Vancomycin-Induced Profound Agranulocytosis!
Location
D.P. Culp Center Ballroom
Start Date
4-5-2024 9:00 AM
End Date
4-5-2024 11:30 AM
Poster Number
84
Name of Project's Faculty Sponsor
Devapiran Jaishankar
Faculty Sponsor's Department
Division of Medical Oncology
Competition Type
Competitive
Type
Poster Presentation
Presentation Category
Health
Abstract or Artist's Statement
A 31-year-old man with no significant medical history presented with fevers, malaise, back pain, and elevated outpatient blood pressure. He recently was admitted for osteomyelitis/diskitis of T11-T12 vertebrae and was on treatment with IV vancomycin and cefepime for six weeks. He also took Percocet and furosemide as needed. He denied IV drug use but admitted to occasional marijuana use. On admission, he had a normal temperature but a low white blood cell count (WBC) of 1.2 K/uL with an absolute neutrophil count (ANC) of 0 K/uL and a positive urine drug screen for cannabinoids and opioids. Erythrocyte sedimentation rate was elevated at 36 mm/hr and C- Reactive protein at 65.8 mg/dL. Imaging showed ankylosing spondylitis, hepatosplenomegaly, and a non-obstructing kidney stone. Echocardiogram was negative for infective endocarditis. Iron profile, ferritin, vitamin B12, and folate levels were within normal limits. A peripheral blood smear revealed significant leukopenia with neutropenia and did not show any blasts or dysplasia. Autoimmune workup revealed mildly elevated anti-ds-DNA antibody level. Drug-induced neutropenia was suspected, therefore vancomycin and cefepime were switched to daptomycin. A subsequent rash led to a change to minocycline, resolving the rash. WBC on day 4 came up to 5.9 K/uL with ANC 2.5 K/uL. Discharged with four weeks of minocycline, neutropenia was deemed likely drug-related, potentially due to vancomycin. Neutropenia is defined as a significant reduction in neutrophils, often indicated by an ANC below 1500 K/uL. It can be classified as severe neutropenia, and agranulocytosis with ANC less than 500 K/uL and 200 K/uL, respectively. Furthermore, an ANC of 0 K/uL is known as profound agranulocytosis. Non-chemotherapy drug-induced agranulocytosis is a rare but serious adverse effect and has a 5% mortality rate. Drugs associated with neutropenia include anti-psychotics, anti-thyroid medications, and anti-infectives like beta-lactams, sulfamethoxazole-trimethoprim, and vancomycin. Vancomycin, a glycopeptide antibiotic, is effective against various gram-positive bacteria, including Methicillin-Resistant Staphylococcus aureus. It carries rare but severe adverse effects such as ototoxicity, nephrotoxicity, and hypersensitivity reactions. Neutropenia is seen in about 2% of patients using vancomycin, with potential complications like febrile agranulocytosis. The average onset of neutropenia has been noted to be around 20 days after vancomycin exposure. Although its mechanism remains incompletely understood, hypotheses suggest immune-mediated damage or direct myeloid cell line injury. Owing to their complexity and unavailability, assays like flow cytometry, ELISA, immunoblotting, and granulocyte agglutination, to detect neutrophil drug-dependent antibodies are scarcely performed. Patients may present with infection-like symptoms with a risk of septicemia, necessitating prompt management involving discontinuation of the offending agent, administration of broad-spectrum antibiotics, and in high-risk cases, granulocyte colony-stimulating factors. In our case, although cefepime could have been the inciting agent, vancomycin induced cytopenias are more reported in clinical practice Our case highlights profound agranulocytosis as a possible severe adverse effect of vancomycin. It warrants vigilance, and regular monitoring of white blood cell counts with prompt recognition and aggressive management vital to mitigate the risk of septicemia and mortality.
Vancomycin-Induced Profound Agranulocytosis!
D.P. Culp Center Ballroom
A 31-year-old man with no significant medical history presented with fevers, malaise, back pain, and elevated outpatient blood pressure. He recently was admitted for osteomyelitis/diskitis of T11-T12 vertebrae and was on treatment with IV vancomycin and cefepime for six weeks. He also took Percocet and furosemide as needed. He denied IV drug use but admitted to occasional marijuana use. On admission, he had a normal temperature but a low white blood cell count (WBC) of 1.2 K/uL with an absolute neutrophil count (ANC) of 0 K/uL and a positive urine drug screen for cannabinoids and opioids. Erythrocyte sedimentation rate was elevated at 36 mm/hr and C- Reactive protein at 65.8 mg/dL. Imaging showed ankylosing spondylitis, hepatosplenomegaly, and a non-obstructing kidney stone. Echocardiogram was negative for infective endocarditis. Iron profile, ferritin, vitamin B12, and folate levels were within normal limits. A peripheral blood smear revealed significant leukopenia with neutropenia and did not show any blasts or dysplasia. Autoimmune workup revealed mildly elevated anti-ds-DNA antibody level. Drug-induced neutropenia was suspected, therefore vancomycin and cefepime were switched to daptomycin. A subsequent rash led to a change to minocycline, resolving the rash. WBC on day 4 came up to 5.9 K/uL with ANC 2.5 K/uL. Discharged with four weeks of minocycline, neutropenia was deemed likely drug-related, potentially due to vancomycin. Neutropenia is defined as a significant reduction in neutrophils, often indicated by an ANC below 1500 K/uL. It can be classified as severe neutropenia, and agranulocytosis with ANC less than 500 K/uL and 200 K/uL, respectively. Furthermore, an ANC of 0 K/uL is known as profound agranulocytosis. Non-chemotherapy drug-induced agranulocytosis is a rare but serious adverse effect and has a 5% mortality rate. Drugs associated with neutropenia include anti-psychotics, anti-thyroid medications, and anti-infectives like beta-lactams, sulfamethoxazole-trimethoprim, and vancomycin. Vancomycin, a glycopeptide antibiotic, is effective against various gram-positive bacteria, including Methicillin-Resistant Staphylococcus aureus. It carries rare but severe adverse effects such as ototoxicity, nephrotoxicity, and hypersensitivity reactions. Neutropenia is seen in about 2% of patients using vancomycin, with potential complications like febrile agranulocytosis. The average onset of neutropenia has been noted to be around 20 days after vancomycin exposure. Although its mechanism remains incompletely understood, hypotheses suggest immune-mediated damage or direct myeloid cell line injury. Owing to their complexity and unavailability, assays like flow cytometry, ELISA, immunoblotting, and granulocyte agglutination, to detect neutrophil drug-dependent antibodies are scarcely performed. Patients may present with infection-like symptoms with a risk of septicemia, necessitating prompt management involving discontinuation of the offending agent, administration of broad-spectrum antibiotics, and in high-risk cases, granulocyte colony-stimulating factors. In our case, although cefepime could have been the inciting agent, vancomycin induced cytopenias are more reported in clinical practice Our case highlights profound agranulocytosis as a possible severe adverse effect of vancomycin. It warrants vigilance, and regular monitoring of white blood cell counts with prompt recognition and aggressive management vital to mitigate the risk of septicemia and mortality.