Can osteomyelitis cause an elevation in B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP)?

Can Osteomyelitis Elevate BNP?

Yes, osteomyelitis can elevate BNP through the systemic inflammatory response and sepsis it triggers, even in patients without heart failure or cardiac dysfunction. 1, 2

Mechanism of BNP Elevation in Infection

• Systemic inflammation from bacterial infections directly stimulates BNP production, independent of cardiac dysfunction or volume overload. 2, 3
• Microbial infections cause BNP elevation through inflammatory mediators and cytokine release, with the presence of bacterial infection being an independent predictor of elevated BNP (adjusted odds ratio 9.8). 2
• In experimental models of bacterial endotoxemia, NT-proBNP increases continuously over 6 hours in healthy volunteers with normal cardiac function, correlating with body temperature, heart rate, and inflammatory markers like C-reactive protein. 3

Clinical Evidence from Infection Studies

• BNP levels are significantly elevated in patients with community-acquired bacterial infections without severe sepsis or shock (median 25 pg/mL vs. 13 pg/mL in controls, p=0.01), and these levels decrease with infection resolution (to 16 pg/mL pre-discharge, p=0.0002). 2
• The magnitude of BNP elevation in bacterial infections is influenced by infection location (lower respiratory tract infections cause higher elevations) and comorbidities like diabetes mellitus. 2
• Sepsis independently elevates BNP and reduces its diagnostic accuracy for heart failure, requiring cautious interpretation in infected patients. 1

Diagnostic Implications for Osteomyelitis

• When interpreting elevated BNP in a patient with osteomyelitis, the elevation reflects "cardiorenal distress" from systemic inflammation rather than necessarily indicating heart failure. 4
• Multiple disorders in critically ill patients—including sepsis, shock, and various infections—cause elevated BNP and NT-proBNP to different degrees, serving as markers of illness severity and prognosis rather than purely cardiac dysfunction. 5
• BNP elevation in the setting of infection does not represent a "false positive" but rather a pathological process causing ventricular stress that requires different interpretation, analogous to troponin elevations from non-ACS causes. 1

Critical Clinical Pitfalls

• Do not assume elevated BNP in osteomyelitis patients automatically indicates heart failure—echocardiography is required for definitive cardiac assessment. 4
• Consider that osteomyelitis with bacteremia or sepsis can elevate BNP through multiple mechanisms: direct inflammatory effects, increased metabolic demand, potential myocardial depression from sepsis, and cytokine-mediated cardiac stress. 2, 3, 5
• Renal dysfunction commonly accompanies severe infections and further elevates BNP through decreased clearance, compounding the interpretation challenge. 1, 4, 6
• Serial BNP measurements may help distinguish infection-related elevation from cardiac dysfunction: BNP should decrease as the infection resolves if cardiac dysfunction is not the primary driver. 2

Practical Approach

• In patients with osteomyelitis and elevated BNP, obtain echocardiography rather than relying on BNP alone to determine if cardiac dysfunction is present. 4
• Check renal function (creatinine, eGFR) because kidney dysfunction significantly amplifies BNP elevation (patients with renal dysfunction and normal hearts have BNP 258.6 pg/mL vs. 92.4 pg/mL without renal dysfunction). 4, 6
• Measure cardiac troponins to assess for concurrent myocardial injury, as sepsis can cause myocardial depression. 1
• Expect BNP to normalize as osteomyelitis is treated and systemic inflammation resolves—persistent elevation after infection control suggests underlying cardiac pathology. 2