I am eager to contribute to the research on the causes of thrombosis, drawing from my personal experiences with clots that began following surgeries in 2011 and 2016. These incidents were complicated by infections with Staph epidermidis, Peptostreptococcus, a single colony of Staph caprae,…
I am eager to contribute to the research on the causes of thrombosis, drawing from my personal experiences with clots that began following surgeries in 2011 and 2016. These incidents were complicated by infections with Staph epidermidis, Peptostreptococcus, a single colony of Staph caprae, and Corynebacterium species, all culminating in sepsis.
The pivotal question I grapple with is whether the clots were precipitated by the sepsis or by the treatments I received: oral Ciprofloxacin and Vancomycin administered through a Peripherally Inserted Central Catheter (PICC) line. Sepsis, a critical response to infection, triggers widespread inflammation that can enhance the risk of clotting as part of the body's inflammatory response. This inflammatory cascade can significantly elevate the likelihood of thrombosis, particularly venous thromboembolism (VTE), as the body's defense against infection inadvertently fosters clot formation.
Complications with the PICC line, which required frequent clearance with heparin every other day to maintain vancomycin therapy, further complicated my situation. A sonogram detected clotting at the site of the PICC line insertion in my arm, a known risk factor for clot development, as well as deep vein thrombosis (DVT) in my legs.
My thrombosis recurred in 2020 after contracting COVID-19 (with a D-Dimer level of 3800) and intensified following the Pfizer vaccine, manifesting alongside petechiae. This sequence of events underscores the complex interplay between infections, inflammation, and the risk of clot formation. While some medications may indirectly elevate the risk of clotting, this is generally less common and not typically a major concern with antibiotics such as Ciprofloxacin or Vancomycin.
Further complicating my medical history are previous diagnoses of Von Willebrand Factor (VWF) types II and V, Lupus, Rheumatoid arthritisand psoriasis. These conditions are known to activate the CYP450 enzyme system, potentially contributing to endothelial dysfunction and further complicating the risk of thrombosis.
Thus far, the question of whether hydrogel or polyethylene glycol (PEG) present in medications can contribute to the formation of microclots or macroclots remains unanswered. The Cytochrome P450 enzymes are involved in the metabolism of various substances, including medications.
Through sharing my story, I aim to deepen the understanding of thrombosis's multifaceted causes, hoping to contribute valuable insights into its complex etiology and potential preventive measures.
Contributing to Clot Research: A Personal Journey
I am eager to contribute to the research on the causes of thrombosis, drawing from my personal experiences with clots that began following surgeries in 2011 and 2016. These incidents were complicated by infections with Staph epidermidis, Peptostreptococcus, a single colony of Staph caprae, and Corynebacterium species, all culminating in sepsis.
The pivotal question I grapple with is whether the clots were precipitated by the sepsis or by the treatments I received: oral Ciprofloxacin and Vancomycin administered through a Peripherally Inserted Central Catheter (PICC) line. Sepsis, a critical response to infection, triggers widespread inflammation that can enhance the risk of clotting as part of the body's inflammatory response. This inflammatory cascade can significantly elevate the likelihood of thrombosis, particularly venous thromboembolism (VTE), as the body's defense against infection inadvertently fosters clot formation.
Complications with the PICC line, which required frequent clearance with heparin every other day to maintain vancomycin therapy, further complicated my situation. A sonogram detected clotting at the site of the PICC line insertion in my arm, a known risk factor for clot development, as well as deep vein thrombosis (DVT) in my legs.
My thrombosis recurred in 2020 after contracting COVID-19 (with a D-Dimer level of 3800) and intensified following the Pfizer vaccine, manifesting alongside petechiae. This sequence of events underscores the complex interplay between infections, inflammation, and the risk of clot formation. While some medications may indirectly elevate the risk of clotting, this is generally less common and not typically a major concern with antibiotics such as Ciprofloxacin or Vancomycin.
Further complicating my medical history are previous diagnoses of Von Willebrand Factor (VWF) types II and V, Lupus, Rheumatoid arthritisand psoriasis. These conditions are known to activate the CYP450 enzyme system, potentially contributing to endothelial dysfunction and further complicating the risk of thrombosis.
Thus far, the question of whether hydrogel or polyethylene glycol (PEG) present in medications can contribute to the formation of microclots or macroclots remains unanswered. The Cytochrome P450 enzymes are involved in the metabolism of various substances, including medications.
Through sharing my story, I aim to deepen the understanding of thrombosis's multifaceted causes, hoping to contribute valuable insights into its complex etiology and potential preventive measures.