Once it became clear that inflammation takes place in the modulation of different degenerative disease including neurodegenerative, cardiovascular, diabetes and cancer the researchers has started intensive programs evaluating potential role of non-steroidal anti-inflammatory drugs (NSAIDs) in the prevention or therapy of these diseases. This review discusses the novel mechanism of action of NSAIDs and its potential use in the pharmacotherapy of neurodegenerative, cardiovascular, diabetes and cancer diseases. Many different molecular and cellular factors which are not yet fully understood play an important role in the pathogenesis of inflammation, axonal damage, demyelination, atherosclerosis, carcinogenesis thus further NSAID studies for a new potential indications based on precise pharmacotherapy model are warranted since NSAIDs are a heterogeneous group of medicines with relative different pharmacokinetics and pharmacodynamics profiles. Hopefully the new data from studies will fill in the gap between experimental and clinical results and translate our knowledge into successful disease therapy.

Background and objective: Irrational use of nonsteroidal anti-inflammatory drugs (NSAIDs) is the main cause of adverse effects-associated hospitalizations among all medication groups leading to extremely increased costs for health care. Pharmacoepidemiological studies can partly reveal such issues and encourage further decisions. Therefore, the aim of our study was to evaluate the utilization of non-opioid analgesics (ATC classification N02B and M01A) in Lithuania, and to compare it with that of other Baltic and Scandinavian countries in terms of compliance to the WHO pain treatment guidelines and the EMA safety recommendations on NSAID use. Materials and methods: The dispensing data were obtained from the sales analysis software provider in the Baltic countries (SoftDent, Ltd., Kaunas, Lithuania); State Medicine Control Agencies of Lithuania, Latvia, and Estonia; Norwegian Prescription Database; Swedish Database for Medicines; and Danish Prescription Database. Data included the utilization of both prescription and over-the-counter drugs. Utilization was expressed in defined daily doses (DDD)/1000 inhabitants/day. Results: During the 11-year period, the utilization of drugs belonging to the N02B and M01A groups increased by 22.8%, from 58.37 in 2005 to 71.68 DDD/1000 inhabitants/day in 2016 in Lithuania. Contrary to the WHO guidelines on pain management, all Baltic countries were more likely to use NSAIDs than other analgesics and antipyretics: in 2015, the drugs of the M01A group were used 6.04, 5.79, and 6.11 times more than those of N02B in Lithuania, Estonia, and Latvia, respectively, whereas the Scandinavian countries preferred the N02B to the M01A group: in Denmark and Sweden, the utilization of other analgesics and antipyretics was 2.33 and 1.24, respectively, times higher than that of NSAIDs. In Norway, the use of both groups was similar. In the Scandinavian countries, paracetamol was the analgesic of first choice, whereas, in Lithuania, it took only the third place. The most popular drug in Lithuania was diclofenac, and its utilization accounted for 30.04% of all non-opioid analgesics in 2016. Although the European Medicines Agency (EMA) restricted the use of certain NSAIDs, i.e., cyclooxygenase-2 (COX-2) inhibitors, nimesulide, and diclofenac, their use consistently increased by 15.91, 2.83, and 1.41 times, respectively, showing incompliance with the international guidelines. Conclusions: Neither the EMA safety policy on NSAID use nor the WHO pain treatment guidelines had a sufficient impact on the rational use of NSAIDs in Lithuania. The use of NSAIDs restricted by the EMA (diclofenac, COX-2 inhibitors, nimesulide, and piroxicam) remains high or even increases, while the utilization of safer alternatives (paracetamol and naproxen) remains relatively low as compared with the Scandinavian countries. Incompliance with international guidelines may result in increased morbidity, mortality and higher costs for health care.

About half a century ago, Eugene Braunwald, a father of modern cardiology, shared a revolutionary belief that “time is muscle”, which predetermined never-ending effort to preserve the unaffected myocardium. In connection to that, researchers are constantly trying to better comprehend the ongoing changes of the ischemic myocardium. As the latest studies show, metabolic changes after acute myocardial infarction (AMI) are inconsistent and depend on many constituents, which leads to many limitations and lack of unification. Nevertheless, one of the promising novel mechanistic approaches related to iron metabolism now plays an invaluable role in the ischemic heart research field. The heart, because of its high levels of oxygen consumption, is one of the most susceptible organs to iron-induced damage. In the past few years, a relatively new form of programmed cell death, called ferroptosis, has been gaining much attention in the context of myocardial infarction. This review will try to summarize the main novel metabolic pathways and show the pivotal limitations of the affected myocardium metabolomics.

