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BACKGROUND: Transient transaminitis is an expected outcome from liver retraction after foregut surgeries. However, severe thrombocytopenia is usually not a sequela of that. We present a case in which sevoflurane is suspected of inducing thrombocytopenia as it was the only newly introduced medication to the patient during the hospital course. Thrombocytopenia may present in a variety of settings in hospitalized patients. However, managing this occurrence requires deep exploration of pathophysiology that can cause decreased platelets, which may be a challenging task in certain circumstances. The liver plays an important role in thrombopoiesis by releasing megakaryocyte growth factors. Therefore, liver dysfunction can present as thrombocytopenia or other platelet dysfunctions. OBJECTIVE: To describe a presentation of thrombocytopenia possibly associated with anesthesia-induced transaminitis after a robotic paraesophageal hernia repair with mesh and fundoplasty with intraoperative esophagogastroduodenoscopy (EGD). METHODS: A 55-year-old presented to the ED with abdominal pain and was found to have a large type IV paraesophageal hernia that was surgically treated with a robotic paraesophageal hernia repair with mesh. However, on the first postoperative day (POD) (#1), the patient developed new onset thrombocytopenia with transaminitis. Workup for thrombocytopenia failed to determine an etiology. With platelet transfusion, platelet count showed an upward trend. The patient was then evaluated and cleared for discharge by POD#5. RESULTS: The patient's POD#1 daily labs showed elevated values for liver function tests and a low platelet count of 10,000 platelets per microliter with an international normalized value (INR) of 1.3. She had received two doses of intravenous acetaminophen just prior to surgery. Her platelet count responded to two units of platelets but decreased again immediately after. She continued to have transaminitis with down-trending liver enzymes. Peripheral smear on review showed no evidence of schistocytes. A heparin-induced thrombocytopenia (HIT) screening was negative. The patient was regularly evaluated, and the platelets stabilized and slowly started to trend up. The patient recovered by the morning of her POD#5 and was cleared for discharge. CONCLUSION: We are reporting on a case of acute postoperative thrombocytopenia that was associated with transaminitis and elevated liver enzymes. We are linking the role of the liver dysfunction in noncirrhotic patients with surgical abdominal procedures. Although liver retraction transaminitis possibly played a role in the laboratory findings in the patient, the acute drop in her platelet count could be closely related to the use of sevoflurane anesthetic considering its potential hepatotoxic side effects. We also cannot rule out the sevoflurane directly affecting the platelet count.
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Breast cancer is the leading cause of death in women among all cancer types. Obesity is one of the factors that promote progression of breast cancer, especially in post-menopausal women. Increasingly, adipose tissue is recognized for its active role in the tumor microenvironment. We hypothesized that adipocytes conditioned medium can impact breast cancer progression by increasing inflammatory cytokines production by cancer cells, and subsequently increasing their motility. By contrast, eicosapentaenoic acid (EPA), an anti-inflammatory n-3 polyunsaturated fatty acid, reduces adipocyte-secreted inflammatory factors, leading to reduced cancer cell motility. To test these hypotheses, we investigated the direct effects of EPA on MCF-7 and MDA-MB-231 breast cancer cells and the effects of conditioned medium from 3 T3-L1 or human mesenchymal stem cells (HMSC)-derived adipocytes treated with or without EPA supplementation on breast cancer cells. We observed that conditioned medium from HMSC-derived adipocytes significantly increased mRNA transcription levels of cancer-associated genes such as FASN, STAT3 and cIAP2, while EPA-treated HMSC-derived adipocytes significantly reduced mRNA levels of these genes. However, direct EPA treatment significantly reduced mRNA content of these tumor-associated markers (FASN, STAT3, cIAP-2) only in MDA-MB-231 cells not in MCF-7 cells. Conditioned medium from EPA-treated 3 T3-L1 adipocytes further decreased inflammation, cell motility and glycolysis in cancer cells. Our data confirms that adipocytes play a significant role in promoting breast cancer progression and demonstrates that EPA-treated adipocytes reduced the negative impact of adipocyte-secreted factors on breast cancer cell inflammation and migration.