Venous thromboembolism and sarcoidosis: co-incidence or coexistence?

Goljan-Geremek, Anna; Geremek, Marcin; Puścińska, Elżbieta; Śliwiński, Paweł

doi:10.5114/ceji.2015.56972

Cited by 20 publications

(18 citation statements)

References 34 publications

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“…An important argument in favor of the impact of inflammation in venous thromboembolism is the elevated risk of venous thrombosis and embolism in different inflammatory diseases, such as vasculitis, sarcoidosis, rheumatoid arthritis, inflammatory myopathies, gout, celiac and inflammatory bowel disease and perhaps other autoimmune diseases [5][6][7][8][9][10][11][12].…”

Section: Inflammation -The Connection Between Arterial and Venous Thrmentioning

confidence: 99%

“…Moreover, the metabolic syndrome -abdominal obesity, insulin resistance, arterial hypertension, hypertriglyceridemia, low HDL (high density lipoprotein) cholesterol -an important risk factor of the atherosclerotic disease, has been recently associated with venous thromboembolism [4][5][6][7][8][9][10][11][12][13][14][15].…”

Section: Inflammation -The Connection Between Arterial and Venous Thrmentioning

confidence: 99%

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Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Cocoi

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Cocoi³

et al. 2017

Revista Romana De Medicina De Laborator

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Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha)

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Section: Inflammation -The Connection Between Arterial and Venous Thrmentioning

confidence: 99%

Section: Inflammation -The Connection Between Arterial and Venous Thrmentioning

confidence: 99%

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Cocoi

Pop

Cocoi³

et al. 2017

Revista Romana De Medicina De Laborator

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“…There is an elevated risk of venous thromboembolism in chronic inflammatory conditions such as vasculitis, sarcoidosis, rheumatoid arthritis, inflammatory myopathies, celiac disease, and inflammatory bowel disease [1][2][3], as well as an up-regulation of inflammatory mediators during acute thrombosis. The modulation of inflammation with antiplatelets [4] and statins [5] was found to reduce the risk of thrombotic events.…”

Section: Introductionmentioning

confidence: 99%

Association of Serum Albumin and Severity of Pulmonary Embolism

Omar¹,

Mirsaeidi

Rashad

et al. 2020

Medicina

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Background and Objectives: Inflammation is considered a risk factor for venous thromboembolism. The association between inflammatory markers and the severity of acute pulmonary embolism (APE) has not been explored. Methods: We studied the association between two crude markers of inflammation, serum albumin, and red cell distribution width (RDW) and massive versus non-massive APE. Results: Among 552 consecutive cases of CT-angiogram-confirmed APE, a total of 46 cases (8.3%) had massive APE. Despite similar demographics and comorbidities, patients with massive APE had higher frequency of acute kidney injury (P = 0.005), higher lactic acid (P = 0.011), higher troponin (P = 0.001), higher BNP (P < 0.001), higher frequency of RV dilation (P = 0.017) and hypokinesis (P = 0.003), and higher in-hospital mortality (15.2% vs. 2%, P < 0.001). Patients with massive APE had significantly lower albumin level (median (IQR): 2.8 (2.2, 3.0) vs. 3.2 (2.8, 3.6) gm/dL, P < 0.001) and higher RDW (median (IQR): 14.7 (13.8, 17.1) vs. 14.2 (13.3, 15.6), P = 0.006) compared with non-massive APE. ROC curves showed that albumin and RDW had an AUC of 0.750 (P < 0.001) and 0.621 (P = 0.006) in predicting a massive APE, respectively. The optimal cutoff values for albumin and RDW that had the highest combined sensitivity and specificity for predicting APE was ≤3 gm/dL and >14, for albumin and RDW, respectively. Restricted cubic splines showed a significant association between albumin (P = 0.0002) and RDW (P = 0.0446) and the occurrence of massive APE. After adjustment for patients’ age, body mass index, white blood cell count, the requirement of antibiotics during hospitalization, diabetes, RDW, and peak creatinine, serum albumin was independently associated with massive APE (OR 0.234, 95% CI 0.129–0.4242, P < 0.001). Conclusion: low serum albumin is associated with massive APE. This association is likely a proxy for higher inflammatory state in massive compared with non-massive APE.

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“…Firstly, the local inflammatory profile of sarcoid lesions is hypothesized to alter factors associated with coagulability [ 27 ]. A correlation between the location of sarcoid lesions and the location of thrombus formation has been reported [ 28 ]. These anatomic relationships suggest that local inflammation produced by sarcoid lesions modifies the surrounding environment into a hypercoagulable state [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Recurrent Superior Vena Cava Syndrome in a Patient with Sarcoidosis and Pancreatic Adenocarcinoma: A Case Report and Literature Review

et al. 2020

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Background: Superior vena cava (SVC) syndrome may result from extravascular compression or intravascular obstruction such as thrombosis. Recurrent venous thrombosis is typically associated with a hypercoagulable state such as malignancy, and inheritable or acquired coagulopathy. Sarcoidosis is a derangement of the immune system, and it has been associated with malignant diseases and hypercoagulation. The association of pancreatic cancer and sarcoidosis with SVC syndrome has not been reported previously. Here, we present a case of recurrent venous thrombosis causing SVC syndrome in a patient with pancreatic ductal adenocarcinoma and underlying thoracic sarcoidosis. Methods: The patient’s electronic health record was retrospectively analyzed. Results: A 66-year-old woman with pancreatic adenocarcinoma was treated with neoadjuvant chemotherapy followed by Whipple procedure, before developing tumor recurrence in the liver. Her treatment course was complicated with repeated incidents of venous thrombosis in the presence of a central venous catheter leading to recurrent SVC syndrome, which resolved with anti-coagulation. Conclusions: This case raises a plausible inter-relationship between sarcoidosis, pancreatic cancer, and hypercoagulable state. We suggest that patients with multiple risk factors for developing venous thrombosis should be carefully monitored for any thrombotic event, and they may benefit from prophylactic anti-coagulation.

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Venous thromboembolism and sarcoidosis: co-incidence or coexistence?

Cited by 20 publications

References 34 publications

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Association of Serum Albumin and Severity of Pulmonary Embolism

Recurrent Superior Vena Cava Syndrome in a Patient with Sarcoidosis and Pancreatic Adenocarcinoma: A Case Report and Literature Review

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