The lithium ions concentration in human serum and saliva was determined using dry-slide technology Vitros 250 Analyser (Ortho Clinical Diagnostic) and atomic absorption spectrometry Perkin Elmer 403 (AAS). We analyzed lithium ions in 100 serum and saliva specimens of patients after oral administration of lithium carbonate (3 x 300 mg) Jadran, Galen Laboratory Rijeka. Saliva and blood were taken 2 and 12 hours after the last dose. At the same time lithium ions at samples of blood and saliva were determined with both methods which showed high level of correlation. The mean difference of lithium ions between saliva and serum was statistically significant for p<0.05 using t student test. At saliva we got constant of elimination Kel = 0.02(-1)h and elimination half life (t(1/2)) was t(1/2)=34.6 h. For serum was t(1/2)= 24 h what means that lithium ions elimination is slower from saliva then from serum. That is the reason why probably concentration at saliva is higher then at serum. Lithium elimination is two compartment pharmacokinetic model where important part of compartment are saliva and salivary glands. At a certain point in medical treatment it could be expected to use controlled determination of lithium ions in saliva with serum as control.

Recently identified soluble circulating osteoprotegerin (OPG), a member of tumor necrosis factor receptor family, is the osteoclastogenesis inhibitory factor (OCIF). It acts as a "decoy" receptor for receptor activator of NF-kappaB ligand (RANKL) and antagonises RANKL/RANK activity. This way OPG exerts the protective effect on bone, which is also important in hyperparathyroidism. The studies measuring OPG levels in secondary hyperparathyroidism have shown contradictory results and inconsistent conclusions. The aim of our work was to evaluate OPG levels in hemodialysis patients and their correlation with the intensity of bone turnover, bone formation and bone resorption. Serum OPG levels, bone alkaline phosphatase activity (bALP) and beta-CrossLaps (CTx) were measured in a control group (n = 20, age 30+/-6.7 years) and in two groups of dialysis patients: the first group with serum intact parathyroid hormone (iPTH) concentration below 200 pg/ml (n = 28, age 62.6+/-14.8 years) and the second group with iPTH concentration above 200 pg/ml (n = 16, age 63.7+/-14.8 years). Compared to controls, serum OPG levels were 6.4-fold higher in dialysis patients. OPG levels in patients with high PTH were approximately 1.2-fold higher than in the low-PTH group. OPG correlated weakly with bALP (r = 0.277, p = 0.153), as well as with CTx (r = 0.018, p = 0.929) in the low-PTH group, and there was an insignificant negative correlation in the high-PTH group (r = -0.145, p = 0.593 and r = -0.219, p = 0.416, respectively). In conclusion, 6.4-fold increase in OPG might protect bone against intensive bone loss in hemodialysis patients, but this increase is probably not mediated by the increased bone formation; rather, it seems to be the consequence of the imbalance of bone kinetics in renal disease. The precise role of OPG in the pathogenesis of renal osteodystrophy remains unknown and establishing it requires further studies.

A statistically significant fast decrease of GLDH serum activity after a break in alcohol consumption has been confirmed. It is estimated that increased GLDH activity in the sera of alcohol dependents and its fast decrease after total abstinence has been restored are specific for alcohol addiction.

GLDH is an equally accurate marker of alcoholism in comparison to others, if its significantly faster decrease is taken into consideration. We strongly believe that watching changes in the activity of laboratory markers of alcoholism is an effective yet overlooked aid.

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