpura.

Idiopathic thrombocytopenic purpura (ITP), caused by autoantibodies directed against certain platelet antigens, is the most common entity of the immune thrombocytopenias. ITP is an acquired disorder and can affect both children and adults. However, the clinical syndromes of ITP are distinct between children and adults. Childhood (acute) ITP characteristically is acute in onset, occurs within 1-2 weeks of an infection, usually of viral origin, resolves spontaneously within 6 months. Adult (chronic) ITP has an insidious onset and rarely resolves spontaneously. Over the last decade considerable new information has accumulated as to the pathophysiological mechanisms of immune thrombocytopenias. In addition, most of the knowledge on this disorder has been obtained from studies of adult patients with chronic ITP. The present work gives an updated overview of the platelet autoantigens and the molecular immunological reactions in ITP.

Acute Disease↗