The Platelet-to-Lymphocyte Ratio as an Inflammatory Marker in Rheumatic Diseases.

The platelet-to-lymphocyte ratio (PLR) has emerged as an informative marker revealing shifts in platelet and lymphocyte counts due to acute inflammatory and prothrombotic states. PLR has been extensively examined in neoplastic diseases accompanied by immune suppression and thrombosis, which can be predicted by combined blood cell counts and their ratios. Several large observational studies have demonstrated the value of shifts in PLR in evaluating the severity of systemic inflammation and predicting infections and other comorbidities, in inflammatory rheumatic diseases. The value of PLR as an inflammatory marker increases when its fluctuations are interpreted along with other complementary hematologic indices, particularly the neutrophil-to-lymphocyte ratio (NLR), which provides additional information about the disease activity, presence of neutrophilic inflammation, infectious complications, and severe organ damage in systemic lupus erythematosus. PLR and NLR have high predictive value in rheumatic diseases with predominantly neutrophilic inflammation (e.g., Behçet disease and familial Mediterranean fever). High PLR, along with elevated platelet count, is potentially useful in diagnosing some systemic vasculitides, particularly giant-cell arteritis. A few longitudinal studies on rheumatic diseases have demonstrated a decrease in PLR in response to anti-inflammatory therapies. The main limitations of PLR studies are preanalytical faults, inadequate standardization of laboratory measurements, and inappropriate subject selection. Nonetheless, accumulating evidence suggests that PLR can provide valuable information to clinicians who encounter multisystem manifestations of rheumatic diseases, which are reflected in shifts in platelet, lymphocyte, neutrophil, or monocyte counts. Interpretation of PLR combined with complementary hematologic indices is advisable to more accurately diagnose inflammatory rheumatic diseases and predict related comorbidities.

Colchicine as an anti-inflammatory and cardioprotective agent.

INTRODUCTION: Colchicine has been successfully used for the treatment of neutrophilic disorders such as familial Mediterranean fever (FMF), Behçet disease (BD) and gout. There is a growing interest in its cardiovascular effects. AREAS COVERED: A MEDLINE/PubMed search for English articles published from January 1972 to June 2015 was completed using the following terms: therapy, pharmacokinetics, efficiency, side effects, toxicity, heart, colchicine, inflammation, FMF, amyloidosis, BD, gout, cardiovascular disorders, pericarditis, arrhythmias, inflammation, neutrophils, platelets. EXPERT OPINION: By targeting neutrophils, endothelial cells and platelets, inhibiting mitosis, vascular hyperplasia and fibrosis, colchicine improves outcomes of pericarditis, myocardial ischemia and coronary interventions. Studies in neutrophilic rheumatic diseases and cardiovascular disorders demonstrated that oral colchicine at doses of 0.5 - 2.5 mg/daily is useful for treating pericarditis, myocardial ischemia and coronary occlusion. In rheumatic and cardiovascular disorders, therapeutic doses of the drug reduce C-reactive protein to levels below 2 mg/L, prevent myocardial damage and preserve normal values of atrial and ventricular impulse generation. One of the drug's frequent side effects is diarrhea, which is treated by diet modification or temporary discontinuation of the therapy. Certain drugs (macrolides, statins), comorbidities and certain genetic factors increase risk of colchicine toxicity.

Mean platelet volume: a link between thrombosis and inflammation?

Platelet activation is a link in the pathophysiology of diseases prone to thrombosis and inflammation. Numerous platelet markers, including mean platelet volume (MPV), have been investigated in connection with both thrombosis and inflammation. This review considers MPV as a prognostic and therapeutic marker as well as the factors influencing its measurement. Established cardiovascular risk factors, such as smoking, hypertension, dyslipidemia, and diabetes, can influence MPV, depending on confounding factors. Low-grade inflammation is one such factor. Evidence, particularly derived from prospective studies and a meta-analysis, suggest a correlation between an increase in MPV and the risk of thrombosis. High MPV associates with a variety of established risk factors, cardio- and cerebrovascular disorders, and low-grade inflammatory conditions prone to arterial and venous thromboses. High-grade inflammatory diseases, such as active rheumatoid arthritis or attacks of familial Mediterranean fever, present with low levels of MPV, which reverse in the course of anti-inflammatory therapy. Lifestyle modification, antihypertensive, lipid lowering and diet therapies can also affect MPV values, but these effects need to be investigated in large prospective studies with thrombotic endpoints.