Pruritus in dialysis patients — ethiopathogenesis, clinical aspects and treatment

Świąd mocznicowy jest powszechnym powikłaniem u chorych poddawanych dializie. Dolegliwość obniża jakość życia chorych, może również pogarszać rokowanie związane z przeżyciem. Mechanizmy patofizjologiczne świądu u chorych dializowanych z powodu schyłkowej niewydolności nerek pozostają nieznane. Rozważa się rogowacenie i nadmierną suchość skóry, zaburzenia immunologiczne, zaburzenia systemu endogennych opioidów, neuropeptydów, równowagi elektrolitów, jonów dwuwartościowych, wtórną nadczynność przytarczyc, niedokrwistość z niedoboru żelaza oraz zmiany pH skóry. W związku z różnorodnością możliwych przyczyn brak również metod leczenia przyczynowego. W pracy dokonano przeglądu dyskutowanych czynników patogenetycznych świądu mocznicowego u chorych z przewlekłą niewydolnością nerek oraz podejmowanych prób terapeutycznych.Uraemic pruritus is a common complication in dialysis patients which reduces the quality of life and increases the mortality. The ethiopathogenesis of uremic pruritus has not been well explained. Several explanations for ureamic pruritus have been proposed like keratosis, xerosis, dysfunction of immune system, dysfunction of endogenous opioid system, nueropeptide disturbances, water-electrolyte imbalance, dysfunction of divalent cations metabolism, iron-deficiency anaemia and skin surface pH changes. Because of complex pathomechanism there is no known causal treatment of uraemic pruritus. The paper synthesizes the current data regarding ethiopathogenesis and treatment of uraemic pruritus

Recurrent syncope and hypocalcaemic cardiomyopathy as manifestations of Fahr's syndrome

In our report we would like to present a case of a 60-year-old patient with epileptic seizures, affective disturbances, only mild neurocognitive disorders and cardiomyopathy. A female patient was taken to the internal ward with a tentative diagnosis of recurrent syncope. Laboratory results disclosed severe hypocalcaemia, hypoparathyroidism, and hypothyroidism. An echocardiogram revealed left ventricle systolic dysfunction. Computed tomography revealed massive intracranial calcifications typical for Fahr's syndrome. Our patient demonstrated only mild neurological and psychiatric symptoms, but developed hypocalcaemic heart failure. It is possible that some cases of Fahr's syndrome remain undiscovered, particularly patients taken to internal wards with mild neurological or psychiatric signs

The impact of chronic alcohol overuse on heart function and prognosis: layer-specific longitudinal strain and mid-term outcome analysis

Background: The exact effects of alcohol drinking on cardiac function are not clear.Aims: This study aimed to determine the relationship between consumed amount of alcohol, myocardial injury, and prognosis.Methods: Myocardial function and cardiac outcomes were examined in subjects with chronic alcoholism by classical and strain echocardiographic parameters, including global (GLS) and layer-specific longitudinal strain of the endocardial (GLSendo) and epicardial (GLSepi) layer. One group of 65 alcohol-overusers (ALC), median (IQR, interquartile range) age 44 (38–51) years, was compared with 30 controls (CG).Results: Median (IQR) alcohol dose (in alcohol units, 1 AU = 1 g of ethanol) per week was 30 (12–51) AU in ALC and 0 in CG; P <0.001, and the mean (SD, standard deviation) drinking period was 16 (9) years. ALC patients demonstrated higher left ventricular (LV) mass and impaired diastolic function. The ALC group demonstrated lower median (IQR) LV ejection fraction (EF): 52% (37%–57%) vs 60% (55%–63%) (P <0.001); GLS: 17% (9%–20%) vs 19% (18%–21%) (P = 0.01); absolute layer-specific strain values. GLSendo <19% and GLSepi <15% predicted worsened mid-term prognosis, as did elevated N-terminal brain natriuretic peptide (NT-proBNP) and lower EF and GLS.Conclusions: Long-term alcohol overuse, even with a rather low reported median (IQR) dose of 4 (2–7) AU per day resulted in LV hypertrophy, diastolic and systolic dysfunction. Diminished GLS <18%, endocardial <19% and epicardial <15% layer strain predicted combined endpoints but did not significantly improve the prognostic power of tested models, based on NT-proBNP and EF in follow-up

Key Learning Outcomes for Clinical Pharmacology and Therapeutics Education in Europe: A Modified Delphi Study.

