Can Kidney Stones Cause High Platelet Count

Can Kidney Stones Cause High Platelet Count – Whole-transcriptome sequencing-based analysis of DAZL and its interacting genes during germ cell specification and zygotic genome activation in chicken

Downregulation of CTRP-3 by weight loss in vivo and by bile acids and incretins in adipocytes in vitro

Can Kidney Stones Cause High Platelet Count

Can Kidney Stones Cause High Platelet Count

Extracellular Matrix-Specific Platelet Activation Induces Differential Translational Response and De Novo Protein Synthesis in Human Platelets

Obstructive Nephropathy And Molecular Pathophysiology Of Renal Interstitial Fibrosis

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Platelets Test Purpose, Procedure, Results And More

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By Demetra H. Hufnagel Demetra H. Hufnagel Scilit Google Scholar View Publications 1, Gabriella D. Cozzi Gabriella D. Cozzi Scilit Google Scholar View Publications 1, Marta A. Crispens Marta A. Crispens Scilit Google Scholar View Publications 2, 3 and Alicia Beeghly-Fadiel Alicia Beeghly-Fadiel Scilit Google Scholar View Publications 3, 4, *

Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN 37232, USA

Can Kidney Stones Cause High Platelet Count

Department of Medicine, Division of Epidemiology, Vanderbilt University Medical Center, 2525 West End Avenue, Nashville, TN 37203, USA

The Role Of Platelets In The Regulation Of Tumor Growth And Metastasis: The Mechanisms And Targeted Therapy

Received: October 3, 2020 / Revised: October 26, 2020 / Accepted: October 27, 2020 / Published: October 31, 2020

Platelets are critical components of many physiological processes, including tissue remodeling after injury, wound healing, and maintenance of vascular integrity. Increasing evidence suggests that platelets may also play an important role in cancer. In ovarian cancer, thrombocytosis, both at the time of initial diagnosis and at recurrence, was associated with a worse prognosis. This review describes the current evidence for associations between thrombocytosis and ovarian cancer prognosis and discusses the clinical relevance of platelet count thresholds and timing of assessment. Furthermore, we discuss several mechanisms from in vitro, in vivo, and clinical studies that may underlie these associations and recommend possible approaches for new therapeutic targets for this deadly disease.

Circulating anucleated cytoplasmic fragments of megakaryocytes, platelets, play a critical and well-defined role in wound healing and maintenance of vascular integrity by adhering, activating, and aggregating at sites of vascular injury to form blood clots and stop bleeding [1]. While unprovoked thrombosis has long been associated with an increased risk of malignancy, as first described by Armand Trousseau in 1865, increasing evidence has shown a widespread role for platelets in promoting inflammation, tumorigenesis, and cancer metastasis [ 2 , 3 , 4 , 5 ]. Although platelets are anucleated, they have a number of cell surface receptors through which they interact with the environment, including integrins, selectins, immunoglobulin receptors, and glycoproteins; they also contain a rich selection of growth factors and mitogenic proteins in the granules, which they release after activation [1, 6, 7, 8, 9]. A high platelet count, or thrombocytosis, is most commonly defined as > 400,000 platelets per microliter and is largely associated with poor cancer prognosis in a variety of solid tumors, including non-small cell lung cancer, advanced breast cancer, pancreatic cancer, colorectal cancer, and cancer stomach [10, 11, 12, 13, 14, 15, 16, 17, 18]. Although the mechanisms underlying the association between paraneoplastic thrombocytosis and cancer progression are not yet fully understood, there is strong evidence for reciprocal interactions between tumor growth and platelet production and activation; accumulating data suggest that platelets are not only a biomarker of disease burden, with elevated levels at diagnosis falling after primary treatment and rising again at relapse, but also actively contributing to disease progression [19, 20].

