Thrombotic Thrombocytopenic Purpura

Bell, William R.

doi:10.1001/jama.1991.03460010091038

Cited by 17 publications

(8 citation statements)

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“…For many years, the marked increase in serum LDH in patients with TTP has been attributed almost entirely to microangiopathic red blood cell destruction [1][2][3][4][5]. However in his 1979 study of the efficacy of plasma exchange in TTP, Taft [6] obtained LDH isoenzyme profiles from two patients.…”

Section: Discussionmentioning

confidence: 99%

“…In classic cases, patients present with a pentad of clinical and laboratory findings, including fever, neurologic and renal dysfunction, microangiopathic hemolytic anemia, and thrombocytopenia. In some cases, renal and neurologic abnormalities are subtle or variable, and diagnosis is difficult [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

“…As in other hemolytic anemias, the increase in LDH in TTP has been attributed by many authors to the release of LDH from erythrocytes destroyed by intravascular hemolysis [1][2][3][4]. However, this widely accepted belief has not been substantiated by LDH isoenzyme analysis.…”

Section: Introductionmentioning

confidence: 99%

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Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

1998

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

1998

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“…As for the TTP mechanism, it was reported that microthrombi mainly consisting of platelets are formed by injury of vasoendotherial cells due to various causes (4). Recently, a concept of thrombotic microangiopathy (TMA) involving hemolytic uremic syndrome (HUS), TTP, and other lesions also has been advocated (5).…”

Section: Discussionmentioning

confidence: 99%

A Case of Thrombotic Thrombocytopenic Purpura Refractory to Plasma Exchange

Okamoto

Abe

Shouno

et al. 2001

Therapeutic Apheresis

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We experienced a case of thrombotic thrombocytopenic purpura (TTP) finally relieved after 74 sessions of plasma exchange (PE). The patient was a 56‐year‐old male. In August 1999, he was examined in emergency because of brown urine and a lowered level of consciousness. As TTP was suspected according to the laboratory findings of abnormally high lactate dehydrogenase and total bilirubin, decreased platelet counts, and numerous fragmented erythrocytes, he was admitted to the ICU of our hospital. Immediately after admission, PE was started consecutively. Upon concomitant use of antiplatelet drugs and prostacyclin, the level of platelet counts recovered to 100,000/μl once, but decreased again. Thus, in addition to the PE, prednisolone and vincristine were administrated, which elevated the level of platelet counts to 200,000 to 300,000/μl. Since the erythrocyte fragmentation was noted frequently, PE was continued twice a week. From the 60th day of admission onward, however, his body temperature rose above 40°C with a rapid increase of C‐reactive protein. A blood culture detected methicillin‐resistant Staphylococcus aureus (MRSA) which derived from a left lung abscess. During the course of anti‐MRSA treatment, he presented acute renal failure and acute hepatic dysfunction, but survived because of the combined therapy. He was discharged on the 180th day of admission. These results suggest that a combined therapy of steroid and vincristine is effective to treat TTP refractory to PE, but careful attention should be paid to the complications caused by immunosuppression.

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“…Endotel vaskuler yang teraktivasi akibat infeksi virus dengue memberi peluang kepada trombosit dalam sirkulasi pembuluh darah untuk berinteraksi dengan kolagen dalam lapisan sub-endotel yang kemudian memicu agregasi trombosit dan bermuara pada trombositopenia (9,12). Para peneliti telah membuktikan bahwa pada penderita aterosklerosis dan trombosis peningkatan produksi molekul protrombosis vWF dan penurunan produksi molekul antitrombosis PGI2 oleh endotel yang teraktivasi memicu agregasi trombosit (13,14,15,16,17,18). Diduga agregasi trombosit pada penderita DBD juga dipicu oleh perubahan kadar vWF dan PGI2 akibat endotel yang teraktivasi oleh sitokin yang dihasilkan oleh monosit yang mengandung virus DBD dan T helper-1 (TH-1) yang berfungsi sebagai stress cells.…”

