• Cyclic glycopeptides
• C−H activation
• Glycosides
• Palladium
• Peptides

• Cyclization
• Stereoisomerism
• Glycopeptides/chemistry
• Glycopeptides/chemical synthesis
• Catalysis
• Palladium/chemistry
• Peptides, Cyclic/chemistry
• Peptides, Cyclic/chemical synthesis
• Cyclophanes

• Bleeding
• Risk factors
• Thrombocytopenia
• Vancomycin

• Humans
• Vancomycin/adverse effects
• Thrombocytopenia/chemically induced
• Thrombocytopenia/epidemiology
• Risk Factors
• Male
• Female
• Retrospective Studies
• Incidence
• Middle Aged
• Aged
• Case-Control Studies
• Anti-Bacterial Agents/adverse effects
• Adult
• Aged, 80 and over

• ITP
• autoimmune mechanisms
• cancer
• immune system
• immunosuppressive treatment

• DS640 Medical University of Lublin

• Adverse drug reaction
• Bleeding
• Gastrointestinal hemorrhage
• Vancomycin

• Adult
• Humans
• Male
• Anti-Bacterial Agents/adverse effects
• Anti-Bacterial Agents/administration & dosage
• Gastrointestinal Hemorrhage/blood
• Gastrointestinal Hemorrhage/chemically induced
• Gastrointestinal Hemorrhage/diagnosis
• Methicillin-Resistant Staphylococcus aureus
• Staphylococcal Infections/drug therapy
• Staphylococcal Infections/microbiology
• Thrombocytopenia/blood
• Thrombocytopenia/diagnosis
• Vancomycin/adverse effects

• 2022HXFH034 1·3·5 project for disciplines of excellence-Clinical Research Incubation Project, West China Hospital, Sichuan University
• 1·3·5 project for disciplines of excellence–Clinical Research Incubation Project, West China Hospital, Sichuan University

• Posterior spine fusion surgery
• Postoperative spinal infection
• Resistant organism
• SSI prophylaxis
• Vancomycin powder

• Humans
• Vancomycin/therapeutic use
• Anti-Bacterial Agents/therapeutic use
• Powders
• Lumbar Vertebrae/surgery
• Surgical Wound Infection/epidemiology
• Spinal Fusion/adverse effects
• Retrospective Studies

• Humans
• Aged
• Thrombocytopenia/diagnosis
• Thrombocytopenia/therapy
• Thrombocytopenia/chemically induced
• Myelodysplastic Syndromes/diagnosis
• Myelodysplastic Syndromes/therapy
• Myelodysplastic Syndromes/complications
• Purpura, Thrombocytopenic, Idiopathic/diagnosis
• Purpura, Thrombocytopenic, Idiopathic/therapy
• Purpura, Thrombocytopenic, Idiopathic/complications

• Humans
• Purpura, Thrombocytopenic, Idiopathic/diagnosis
• Purpura, Thrombocytopenic, Idiopathic/therapy
• Hemorrhage/diagnosis
• Hemorrhage/therapy
• Thrombocytopenia/diagnosis
• Thrombocytopenia/therapy
• Platelet Count
• Emergency Service, Hospital

• coagulation disorder
• pharmacovigilance
• risk factor
• thrombocytopenia
• tigecycline

• National High Level Hospital Clinical Research Funding

• Humans
• Hemolysis
• Critical Illness
• Thrombocytopenia/complications
• Anemia/complications

• Bleeding complications
• MRSA infections
• Pharmacovigilance analysis
• Thrombocytopenia
• Vancomycin

• Humans
• Vancomycin/adverse effects
• Linezolid/adverse effects
• Daptomycin/pharmacology
• Tigecycline
• Teicoplanin/pharmacology
• Methicillin-Resistant Staphylococcus aureus
• Pharmacovigilance
• Thrombocytopenia/chemically induced
• Anti-Bacterial Agents/adverse effects

• anti-platelet
• immune
• medications
• thrombocytopenia
• vancomycin

• drug discontinuation
• drug-induced thrombocytopenia
• immune-mediated thrombocytopenia
• vancomycin infusion
• vancomycin-induced immune thrombocytopenia

• Impurity
• LC-MS
• NMR
• Two-dimensional preparative liquid chromatography (2D-Prep-LC)
• Vancomycin

• Corynebacterium striatum
• all-cause mortality
• linezolid
• lower respiratory tract infection
• vancomycin