The AUC (area under the concentration time curve) is considered the pharmacokinetic exposure parameter best associated with clinical effects. Unfortunately, no prospective studies of clinical outcomes have been conducted in adult transplant recipients to investigate properly the potential benefits of AUC_(0–12) monitoring compared to the C₀-guided therapy. The aim of the present study was to compare two methods, C₀ (through level) and AUC_(0–12) (area under the concentration time curve), for assessing cyclosporine and tacrolimus concentrations. The study included 340 kidney recipients. The AUC_(0–12) was estimated using a Bayesian estimator and a three-point limited sampling strategy. Therapeutic drug monitoring of tacrolimus performed by using AUC_(0–12) and C₀ showed that tacrolimus in most cases is overdosed when considering C₀, while determination of the AUC_(0–12) showed that tacrolimus is effectively dosed for 27.8–40.0% of patients receiving only tacrolimus and for 25.0–31.9% of patients receiving tacrolimus with MMF (mycophenolate mofetil). In the 1–5 years post-transplantation group, 10% higher CsA (cyclosporine) dose was observed, which was proportionate with a 10% higher AUC_(0–12) exposure value. This indicates good compatibility of the dosage and the AUC(0–12) method. The Bland–Altman plot demonstrated that C₀ and AUC_(0–12) might be interchangeable methods, while the ROC (receiver operating characteristic) curve analysis of the C₀/AUC_(0–12) ratio in the tacrolimus-receiving patient group demonstrated reliable performance to predict IFTA (interstitial fibrosis and tubular atrophy) after kidney transplantation, with an ROC curve of 0.660 (95% confidence interval (CI): 0.576–0.736), p < 0.01. Moreover, AUC_(0–12) and C₀ of tacrolimus depend on concomitant medication and adjustment of the therapeutic range for AUC_(0–12) might influence the results.

Amiodarone is an antiarrhythmic drug which is used to treat and prevent several dysrhythmias. This includes ventricular tachycardia and fibrillation, wide complex tachycardia, as well as atrial fibrillation (AF) and paroxysmal supraventricular tachycardia. Amiodarone may prove to be the agent of choice where the patient is hemodynamically unstable and unsuitable for direct current (DC) cardioversion. Although, it is not recommended for long-term use. The physician might encounter issues when differentiating amiodarone-induced lung toxicity with suspicion of interstitial lung disease, cancer or vasculitis. Adverse drug reactions are difficult to confirm and it leads to serious problems of pharmacotherapy. A 78-year-old Caucasian male pensioner complaining of fever, dyspnea, malaise, non-productive cough, fatigue, weight loss, diagnosed with acute respiratory failure with a 16-year long history of amiodarone use and histologically confirmed temporal arteritis with long-term glucocorticosteroid (GCC) therapy. Patient was treated for temporal arteritis with GCC for ~ 1 year, then fever and dyspnea occurred, and the patient was hospitalized for treatment of bilateral pneumonia. Chest X-ray and chest high resolution computed tomography (HRCT) indicated several possible diagnoses: drug-induced interstitial lung disease, autoimmune interstitial lung disease, previously excluded pulmonary TB. Amiodarone was discontinued. Antibiotic therapy for bilateral pneumonia was started. Fiberoptic bronchoscopy with bronchial washings and brushings was performed. Acid fast bacilli (AFB) were found on Ziehl-Nielsen microscopy and tuberculosis (TB) was confirmed (later confirmed to be Mycobacterium tuberculosis in culture), initial treatment for TB was started. After a few months of treating for TB, patient was diagnosed with pneumonia and sepsis, empiric antibiotic therapy was prescribed. After reevaluation and M. Tuberculosis identification, the patient was referred to the Tuberculosis hospital for further treatment. After 6 months of TB treatment, pneumonia occurred which was complicated by sepsis. Despite the treatment, multiple organ dysfunction syndrome evolved and patient died. Probable cause of death: pneumonia and sepsis. The current clinical case emphasizes issues that a physician may encounter in the differential diagnostics of amiodarone-induced lung toxicity with other lung diseases.