Section: Pendahuluanunclassified

Perubahan Kadar Sitokin Dan Molekul Agregasi Pada Berbagai Tingkat Trombositopenia Pada Demam Berdarah Dengue

Djunaedi

2013

JKB

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The uncovering of the changes in the concentration of aggregation molecules (vWF, PGI2) and cytokines (TNFα, IL-1β, IL-6) in different levels of thrombocytopenia in DHF patients can be used as the basis in predicting the occurrence of thrombocytopenia. A prospective-observational study was undertaken utilizing a 3-day sequentially drawn vein blood of inclusive DHF patients. The TNFα, IL-1β and IL-6 test was conducted utilizing the quantikine high sensitivity human cytokine immunoassay, and the vWF and PGI2 test was conducted utilizing the ELISA procedure. The multivariate and discriminant analyses tests on the deltas between day 1 and 2 observations, and between day 2 and 3 observations of the 6 variables showed Wilks' Lambda =0.638 with p=0.008 and platelets and vWF as the most powerful discriminating variable (70.5.%). The findings of this study indicated that in DHF patients (1) the changing of the concentration of TNFα, IL-1β and IL-6 cytokines do not play a significant role in the mechanism of platelets aggregation, (2) platelets count decreases in a condition in which vWF facilitated platelets aggregation, (3) the changing of a positive contribution of vWF causes a determination of the process of platelets aggregation, and (4) a positive changing of vWF's concentration can be used as a prognostic indicator of a negative changing of platelets count.. PENDAHULUANInsidensi dan penyebaran penyakit demam berdarah dengue (DBD) semakin meningkat dan meluas dari tahun ke tahun (1). Selain berdasarkan kriteria WHO, diagnosis DBD perlu dikonfirmasi dengan penemuan IgM anti dengue positif atau isolasi virus dengue (2,3,4,5). Perdarahan yang terjadi pada penderita DBD akibat agregasi trombosit dapat berkembang menuju DIC dan dapat berakhir dengan kematian (6,7,8). Perkembangan perdarahan tersebut sulit diprediksi dan jika hal itu diketahui, perjalanan penyakit sudah pada tingkat lanjut. Oleh karena itu pengungkapan pengaruh perubahan kadar molekul agregasi vonWillebrand factor, Prostaglandin I2 (vWF, PGI2) terhadap kejadian agregasi trombosit yang menyebabkan trombositopenia pada penderita DBD dapat digunakan sebagai prognostik indikator perdarahan akibat trombositopenia pada penyakit DBD.Trombositopenia pada penderita DBD diduga terjadi melalui mekanisme kompleks imun yang didapatkan pada permukaan trombosit (9,10) dan akibat penurunan produksi trombosit oleh sumsum tulang, peningkatan destruksi trombosit di reticulo endothelial system (RES), serta agregasi trombosit akibat endotel yang teraktivasi (11). Endotel vaskuler yang teraktivasi akibat infeksi virus dengue memberi peluang kepada trombosit dalam sirkulasi pembuluh darah untuk berinteraksi dengan kolagen dalam lapisan sub-endotel yang kemudian memicu agregasi trombosit dan bermuara pada trombositopenia (9,12). Para peneliti telah membuktikan bahwa pada penderita aterosklerosis dan trombosis peningkatan produksi molekul protrombosis vWF dan penurunan produksi molekul antitrombosis PGI2 oleh endotel yang teraktivasi memicu agregasi trombosit (13,14,15,1...

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Thrombotic Thrombocytopenic Purpura

Cited by 17 publications

References 8 publications

Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

A Case of Thrombotic Thrombocytopenic Purpura Refractory to Plasma Exchange

Perubahan Kadar Sitokin Dan Molekul Agregasi Pada Berbagai Tingkat Trombositopenia Pada Demam Berdarah Dengue

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