• Ministry of Science and Technology of China

• GM-CSF
• IL-17A
• antibiotics
• invasive candidiasis
• lymphocytes
• trans-kingdom infections
• vancomycin

• Animals
• Anti-Bacterial Agents/administration & dosage
• Anti-Bacterial Agents/adverse effects
• Bacteria/drug effects
• Bacteria/immunology
• Candida albicans/immunology
• Candidiasis, Invasive/immunology
• Candidiasis, Invasive/microbiology
• Coinfection/immunology
• Coinfection/microbiology
• Granulocyte-Macrophage Colony-Stimulating Factor/immunology
• Granulocyte-Macrophage Colony-Stimulating Factor/therapeutic use
• Humans
• Iatrogenic Disease
• Immunotherapy
• Interleukin-17/immunology
• Interleukin-17/therapeutic use
• Mice
• Th17 Cells/metabolism
• Vancomycin/pharmacology

• MR/V009052/1 Medical Research Council
• R00 AI141622 NIAID NIH HHS
• ZIA AI001175 Intramural NIH HHS

Thrombocytopenia can cause substantial morbidity and mortality in critically ill patients. There are multiple etiology factors and various mechanisms associated with thrombocytopenia, of which drug-induced thrombocytopenia (DITP) deserves attention. Herein, we describe a case of severe thrombocytopenia during intensive care unit (ICU) hospitalization that was likely to be associated with vancomycin. By revealing the process of identifying this case of DITP and reviewing relevant clinical studies, a risk alert of vancomycin-related severe hematotoxicity should be considered.

• adverse drug reaction
• case report
• critically illness
• thrombocytopenia
• vancomycin

• Anti-infective agents
• Clostridioides difficile
• fluid therapy
• hematologic toxicities
• neurocognitive disorders

Several therapeutic agents can cause thrombocytopenia by either immune-mediated or non-immune-mediated mechanisms. Non-immune-mediated thrombocytopenia is due to direct toxicity of drug molecules to platelets or megakaryocytes. Immune-mediated thrombocytopenia, on the other hand, involves the formation of antibodies that react to platelet-specific glycoprotein complexes, as in classic drug-induced immune thrombocytopenia (DITP), or to platelet factor 4, as in heparin-induced thrombocytopenia (HIT) and vaccine-induced immune thrombotic thrombocytopenia (VITT). Clinical signs include a rapid drop in platelet count, bleeding or thrombosis. Since the patient's condition can deteriorate rapidly, prompt diagnosis and management are critical. However, the necessary diagnostic tests are only available in specialized laboratories. Therefore, the most demanding step in treatment is to identify the agent responsible for thrombocytopenia, which often proves difficult because many patients are taking multiple medications and have comorbidities that can themselves also cause thrombocytopenia. While DITP is commonly associated with an increased risk of bleeding, HIT and VITT have a high mortality rate due to the high incidence of thromboembolic complications. A structured approach to drug-associated thrombocytopenia/thrombosis can lead to successful treatment and a lower mortality rate. In addition to describing the treatment of DITP, HIT, VITT, and vaccine-associated immune thrombocytopenia, this review also provides the pathophysiological and clinical information necessary for correct patient management.

Chemotherapy-induced thrombocytopenia (CIT) is a common complication of the treatment of non-hematologic malignancies. Many patient-related variables (e.g., age, tumor type, number of prior chemotherapy cycles, amount of bone marrow tumor involvement) determine the extent of CIT. CIT is related to the type and dose of chemotherapy, with regimens containing gemcitabine, platinum, or temozolomide producing it most commonly. Bleeding and the need for platelet transfusions in CIT are rather uncommon except in patients with platelet counts below 25x10⁹/L in whom bleeding rates increase significantly and platelet transfusions are the only treatment. Nonetheless, platelet counts below 70x10⁹/L present a challenge. In patients with such counts, it is important to exclude other causes of thrombocytopenia (medications, infection, thrombotic microangiopathy, post-transfusion purpura, coagulopathy and immune thrombocytopenia). If these are not present, the common approach is to reduce chemotherapy dose intensity or switch to other agents. Unfortunately decreasing relative dose intensity is associated with reduced tumor response and remission rates. Thrombopoietic growth factors (recombinant human thrombopoietin, pegylated human megakaryocyte growth and development factor, romiplostim, eltrombopag, avatrombopag and hetrombopag) improve pretreatment and nadir platelet counts, reduce the need for platelet transfusions, and enable chemotherapy dose intensity to be maintained. National Comprehensive Cancer Network guidelines permit their use but their widespread adoption awaits adequate phase III randomized, placebo-controlled studies demonstrating maintenance of relative dose intensity, reduction of platelet transfusions and bleeding, and possibly improved survival. Their potential appropriate use also depends on consensus by the oncology community as to what constitutes an appropriate pretreatment platelet count as well as identification of patient-related and treatment variables that might predict bleeding.

