COVID-19 is a disease caused by the SARS-CoV-2 virus. The virus enters the human body through the respiratory system. Virus-loaded pneumocytes release various cytokines and inflammatory markers, resulting in lung injury and diffuse alveolar damage that may eventually culminate in acute respiratory distress syndrome. Calprotectin is a protein released by stimulated neutrophils and monocytes. During viral or bacterial infection of the respiratory system, the expression of calprotectin increases. CRP is an acute phase reactant. Stimulation of proinflammatory cytokines increases the concentration of CRP in plasma. The aim of this study was to analyze the results of serum calprotectin and CRP determined by immunoturbidimetric methods in order to detect differences depending on the severity of the clinical picture in COVID-19 patients or the absence of COVID-19 disease. The remaining samples of 143 subjects were used. Subjects were divided into four groups depending on the severity of the clinical condition, the condition after recovery, or as a group of healthy volunteers. Serum calprotectin and CRP concentrations were determined by immunoturbidimetric methods on the Beckman Coulter AU 5800 analytical system (Beckman Coulter, Brea, USA). The oldest persons were in the group of patients with the most severe clinical picture. Patients with more severe clinical pictures had high concentrations of serum calprotectin and CRP, while subjects who recovered from COVID-19 and subjects in the control group had lower concentrations. Serum calprotectin was higher in subjects who recovered from COVID-19 than in the control group, although these subjects were no longer in the acute phase of inflammation. Serum calprotectin concentrations showed a significant correlation with CRP. There is a greater distribution of more severe forms of COVID-19 disease in the elderly. Serum calprotectin and CRP concentrations are high in patients with severe clinical pictures. Serum calprotectin remains elevated for a longer period in subjects who recovered from COVID-19 and are no longer in the acute phase of inflammation, thus not following the pattern of a classic acute phase marker such as CRP whose concentration is not elevated in conditions without acute inflammation.