Harmonizing clinical pharmacology and therapeutics (CPT) education in Europe is necessary to ensure that the prescribing competency of future doctors is of a uniform high standard. As there are currently no uniform requirements, our aim was to achieve consensus on key learning outcomes for undergraduate CPT education in Europe. We used a modified Delphi method consisting of three questionnaire rounds and a panel meeting. A total of 129 experts from 27 European countries were asked to rate 307 learning outcomes. In all, 92 experts (71%) completed all three questionnaire rounds, and 33 experts (26%) attended the meeting. 232 learning outcomes from the original list, 15 newly suggested and 5 rephrased outcomes were included. These 252 learning outcomes should be included in undergraduate CPT curricula to ensure that European graduates are able to prescribe safely and effectively. We provide a blueprint of a European core curriculum describing when and how the learning outcomes might be acquired

The Effects of Simvastatin and Bisoprolol Therapy on the Lipids in Serum, Hepatic Biotransformation in Patients with Essential Hypertension and Hypercholesterolaemia Type ll

Wstęp: Celem badania była ocena hipolipemicznej interakcji simwastatyny i bisoprololu podczas leczenia obu lekami osób z łagodnym nadciśnieniem tętniczym ze współistniejącą hiperlipidemią typu II. Metody: Badaniem objęto 43 osoby (kobiety: 18, mężczyźni: 25 ) w wieku od 42 do 68 lat, stosujących dietę hipolipemiczną. Wyodrębniono dwie grupy chorych: I grupa - 20 osób z wyjściowym stężeniem cholesterolu całkowitego (TC) > 270 mg/dl i cholesterolu frakcji LDL (LDL-C) > 170 mg/dl, u których po 3-miesięcznej terapii simwastatyną (10-20 mg/d) dołączono bisoprolol (5-10 mg/d) przez okres 3 miesięcy, i II grupa - obejmująca 23 chorych z wyjściowym stężeniem TC 200-270 i LDL-C 130--170mg/dl, która przez 3 miesiące otrzymywała bisoprolol jako monoterapię (5-10 mg/d). Kontrolowano: lipidy surowicy, testy wątrobowe (AlAT, AspAT, bilirubina, AP, GGTP) i CPK. Ocenę metabolizmu wątrobowego przeprowadzono na podstawie wyników próby antypirynowej. Badania wykonano w grupie I przed rozpoczęciem leczenia oraz po 3 miesiącach terapii simwastatyną i po 3 miesiącach leczenia skojarzonego, zaś w grupie II - przed leczeniem i po 3 miesiącach monoterapii bisoprololem. Wyniki: W grupie I po 3 miesiącach terapii simwastatyną uzyskano istotne obniżenie stężenia TC, średnio o 27,2% i LDL-C o 32,9%. Po dołączeniu bisoprololu obserwowano dalsze znamienne obniżenie stężenia lipidów (TC o 6,8% i LDL-C o 12,2%). W grupie II bisoprolol spowodował nieznamienne obniżenie stężenia TC o 2,7%, LDL-C o 3,6%. W obu grupach nie odnotowano istotnych zmian testów wątrobowych i parametrów kinetyki antypiryny. Wnioski: 1. Bisoprolol nie powoduje zmniejszenia skuteczności hipolipemicznej simwastatyny, a nawet obserwuje się korzystny kierunek zmian cholesterolemii podczas leczenia skojarzonego. 2. Trzymiesięczna skojarzona terapia simwastatyną z bisoprololem nie nasila działań niepożądanych oraz nie wpływa na sprawność metabolizmu wątrobowego.Introduction The aim of the study was to estimate the hypolipemic interaction between simvastatin and bisoprolol during treatment of these drugs the patients with primary mild hypertension and dyslipidemia type II. Methods The study was undertaken in 43 patients (pts) with arterial hypertension (women: 18, men: 25, age 42-68). Patients were divided in two groups: I group-included 20 pts with basal total cholesterol (TC) > 270 mg/dl and LDL-cholesterol (LDL-C) > 170 mg/dl. After one-month run in period on hypolipemic diet they were treated firstly for 3 months with simvastatin (10-20 mg/daily) after that bisoprolol (5-10 mg/daily) was added for the next 3 months. II group - 23 pts with basal TC between 200 and 270 mg/dl; LDL-C between 130 and 170 mg/dl were given bisoprolol at the same dosage for 3 months. The rate of hepatic metabolism was estimated by antipyrine test. Results In group I after simvastatin therapy TC and LDL-C levels decreased significant. Added of bisoprolol caused the further significant decreasing of TC and LDL-C. In group II bisoprolol caused nonsignificant decreasing of TC, LDL-C and HDL-cholesterol and increasing of triglicerydes. In both groups we didn't observed significant changes of antipyrine test. Conclusions Bisoprolol doesn't change the hypolipemic efficacy of simvastatin and it is observed the positive effects therapy simvastatin with bisoprolol on lipids and hepatic biotransformation in patients with hypertension and hypercholesterolaemia type II

