Neutrophil Elastase

(DOCX 18 kb) Acknowledgements Not applicable

(DOCX 18 kb) Acknowledgements Not applicable. Funding This was an unfunded study. Availability of data and materials Data sharing is not applicable to this article, because no datasets were generated or analyzed. Abbreviations CBCComplete blood countCIDPChronic inflammatory Tanshinone IIA sulfonic sodium demyelinating polyneuropathyCTComputed tomographyDMDiabetes mellitusHTHypertensionITPImmune thrombocytopeniaIVIgIntravenous immunoglobulin Authors contributions TR collected and provided all patient data and imaging and drafted the manuscript. of intravenous immunoglobulin infusion, the individuals sister complained that the patient was unconscious and could not move both legs and Tanshinone IIA sulfonic sodium arms. Emergency computed tomography of the brain showed no irregular findings, such as mind edema, intracranial hemorrhage, or infarction. One day later on, repeat computed tomography of the brain displayed extensive acute ischemic changes and loss of gray-white differentiation of bilateral cerebral hemispheres. Conclusions We performed an extensive literature review to determine the possible causes of serious thrombotic events in immune thrombocytopenia between the predictive factors of the disease and intravenous Tanshinone IIA sulfonic sodium immunoglobulin. Although intravenous immunoglobulin is an effective treatment, thrombotic complications can occur. We emphasize that in individuals with atherosclerosis risk factors or thrombophilia, the appropriateness of administering an intravenous immunoglobulin infusion should be cautiously evaluated. Electronic supplementary material The online version of this article (10.1186/s13256-018-1955-x) contains supplementary material, which is available to authorized users. December, intravenous immunoglobulin, January, liter, microliter, mg/kg/day time, November, October Open in a separate windowpane Fig. 2 Bone marrow aspiration demonstrating improved quantity of megakaryocytes One hour after completion of the IVIg infusion, the individuals sister complained Tanshinone IIA sulfonic sodium that the patient was unconscious and had not been able to move both legs and arms. A neurological exam showed a Glasgow Coma Level score of E3V3M5 and engine power of grade 2 on both sides; both pupils were 5?mm and semireactive to lights. Emergency computed tomography (CT) of the brain showed no irregular findings, such as mind edema, intracranial hemorrhage, or infarction. One day later on, repeat CT of the brain displayed extensive acute ischemic changes and loss of gray-white differentiation of bilateral cerebral hemispheres (Fig.?3). The individuals consciousness was deteriorating. The decision was made to forgo intubation in the request of the family and in accordance with the individuals advance care and attention directive. Consequently, her blood pressure fallen rapidly, and she died within a few hours. Her family members declined an autopsy. A timeline of the long-term treatment of the patient is offered in Additional?file?1. Open in a separate windowpane Fig. 3 Computed tomography of the brain. a Decrease in attenuation and loss of gray-white differentiation of bilateral cerebral hemispheres supplied by the middle cerebral artery territories, having a narrowing of the bilateral lateral ventricle Tanshinone IIA sulfonic sodium due to compression by swelling mind parenchyma. b The infarction in the right and remaining middle cerebral artery distribution, with sparing of the bilateral frontal and occipital lobes Conversation We present a case of a 49-year-old female with relapsed/refractory ITP who experienced severe thrombocytopenia and a large hematoma on her ideal buttock. After IVIg therapy for active ITP, she unexpectedly developed acute ischemic stroke. Many case Rabbit polyclonal to USP53 reports have explained thrombotic events after IVIg administration, including venous and arterial thrombosis [8C11]. The incidence rate of post-IVIg thrombosis varies between 0.6% and 3% of individuals. Our literature review exposed that IVIg-related arterial thromboses are more common than venous thromboses, including myocardial infarction, stroke, and peripheral arterial disease [6, 12]. Focusing on the several reports available on ischemic stroke event after IVIg therapy, we found five cases in all, including our individuals [8C10, 13]. All earlier cases experienced no underlying bleeding disorders and experienced normal platelet counts. Interestingly, only our patient experienced very low platelet figures having a recently developed bleeding history, but she experienced an ischemic stroke after IVIg therapy. In contrast to the four additional cases, our individual also experienced atherosclerosis risks, including diabetes mellitus type 2 and hypertension, which might be possible additive risks for thrombosis. Furthermore, it seemed that she received a.