Immune thrombocytopenia (ITP) is a leading cause of isolated thrombocytopenia characterized by autoantibody-mediated destruction of platelets, impaired megakaryocyte function, and pathologic T-cell recognition of platelet antigens. Several triggers for ITP have been identified. Treatment of the inciting cause decreases the antibodies responsible for molecular mimicry, and these cases are usually associated with a better outcome with a decreased probability of progression to chronic ITP. Mycoplasma pneumoniae infection is known to have extrapulmonary manifestations, and growing evidence suggests it can be a cause of secondary ITP. Many of the described cases report evidence of a pulmonary infection with severe mucosal bleeding. Here, we describe an interesting case of a patient presenting with isolated thrombocytopenia with mild mucosal bleeding, later found to be positive for Mycoplasma immunoglobulin M without clinically significant evidence of active infection. Currently, mycoplasma testing is not routinely performed as a workup for ITP. However, clinicians may consider this before proceeding with more aggressive treatment for refractory ITP (i.e., prolonged immunosuppression, splenectomy). This case illustrates that mild/asymptomatic Mycoplasma infection can also be associated with ITP.

Vancomycin is used for the treatment of gram-positive infections. The increasing prevalence of methicillin-resistant Staphylococcus aureus since the 1980 s has led to a significant increase in the clinical utility of vancomycin in the United States. The diagnosis of vancomycin induced thrombocytopenia (VIT) poses a challenge since it requires the exclusion of other etiologies of thrombocytopenia, such as infectious or immunologic diseases and alternative drugs. Physicians should be aware that VIT is a rare but important complication of IV vancomycin therapy and failure to recognize this diagnosis may lead to a delay in discontinuation of vancomycin and serious complications

Vancomycin is a glycopeptide antibiotic used against multi-drug resistant gram-positive bacteria such as Staphylococcus aureus (MRSA). Although invaluable against resistant bacteria, vancomycin harbors adverse drug reactions including cytopenia, ototoxicity, as well as nephrotoxicity. Since nephrotoxicity is a rarely occurring side effect, its mechanism is incompletely understood. Only recently, the actual clinically relevant concentration the in kidneys of patients receiving vancomycin was investigated and were found to exceed plasma concentrations by far. We applied these clinically relevant vancomycin concentrations to murine and canine renal epithelial cell lines and assessed metabolic and lipidomic alterations by untargeted and targeted gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry analyses. Despite marked differences in the lipidome, both cell lines increased anabolic glucose reactions, resulting in higher sorbitol and lactate levels. To the best of our knowledge, this is the first endometabolic profiling of kidney cells exposed to clinically relevant vancomycin concentrations. The presented study will provide a valuable dataset to nephrotoxicity researchers and might add to unveiling the nephrotoxic mechanism of vancomycin.

• GC/MS
• LC/MS
• lipidomics
• mass spectrometry
• metabolomics
• nephrotoxicity
• tubule
• vancomycin

• haematology (incl blood transfusion)
• infection (neurology)
• infections

• Anti-Bacterial Agents/adverse effects
• Humans
• Meningitis/drug therapy
• Platelet Count
• Thrombocytopenia/chemically induced
• Thrombocytopenia/drug therapy
• Vancomycin/adverse effects

• haematology (drugs and medicines)
• infections

• bacteraemia
• bactericidal antibodies
• fully human antibody
• methicillin‐resistant Staphylococcusaureus
• single‐chain fragment variable

