In the last ten years significant progress has been made in understanding of role of neutrophil granulocytes and their enzyme myeloperoxidase in the evolution and complications of atherosclerosis. Myeloperoxidase plays the role in the development of vulnerable plaque associated with the development of acute coronary syndrome. There is much evidence that suggests the role of myeloperoxidase in the development of vulnerable plaque. We investigate the value of myeloperoxidase as marker of the presence of vulnerable plaques in patients with acute coronary syndrome. Myeloperoxidase activity was significantly high in serum of the patients with the diagnosis of acute coronary syndrome as reflection of the presence of vulnerable plaques. Increase in myeloperoxidase activity in serum of patients with the diagnosis of acute coronary syndrome precedes to myocardial damage.

The increased protein concentration in cerebrospinal fluid is among most prominent biochemical parameter of intensified passage of macromolecules through blood-brain barrier. It is often found in cases of meningeal inflammation, neurodegeneration, neoplastic and traumatic processes developed on brain or spinal cord structures. Protein concentration in cerebrospinal fluid is often determined, but determination of albumin concentrations as well as mathematical models utilizing albumin are more reflective to the pathologic processes on the brain and spinal cord. Our study was limited to the determination of referent values for our laboratory for cerebrospinal fluid albumin concentrations, albumin quotient, as well as albumin transudat and exudat in the function of the age of probands. The results of the study show great agreement with previously published data.

Myeloperoxidase (MPO), a heme enzyme present in the primary granules of polymorphonuclear leukocytes (PMNs) participate in oxygen-dependent microbicidal activity of these cells. During the course of bacterial meningitis plenty of PMNs leave blood vessels and migrate to cerebrospinal fluid (CSF) space, and some of their MPO may become, extracellular. MPO activity in control CSF is low (Me = 0.5 U/L), comparing with patients CSF samples of all three groups of proteinorrachia where elevated values were found already on admission (3.5 U/L, 5.0 U/L and 12.0 U/L, respectively), with highest values found during second lumbal punction (5.5 U/L, 7.5 U/L and 14.0 U/L, respectively). Poor correlation was found between albumin quotient and MPO activity CSF/serum, but significant correlation between MPO in CSF and CSF PMNs count.

Bone tissue infections caused by non-specific agents (non-specific osteomyelitis) occur most frequently among children and young individuals demanding surgical and antibiotic therapy, although with unpredictable clinical outcome. While mobilization of cellular response to infectious agents takes place, a bulk of oxygen-derived free radicals emerge with concomitant participation of various elements of endogenous antioxidative defense. Vitamin C is an endogenous antioxidant active in the aqueous phase. It is very likely that ostoemyelitic patients already have some kind of disorder in specific antioxidant system due to hematogenic origin of non-specific osteomyelitis. Our results show that serum total vitamin C concentrations among patients with non specific osteomyelitis are not significantly different from those obtained among control subjects. However, we found significantly different concentrations of ascorbate, dehyroascorbate and their concentration ratio in serum within osteomyelitic patients that points to enlarged consumption of ascorbate even before the bone localization of infection took place