Vancomycin is one of the most empirically used antibiotics in severely ill patients in hospitalized settings. Vancomycin-induced thrombocytopenia (VITP) is a rare and potentially life-threatening complication that requires immediate recognition. Platelet destruction is largely immune-mediated and results in a precipitous drop in the platelet count over a short period of time. Most cases of VITP are drug-dependent, as discontinuation of the offending agent frequently results in a timely return to baseline to pre-exposure platelet levels. Here, we present a case of severe vancomycin-induced thrombocytopenia in a 35-year-old female with a history of multiple comorbidities who presented with pneumonia. She was undergoing treatment with vancomycin and piperacillin-tazobactam and developed thrombocytopenia within 24 hours of hospitalization. The patient was on a loading dose of 1250 mg intravenous vancomycin every 24 hours and piperacillin-tazobactam 3.375 g intravenously every six hours for presumed community-acquired pneumonia. Her other medications included ondansetron, bupropion, sertraline, tamsulosin, pantoprazole, ergocalciferol, and insulin glargine. Additionally, the patient was placed on a prophylactic dose of enoxaparin while in-patient. The patient\'s thrombocytopenia resolved with discontinuation of vancomycin. Clinicians should be well-informed about which medications can trigger thrombocytopenia whenever starting a medication in such cases.

BACKGROUND: We report the case of a postmenopausal female with a hemorrhagic Bartholin\'s cyst who has been using an antiplatelet medication.
METHODS: A postmenopausal woman, 84 years of age, had a medical history of hypertension, diabetes mellitus, coronary artery disease (three-vessel disease), chronic kidney disease (stage 3), and dementia. The patient has been taking clopidogrel, an antiplatelet medication, for several years. She presented at our outpatient clinic complaining of painful swelling over her left vulva for several days. A Bartholin\'s cyst over the left vulva was suspected, and the patient underwent marsupialization under local anesthesia, which was well-tolerated. During the incision procedure, bright-red blood with some blood clots was discharged, and a hemorrhagic Bartholin\'s cyst was observed. There was no recurrence of the hemorrhagic Bartholin\'s cyst during the 6-mo subsequent follow-up period.
CONCLUSIONS: Hemorrhagic Bartholin\'s cysts rarely occur. We report the case of a postmenopausal female with a hemorrhagic Bartholin\'s cyst who had been on antiplatelets and was successfully treated with marsupialization. No recurrence was noted during the 6-mo follow-up period. Older females taking antiplatelets should be cautious of bleeding when presenting with a Bartholin\'s cyst.

To study the influence of blood lipid levels on hemorrhagic transformation (HT) and prognosis after acute cerebral infarction (ACI).
Patients with ACI within 72 h of symptoms onset between January 1st, 2015, and December 31st, 2016, were retrospectively analyzed. Patients were divided into group A (without HT) and group B (HT). The outcomes were assessed after 3 months of disease onset using the modified Rankin Scale (mRS). An mRS score of 0-2 points indicated excellent prognosis, and an mRS score of 3-6 points indicated poor prognosis.
A total of 732 patients conformed to the inclusion criteria, including 628 in group A and 104 in group B. The incidence of HT was 14.2%, and the median onset time was 2 d (interquartile range, 1-7 d). The percentages of patients with large infarct size and cortex involvement in group B were 80.8 and 79.8%, respectively, which were both significantly higher than those in group A (28.7 and 33.4%, respectively). The incidence rate of atrial fibrillation (AF) in group B was significantly higher than that in group A (39.4% vs. 13.9%, P < 0.001). The adjusted multivariate analysis results showed that large infarct size, cortex involvement and AF were independent risk factors of HT, while total cholesterol (TC) was a protective factor of HT (OR = 0.359, 95% CI 0.136-0.944, P = 0.038). With every 1 mmol/L reduction in normal TC levels, the risk of HT increased by 64.1%. The mortality and morbidity at 3 months in group B (21.2 and 76.7%, respectively) were both significantly higher than those in group A (8.0 and 42.8%, respectively). The adjusted multivariate analysis results showed that large infarct size (OR = 12.178, 95% CI 5.390-27.516, P < 0.001) was an independent risk factor of long-term unfavorable outcomes, whereas low-density lipoprotein cholesterol (LDL-C) was a protective factor (OR = 0.538, 95% CI 0.300-0.964, P = 0.037). With every 1 mmol/L reduction in normal LDL-C levels, the risk of an unfavorable outcome increased by 46.2%. Major therapies, including intravenous recombinant human tissue plasminogen activator (rTPA), intensive lipid-lowering statins and anti-platelets, were not significantly related to either HT or long-term, post-ACI poor prognosis.
For patients with large infarct sizes, especially those with cortex involvement, AF, or lower levels of TC, the risk of HT might increase after ACI. The risk of a long-term unfavorable outcome in these patients might increase with a reduction in LDL-C.