Ovarian cancer is the deadliest gynecological cancer, with recent estimates of relative 5-year survival of 48%, often due to late-stage diagnosis due to nonspecific symptoms and lack of sensitive population screening tools [ 21 , 22 , 23 ]. , 24]. Although overall cancer mortality has decreased dramatically in recent decades, ovarian cancer mortality has largely remained unchanged [21]. A better understanding of the pathogenesis of this disease is needed to develop additional therapeutic strategies. As with many other cancers, thrombocytosis is common during the preoperative evaluation of women with epithelial ovarian cancer and affects approximately 30% of patients [25]. Thrombocytosis has also been found to be associated with cancer risk in the setting of an adnexal mass, as well as features of aggressive malignancy, including advanced stage, higher grade, larger ascites volume, extensive residual disease after debulking, and chemoresistance [ 26 , 27 , 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38]. A study of 30-day outcomes after surgery among 1072 cases of ovarian cancer showed an association between thrombocytosis and major complications [39]. In addition, thrombocytosis has been shown in several studies to be a predictive factor for several outcomes (Table 1) with significant associations from univariate and multivariate analyses, indicating independent associations with disease outcomes. The mechanisms behind these associations are now under investigation; therapeutics with antiplatelet activity, such as nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have been associated with better prognosis in epidemiological studies, and antiplatelet therapies are now being investigated in the clinical setting of ovarian cancer [40, 41, 42, 43].

Sex Differences In Midterm Prognostic Implications Of High Platelet Reactivity After Percutaneous Coronary Intervention With Drug‐eluting Stents In East Asian Patients: Results From The Ptrg‐des (platelet Function And Genotype‐related Long‐term

Despite substantial evidence supporting a role for thrombocytosis in ovarian cancer prognosis, clinical guidelines for platelet monitoring as a prognostic indicator to inform patient discussions remain to be established. While previous meta-analyses and reviews have supported associations between pretreatment thrombocytosis and survival in ovarian or gynecologic cancer, in this review we discuss the timing of platelet count measurements and thrombocytosis thresholds in relation to survival among women with epithelial ovarian cancer, taking into account statistical adjustment and other important methodological differences [44, 45]. We also describe a number of mechanisms that could underlie these associations, suggesting that platelets actively contribute to disease progression and may represent novel therapeutic targets in ovarian cancer.

To our knowledge, 29 studies have evaluated the prognostic utility of thrombocytosis for ovarian cancer in the preoperative setting—either primary staging and/or cytoreduction—or before treatment. We focus primarily on the 27 that performed Kaplan–Meier and/or Cox proportional hazards regression to assess associations with progression-free survival (PFS), disease-free survival (DFS), disease-specific survival (DSS), and/or overall survival. (OS). To facilitate the review of studies with different methodologies, we presented the relevant literature divided by thrombocytosis threshold (below 400, 400, above 400 and more thresholds or continuous measurements), taking into account the time frame in which the platelet count was included .

Among the 27 studies that evaluated pretreatment thrombocytosis in relation to ovarian cancer survival, only 12 (44%) provided a specific time frame during which platelet counts were included; these ranged from the date of diagnosis to 8 weeks or 3 years prior to diagnosis [ 26 , 46 ]. Many studies used a time frame within 7 or 14 days of initial staging and/or cytoreductive surgery, but it was rarely stated whether the date of diagnosis was included. The remaining studies examined platelet counts in a “preoperative” or “preworkup” setting without further specification.

Can Kidney Stones Cause High Platelet Count

/L for thrombocytosis in association with ovarian cancer prognosis had significant findings. In a small study of 97 patients in Poland with platelet counts measured 1 day before staging and/or debulking surgery, thrombocytosis (≥350) was found to be a negative prognostic factor for OS, although regression was not performed [47]. In a Swiss study of 91 advanced-stage serous cases, thrombocytosis (>350) was an independent negative prognostic factor for two-fold worse PFS and OS, even after multivariable regression including adjustment for age, stage, menopausal status, CA-125, and optimal tumor removal [27]. In a study of 104 patients in China with recurrent disease, preprimary thrombocytosis (≥300) resulted in significantly worse progression-free survival and OS, even when regression models included adjustment for age, stage, stage, residual disease after cytoreduction, and decreased platelet count after completion of first-line therapy [48]. Similarly, in a study of 190 patients in China with platelet measurements up to 7 days before treatment, thrombocytosis (>300) was significantly associated with approximately 50% worse 3-year progression-free survival and OS in models that included adjustment for age, stage, grade , optimal debulking, operation time,

Why Platelet Count Decreases In Dengue Fever?

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