Infective endocarditis (IE) can cause life-threatening intracerebral hemorrhage via the transformation of an embolic ischemic stroke. Navigating anticoagulant therapy for IE patients is challenging due to this risk. Hospitalized patients often receive anticoagulation to minimize venous thromboembolism (VTE). Those at higher VTE risk may require full anticoagulation, particularly if there is an initial suspicion of a blood clot. A timely IE diagnosis is crucial but is often delayed during inpatient stays, with the patient potentially already on anticoagulants for other conditions. Our case discusses a hemorrhagic stroke in a patient with IE while receiving therapeutic enoxaparin. Clinical signs and symptoms, echocardiographic findings, laboratory workup and microbiological data, and possibly other imaging techniques such as cerebral magnetic resonance imaging (MRI) need to be employed in a timely manner in determining endocarditis as a cause of stroke.

BACKGROUND: Although the correlation between liver toxicity and vancomycin is generally considered low, it has been observed that the use of vancomycin can lead to abnormal liver function indicators, such as elevated aspartate aminotransferase, alanine aminotransferase, alpha fetoprotein, and jaundice. To further understand the clinical features associated with vancomycin-induced liver toxicity and to provide clinical guidance, we conducted an analysis of the characteristics and clinical manifestations of vancomycin-induced liver injury.
METHODS: Patients with liver function injury who received vancomycin treatment at the Third Xiangya Hospital of Central South University and Hunan Maternal and Child Health Hospital between 2016 and 2021 were selected for retrospective analysis of their general characteristics, vancomycin course, dose, liver function index, severity of liver injury, and concomitant medications.
RESULTS: Of the 4562 patients who received vancomycin, 17 patients were finally included, with an incidence rate of 0.37%. Of these patients, 12 were male (70.6%) and 5 were female (29.4%), ranging in age from 17 to 84 years with a mean average age of 45.41 ± 20.405 years. All patients were evaluated using Naranjo\'s score, with score ≥ 3. The dosage, time, and plasma concentration of vancomycin were analyzed and it was found that nine patients (52.94%) had abnormal liver function when initially given a dose of 1 g every 12 hours. In total, 14 patients (82.35%) with liver injury were taking vancomycin in combination with two to four drugs, and severe liver injury occurred in patients taking vancomycin in combination with two drugs. The occurrence time of liver injury was 2-12 days after starting vancomycin, with a mean of 4.53 ± 2.401 days. Of these patients, 16 patients (94.1%) showed liver function abnormalities within 7 days of taking the drug, and 2 patients with grade 3-4 liver injury both showed liver function abnormalities within 3 days of taking the drug. Only 4 of the 17 patients (23.53%) had vancomycin blood concentrations within the normal range, and there was no correlation found between blood concentration and severity of liver injury. Analysis of the correlation between the severity of liver injury and vancomycin showed that none of the patients had allergies such as rash, two patients (11.76%) had jaundice, and fatigue occurred in five patients (29.41%). The remaining ten patients (58.82%) had no symptoms related to liver injury. All 17 patients had abnormal aspartate aminotransferase/alanine aminotransferase levels and 9 patients also had abnormal bilirubin levels. In 15 patients (88.24%), the severity of liver injury was grade 1, indicating mild liver injury, and no correlation was observed between the severity of liver injury and creatinine. Of the 17 patients, 1 patient received no intervention, 4 patients stopped taking vancomycin after developing liver injury, 1 patient reduced the dose, and 11 patients (64.7%) were treated with hepatic protectant.
CONCLUSIONS: Although the study concluded that the incidence of liver injury was not high, the liver toxicity of vancomycin should still be considered and liver function indicators should be monitored during the clinical use of vancomycin.

We present a case of endogenous endophthalmitis with urinary tract infection (UTI) caused by group B Streptococcus (GBS). An 86-year-old female initially presented with ocular pain and sudden visual disturbance of the left eye. The patient did not complain of other symptoms and had no history of recent ocular surgery or trauma. Endogenous endophthalmitis was clinically diagnosed based on ophthalmic examination, history, and lab results showing systemic infection. A few days later, GBS was identified in her aqueous humor, blood, and urine cultures. Intravitreal ceftazidime and vancomycin injections, as well as fortified ceftazidime and vancomycin eye drops, were used immediately after clinical diagnosis. However, the symptoms worsened despite repeated intravitreal injections, so evisceration was performed. Endogenous endophthalmitis caused by GBS is very virulent and may present without evident systemic symptoms. The early recognition of the disease and systemic work up, followed by prompt treatment, is necessary.

Vancomycin is a bactericidal antibiotic used for various infections but can cause hypersensitivity reactions, including vancomycin flushing syndrome (VFS) and anaphylaxis. VFS, previously known as red man syndrome, is a pseudoallergic reaction characterized by flushing, erythema, and pruritus. We present a case of VFS in a female patient with recurrent Methicillin-resistant Staphylococcus aureus (MRSA) infections receiving vancomycin for back abscesses. Following the second dose, she developed a pruritic rash on her face, neck, and torso, which resolved with treatment. The differential diagnosis included hydromorphone allergy, ruled out due to previous tolerance. Anaphylaxis was unlikely due to the absence of respiratory distress, hypotension, or angioedema. Management involved discontinuing vancomycin, administering corticosteroids and antihistamines, and monitoring for anaphylaxis. The patient was transferred for surgical intervention and alternative antibiotic therapy. This case highlights the importance of recognizing and managing VFS, the significance of differential diagnoses, and the need for enhanced documentation and clinical support in managing vancomycin hypersensitivity reactions.