• Pasteur Institute of Iran

Patient: Female, 46-year-old

Final Diagnosis: Adverse drug reaction • epidural abscess

Symptoms: Eosinophilia • neutropenia • thrombocytopenia

Medication: —

Clinical Procedure: —

Specialty: General and Internal Medicine

• ADAMTS13
• cardiac surgery
• clopidogrel
• thrombotic thrombocytopenic purpura

• Vancomycin
• dose optimization
• dose prediction
• machine learning
• xgboost

• Adult
• Aged
• Aged, 80 and over
• COVID-19/complications
• COVID-19/diagnosis
• Critical Illness
• Disease Progression
• Female
• Humans
• Intensive Care Units
• Male
• Middle Aged
• Prognosis
• Retrospective Studies
• SARS-CoV-2/isolation & purification
• Thrombocytopenia/complications

Thrombocytopenia is a serious complication in the medical practice of numerous drugs. Vancomycin is frequently used for the prophylaxis and treatment of suspected or identified methicillin-resistant positive infections. Several cases with vancomycin-induced thrombocytopenia (VIT) have been reported. However, these have rarely been extensively reviewed. The present report describes a case of VIT in endocarditis, and reviews all VIT cases reported in the literature.

A 26-year-old male diagnosed with infective endocarditis was admitted. The patient was treated with multiple drugs, including vancomycin, which was initially intravenously given at 1000 mg every 12 h and subsequently at 500 mg every 8 h on day 3. On day 11, the platelet count decreased to 51 × 10⁹/L, vancomycin was switched to 500 mg every 12 h, and platelet transfusion was given. On day 17, the platelet count dropped to 27 × 10⁹/L, and platelet transfusion was administered again. On day 23, vancomycin was adjusted to 500 mg every 8 h as the trough concentration dropped to the minimum effective concentration. On day 33, the platelet count declined to approximately 40 × 10⁹/L. After platelet transfusion, the platelet count rebounded to 90 × 10⁹/L on day 35 but dropped again to 42 × 10⁹/L on day 43. Based on the time-to-platelet count curve and Naranjo’s Adverse Drug Reaction Probability Scale score, VIT was suspected. After vancomycin discontinuation and platelet transfusion, the platelet count gradually normalized.

The diagnosis of VIT can be achieved through the time-to-platelet count curve and Naranjo’s Adverse Drug Reaction Probability Scale score. The platelet count cannot be normalized simply by platelet transfusion alone, and vancomycin discontinuation is essential.

• Case report
• Vancomycin
• Thrombocytopenia
• Endocarditis
• Platelet transfusion
• Literature review

Stroke is a devastating complication of left ventricular assist device (LVAD) therapy. Understanding the characteristics, risk factors and outcomes of strokes associated with the centrifugal flow LVADs is important to devise better strategies for management and prevention. This is a retrospective cohort study at a single US academic medical center. The cohort includes patients who received a first time Heartmate 3 (HM3) or Heartware (HVAD) LVAD between September 2009 through February 2018 and had a stroke while the LVAD was in place. Descriptive statistics were used when appropriate. A logistic regression analysis was used to determine predictors of poor outcome. Out of a total of 247 patients, 12.1% (N = 30, 24 HVAD and 6 HM3) had a stroke (63% ischemic) and 3 of these patients had pump thrombosis. Events per patient year (EPPY) were similar for HVAD and HM3 patients (0.3 ± 0.1). INR was subtherapeutic in 47.4% of ischemic stroke patients and supratherapeutic in 18.2% of hemorrhagic stroke patients. Concurrent infections were more common in the setting of hemorrhagic stroke than ischemic stroke (45.4% vs 5.3%, p = 0.008). Strokes were severe in most cases, with initial NIH stroke scale (NIHSS) higher in HM3 patients compared to HVAD patients (mean 24.6 vs 16) and associated with high in-patient mortality (21.1% of ischemic stroke vs. 88.8% of hemorrhagic stroke). Predictors of death within 30 days and disability at 90 days included creatinine at stroke onset, concurrent infection, hemorrhaghic stroke, and initial stroke severity (NIHSS). A score derived from these variables predicted with 100% certainty mortality at 30 days and mRS ≥ 4 at 90 days. For patients with centrifugal flow LVADs, ischemic strokes were more common but hemorrhagic strokes were associated with higher in-patient mortality and more frequently seen in the setting of concurrent infections. Infections, sub or supratherapeutic INR range, and comorbid cardiovascular risk factors may all be contributing to the stroke burden. These findings may inform future strategies for stroke prevention in this population.

