Laboratory medicine in arterial hypertension.

In the initial diagnostics of arterial hypertension (AH) laboratory medicine is a cornerstone, along with a blood pressure (BP) measurement and an electrocardiogram. It mainly refers to routine blood and urine tests for diagnosis and monitoring primary hypertension and its associated conditions such as asymptomatic hypertension-mediated organ damage, chronic kidney disease and hypertensive disorders of pregnancy. In addition, long term non-fatal and fatal risks for cardiovascular (CV) events in hypertension are assessed based on clinical and laboratory data. Furthermore, laboratory medicine is involved in the management of hypertension, especially in monitoring the disease progression. However, antihypertensive drugs may interfere with laboratory test results. Diuretics, especially thiazides, can affect blood and urine sodium concentrations, or angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can affect the blood biomarkers of the renin-angiotensin-aldosterone system (RAAS). It's dysfunction plays a critical role in primary aldosteronism (PA), the most common endocrine disorder in secondary hypertension, which accounts for only small proportion of AH in relative terms but substantial proportion of hypertensives in absolute terms, affecting younger population and carrying a higher risk of CV mortality and morbidity. When screening for PA, aldosterone-to-renin ratio still contributes massively to the increased incidence of the disease, despite certain limits. In conclusion, laboratory medicine is involved in the screening, diagnosis, monitoring and prognosis of hypertension. It is of great importance to understand the preanalytical and analytical factors influencing final laboratory result.

Serum bicarbonate stability study at room temperature - influence of time to centrifugation and air exposure on bicarbonate measurement reported according to the CRESS checklist.

OBJECTIVES: The aim was to evaluate the stability of serum bicarbonate at room temperature, depending on time to centrifugation and air exposure. METHODS: Stability study was conducted in the laboratory of Clinical Hospital Centre Rijeka, Croatia in January-February 2022. Nine samples from 10 volunteers were collected in clot activator gel tubes (Greiner Bio-One). Bicarbonate was measured on Beckman Coulter AU480 (Beckman Coulter, Brea, USA). Three tubes were left at room temperature for 30 min, three tubes for 2 h, three tubes for 4 h until centrifugation. First tube from first group (baseline) was measured immediately after centrifugation. Other measurements were expressed as percentage deviation (PD%) from baseline. First tube was remeasured after 1 and 2 h (OT_0h_1h; OT_0h_2h). Second and third tubes were opened 1 and 2 h after centrifugation (C_0h_1h; C_0h_2h). Second group of tubes was processed the same way with 2-hour centrifugation delay (WB_2h; OT_2h_1h; OT_2h_2h; C_2h_1h; C_2h_2h), and third group with 4-hour delay (WB_4h; OT_4h_1h; OT_4h_2h; C_4h_1h; C_4h_2h). PD% was compared to Maximum Permissible Difference (MPD=5.69%). MedCalc statistical software was used (MedCalc, Ostend, Belgium). RESULTS: Bicarbonate baseline mean value (range) was 27.3 (23.4-29.6) mmol/L. Obtained PD% (95%CI) were: C_0h_1h 0.46 (-1.21, 2.12); C_0h_2h 0.18 (-2.22, 2.57); OT_0h_1h -6.46 (-7.57, -5.36); OT_0h_2h -10.67 (-12.13, -9.21); WB_2h -0.15 (-2.04, 1.74); C_2h_1h 0.01 (-1.52, 1.54); C_2h_2h -0.40 (-2.65, 1.85); OT_2h_1h -5.43 (-7.30, -3.55); OT_2h_2h -11.32 (-13.57, -9.07); WB_4h -0.85 (-3.28, 1.58); C_4h_1h -2.52 (-4.93, 0.11); C_4h_2h -3.02 (-5.62, 0.43); OT_4h_1h -7.34 (-9.64, -5.05); OT_4h_2h -11.85 (-14.38, -9.33). CONCLUSIONS: Serum bicarbonate is stable for 4 h in closed uncentrifuged tubes, another 2 h in closed tubes after centrifugation, and is unstable within 1 h in opened tube.

Prevalence of Aminotransferase Macroenzymes in Rheumatoid Arthritis Patients and Impact on Their Management.

INTRODUCTION: Rheumatoid arthritis (RA) treatment can be hepatotoxic, but liver enzymes can be falsely elevated due to macroenzyme presence. Macroenzymes are often found in autoimmune diseases, but prevalence and effect on treatment is unclear. This study aimed to determine aminotransferase macroenzyme prevalence and effect in RA patients. MATERIALS AND METHODS: This study included consecutive RA patients without liver disease sent for laboratory tests. Samples with elevated AST or ALT were processed for macroenzymes. Presence was determined using polyethylene glycol precipitation (PEG). RESULTS: Out of 126 patients, 21 had elevated aminotransferase levels. Due to liver disease, 6 patients were excluded, another 3 were unavailable for informed consent, leaving 12 patients for inclusion. Out of 12 patients, 1 had increased AST levels, 2 increased ALT levels, and 9 both. Macro-ALT was detected in 5/11 patients, 1 also had macro-AST. Out of 5 patients with macroenzymes, treatment change was seen in 3/5 patients, imaging in 2/5, both in 2/5. CONCLUSION: Elevated liver enzymes in RA patients is not always indicative of hepatotoxicity, as shown by the fact that about half of patients in our study had macroenzymes detected. Before assuming drug hepatotoxicity and changing treatment or ordering imaging, rheumatologists could consider macroenzyme presence.