BACKGROUND: Gout is a chronic disease characterized by deposition of monosodium urate crystals. Tophi develop in some individuals with untreated or uncontrolled gout, which leads to ulcerations, cosmetic problems, mechanical obstruction of joint movement, joint damage and musculoskeletal disability. Currently, the treatment of gouty tophi is controversial and challenging. Both surgical and internal medical treatments have limitations and require further exploration in clinical practice.
METHODS: In Case 1, we treated a patient with severe infection of diabetic foot ulcers with concomitant multiple gouty tophi in the same limb. A systematic management strategy was formulated to close the wound and save the limb. The ulcers healed successfully after half a year. In Case 2, a giant gouty tophi located in the first metatarsophalangeal joint of the left foot was removed by surgical treatment and vancomycin-loaded bone cement implantation. In Case 3, we present a case of gouty tophi that was resolved by standardized systemic medical management.
METHODS: Three patients were all diagnosed with gout accompanied by gouty deposition, although there were other different comorbidities.
METHODS: In case 1, we used debridement to gradually remove gouty tophi. In case 2, the giant gouty tophi was removed by surgical operation. In case 3, the gouty tophi disappeared after standardized treatment with medicine, diet and lifestyle management.
RESULTS: Three patients underwent different treatment therapies to remove gouty tophi based on their specific conditions.
CONCLUSIONS: We explored effective interventions for tophi in gout by surgical or other interventions in combination with pharmacotherapy.

A 22-year-old Vietnamese man was referred to our hospital owing to cough, dyspnea, and difficulty moving. The patient was diagnosed with community-acquired Panton-Valentine leukocidin-positive methicillin-resistant Staphylococcus aureus (MRSA) bacteremia and necrotizing pneumonia. Treatment involved vancomycin (VCM) and meropenem, and the MRSA bacteremia improved. However, lung tissue destruction progressed. Therefore, linezolid was added to the VCM regimen, and this intervention led to the patient\'s recovery, and he was discharged from the hospital. Here, we report a case in which the patient was treated with a combination of two anti-MRSA drugs and was cured.

Vancomycin (VCM), an essential antibiotic for antimicrobial-resistant Gram-positive cocci, can lead to complications such as neutropenia. Here, we present a case of a 25-year-old male with noncommunicating hydrocephalus due to an intraventricular tumor who developed neutropenia during VCM therapy. Despite the suspected VCM-induced neutropenia, short-term readministration was deemed necessary for perioperative infection prophylaxis. This patient was readministered without neutropenia. A review of the literature revealed an earlier onset of VCM-induced neutropenia than that previously reported, emphasizing the importance of vigilant monitoring. Although readministration of VCM in patients with neutropenia is uncommon, it may be feasible with careful risk assessment, particularly in cases of mild neutropenia and short-term therapy. However, the mechanisms underlying VCM-induced neutropenia remain unclear, necessitating further research on the optimal management strategies.

The patient, a 43-year-old male, was admitted to the hospital with gradually aggravated exertional palpitations and chest tightness over a 2-day period. Upon hospital admission, a cardiac ultrasound revealed aortic valve redundancy, however multiple blood culture investigations came back negative. Blood mNGS was perfected, revealing Coxiella burnetii, and the diagnosis of Q fever (query fever) was established. The temperature and inflammatory indices of the patient were all normal with the treatment of vancomycin before cardiac surgery. But for the potential liver damage of and the Coxiella burnetii was still positive in the anti-phase II IgG titer, the doxycycline and hydroxychloroquine instead of vancomycin were applied for the patient. Despite receiving standardized anti-infective therapy of doxycycline combined with hydroxychloroquine, this patient had fever and increased leukocytes following surgery. After the addition of vancomycin as an anti-infective treatment, the temperature and leukocytes improved quickly. During the treatment of vancomycin, a discovery of liver injury may have resulted. These findings provide new therapy options for future professionals.

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BACKGROUND: The goal was to report a rare case of lymphadenitis caused by Corynebacterium tuberculostearicum, and the laboratory\'s coping approach in the isolation and identification of this rare pathogen to improve the understanding of the disease.
METHODS: Lymph node biopsy was performed in a patient with suspected tuberculous lymphadenitis, and the biopsy tissue was isolated and cultured.
RESULTS: The culture was Gram positive Corynebacterium, which was identified as Corynebacterium tuberculostearicum by microbial mass spectrometry and 16S rRNA gene sequencing. Antimicrobial susceptibility test showed that the drug was sensitive to daptomycin, doxycycline, gentamicin, linezolid, vancomycin, and meropenem, but resistant to ciprofloxacin, clindamycin, erythromycin, rifampicin, compound sulfamethoxazole, ceftriaxone, and cefepime.
CONCLUSIONS: This is a case of Corynebacterium tuberculostearicum infection. Case reports of Corynebacterium tuberculostearicum infection are relatively rare in China. Through case study, we can provide help for laboratory isolation, identification, clinical diagnosis, and treatment.