Thrombocytopenia is a rare and sometimes life-threatening complication of Vancomycin. A 52-year-old male patient with acute kidney injury was treated with Vancomycin for ventilator-associated pneumonia. Three days later, his platelets decreased from 172 × 10⁹/L to 3 × 10⁹/L over a 36-hour period. The patient developed significant intrapulmonary bleeding leading to profound hypoxemia. Workup was negative for thrombotic thrombocytopenic purpura, disseminated intravascular coagulopathy, atypical hemolytic uremic syndrome, heparin-induced thrombocytopenia, and autoimmune diseases. All recently started medications were discontinued, and the patient was started empirically on methylprednisolone and intravenous immunoglobulin. The patient's platelets increased, and his airway bleeding stopped within 48 hours; his platelet count returned to normal by 18 days. Vancomycin-dependent anti-platelet antibodies were identified in the patient's serum by flow cytometry. Thrombocytopenia is an underrecognized complication of Vancomycin that can lead to life-threating bleeding. Stopping Vancomycin may be sufficient to reverse the thrombocytopenia in patients with normal renal function, but more aggressive measures such as steroids, IVIG, and dialysis may be required to stop bleeding and reverse thrombocytopenia in patients with underlying kidney injury who cannot effectively excrete Vancomycin.

• drugs
• heparin-induced thrombocytopenia
• platelets
• thrombocytopenia

Vancomycin-induced immune thrombocytopenia (ITP) is a rare, potentially life-threatening complication from an antibiotic frequently used in medical practice. We report a case of an 81-year-old male with recent removal of an infected right knee prosthesis and insertion of an articulating antibiotic spacer, presenting from rehabilitation for severe thrombocytopenia (1 X 10³/µL). The patient’s thrombocytopenia was initially falsely attributed to rifampin-induced ITP, a much more common cause of drug-induced thrombocytopenia. Only later, after a second precipitous drop in platelet count, vancomycin was correctly identified as the culprit. The patient’s serum was tested for drug-dependent platelet antibodies with and without vancomycin. A positive reaction for IgG was detected by flow cytometry in the absence of vancomycin, which was potentiated in the presence of vancomycin. The result indicated the presence of vancomycin-dependent and nondrug-dependent platelet reactive antibodies and confirmed the diagnosis of vancomycin-induced ITP. In this case, the correct diagnosis was masked by the simultaneous administration of two drugs that cause drug-induced ITP and highlights the importance of early recognition of rare, vancomycin-induced ITP.

• drug-induced immune thrombocytopenia
• immune thrombocytopenia
• vancomycin
• vancomycin-induced immune thrombocytopenia

Drug-induced thrombocytopenia secondary to antibiotic exposure is a rare complication more commonly associated with other medications. In this review, we present a case of antibiotic-induced thrombocytopenia and discuss the clinical picture and approach to identifying the complication. With increasing use of antibiotics that may be associated with drug-induced thrombocytopenia in perioperative prophylaxis protocols, surgeons need to be cognizant of this cause of thrombocytopenia in the postoperative patient. A delay in recognition and discontinuation of the offending agent can result in significant complications secondary to bleeding and superfluous testing.

• Antibiotic
• Arthroplasty
• Platelet
• Rifampin
• Thrombocytopenia
• Vancomycin

• Anti-Bacterial Agents/chemistry
• Anti-Bacterial Agents/pharmacokinetics
• Anti-Bacterial Agents/pharmacology
• Cell-Penetrating Peptides/chemistry
• Cell-Penetrating Peptides/pharmacokinetics
• Drug Carriers/chemistry
• Drug Compounding/methods
• Escherichia coli/drug effects
• Magnetite Nanoparticles/chemistry
• Microbial Sensitivity Tests
• Staphylococcus aureus/drug effects
• Vancomycin/chemistry
• Vancomycin/pharmacokinetics
• Vancomycin/pharmacology

Vancomycin induced thrombocytopenia (VIT) is an uncommon side effect of vancomycin which can manifest from mild petechiae to life-threatening bleed. Decreased renal clearance of vancomycin results in prolonged thrombocytopenia by antibody-mediated platelet destruction in the presence of vancomycin. Improvement in thrombocytopenia is achieved with the elimination of vancomycin. We describe a patient with end stage renal disease who experienced a protracted course of thrombocytopenia from vancomycin. We illustrate the mechanism of thrombocytopenia and the treatment modalities used by us and those described in literature. VIT is an important differential in patients with thrombocytopenia admitted to the hospital.

• Drug induced thrombocytopenia
• End stage renal disease
• Vancomycin

Prophylactic intracameral injection of antibiotics is commonly used to prevent endophthalmitis after cataract surgery. However, devastating visual complications have been reported including hemorrhagic occlusive retinal vasculitis (HORV).To determine the toxic and inflammatory effects of moxifloxacin, cefuroxime, and vancomycin on human retinal vascular cells, human retinal vascular endothelial cells (RVEC) and pericytes were exposed to three antibiotics, and the adverse effects were assessed by membrane damage, loss of intrinsic esterase activity, kinetic cell viability, and inflammatory cytokine secretion. Their retinal toxicity was examined by live/dead assays after an intravitreal injection of the three antibiotics into mice eyes. In vascular cells in culture, membrane damage and loss of esterase activity were induced after exposure to the three antibiotics. The toxic effects were most obvious after moxifloxacin (RVEC, ≥125 μg/mL; pericytes, ≥1000 μg/mL) at 24 h. Cefuroxime also reduced esterase activity and the membrane integrity of vascular cells but were less toxic than moxifloxacin. Kinetic cell viability testing showed that 500 μg/mL of moxifloxacin exposure induced significant decrease (29%) in the viability as early as 1 h. When the inflammatory effects of the antibiotics were examined, a significant induction of IL-8 was observed especially by RVECs after exposure to cefuroxime or vancomycin which was exacerbated by L-alanyl-γ-D-glutamyl-meso-diaminopimelic acid (Tri-DAP), a NOD1 ligand. Intravitreal injections in mice showed that cefuroxime and vancomycin caused retinal and vascular toxicity extending to the inner nuclear layers. Collectively, moxifloxacin causes immediate damage to retinal vascular cells in vitro, while cefuroxime and vancomycin induced significant inflammatory effects on vascular endothelial cells and caused retinal toxicity. Surgeons need to be cautious of the toxicity when antibiotics are used prophylactically especially by intravitreal administration.

This case involves a 62-year-old male with a prior history of epidural abscess and L1-L2 osteodiscitis who was admitted because of low back pain. The patient was previously treated for methicillin-susceptible Staphylococcus aureus (MSSA) discitis in the L1/L2 vertebral region with intravenous (IV) nafcillin through a peripherally inserted central catheter (PICC). However, he returned after four months with recurrent low back pain along with chills and fever. He was admitted for severe sepsis related to the L1-L2 region osteomyelitis and discitis.

The Infectious Disease department initially started the patient on IV vancomycin and cefepime; however, routine labs on the second day of IV antibiotics showed concern for pancytopenia with white blood cell count (WBC) decreased to 2.5 thou/mm³, Hgb to 6.2 g/dL, Hct to 20.8%, and platelets to 82 thou/mm³ from baseline values of WBC 3.9 thou/mm³, Hgb 8.3 g/dL, Hct 28%, and platelets 126 thou/mm³. Due to concern for pancytopenia in the setting of severe sepsis, extensive hematologic workup was pursued to evaluate for disseminated intravascular coagulation (DIC) and bone marrow suppression. The patient also had a positive fecal occult blood test, so the Gastroenterology department was consulted for esophagogastroduodenoscopy (EGD) and colonoscopy. Furthermore, despite appropriate outpatient treatment for MSSA osteodiscitis, the patient was bacteremic with Staphylococcus aureus. Hence, the Cardiology department was consulted to rule out cardiac valvular vegetation.

This case presents a unique case of pancytopenia involving elements of drug-induced aplastic anemia as well as DIC-related sepsis. The agranulocytosis may have been a consequence of drug reaction to IV vancomycin. The anemia and thrombocytopenia may have been caused by DIC. Repeat computed tomography (CT) guided spinal aspiration confirmed pan-sensitive Staphylococcus aureus infection of the L1/L2 vertebral region. Treatment was reverted to nafcillin monotherapy and fortunately his hematologic function normalized, avoiding the need for advanced treatments such as intravenous immunoglobulin infusion therapy (IVIG) or high dose steroids.

• agranulocytosis
• anemia
• disseminated intravascular coagulation
• drug toxicity
• pancytopenia
• sepsis
• vancomycin

• bone and joint infections
• drugs: infectious diseases
• haematology (incl blood transfusion)
• infections
• unwanted effects / adverse reactions

• AFM
• Antimicrobial peptoids
• Cytotoxicity
• Hydrophobicity
• Lipid membranes
• X-ray scattering