Acquired haemophilia A: a case report

Acquired haemophilia A is rare, autoimmune bleeding disorder caused by the production of autoantibodies against coagulation factor VIII (FVIII). The disorder affects 1.5 people per 1 million population a year, particularly the elderly. Unlike congenital haemophilia, the disease occurs in a similar proportion of men and women. An 86-year-old patient was admitted to the Department of Internal Medicine and Pharmacology with anaemia, progressive weakness, bruising in the subcutaneous tissue, and generaliesd stiffness of joints. Routine blood tests revealed isolated prolongation of activated partial thromboplastin time (aPTT) above 100 s. Activated partial thromboplastin time mixing test also showed prolongation of aPTT equal to 104.2 s. Factor VIII activity was 2%. The patient was referred to the Haematology Department, where a positive titre of anticoagulant 11 (BU) was obtained. After diagnosing acquired haemophilia A, the patient was administered activated prothrombin complex concentrate and prednisone, which resulted in clinical improvement and shortening of aPTT

Neuroprotective Effect of SGLT2 Inhibitors

Patients with diabetes are at higher risk of cardiovascular diseases and cognitive impairment. SGLT2 inhibitors (Empagliflozin, Canagliflozin, Dapagliflozin, Ertugliflozin, Sotagliflozin) are newer hypoglycemic agents with many pleiotropic effects. In this review, we discuss their neuroprotective potential. SGLT2 inhibitors (SGLT2i) are lipid-soluble and reach the brain/serum ratio from 0.3 to 0.5. SGLT receptors are present in the central nervous system (CNS). Flozins are not fully SGLT2-selective and have an affinity for the SGLT1 receptor, which is associated with protection against ischemia/reperfusion brain damage. SGLT2i show an anti-inflammatory and anti-atherosclerotic effect, including reduction of proinflammatory cytokines, M2 macrophage polarization, JAK2/STAT1 and NLRP3 inflammasome inhibition, as well as cIMT regression. They also mitigate oxidative stress. SGLT2i improve endothelial function, prevent remodeling and exert a protective effect on the neurovascular unit, blood-brain barrier, pericytes, astrocytes, microglia, and oligodendrocytes. Flozins are also able to inhibit AChE, which contributes to cognitive improvement. Empagliflozin significantly increases the level of cerebral BDNF, which modulates neurotransmission and ensures growth, survival, and plasticity of neurons. Moreover, they may be able to restore the circadian rhythm of mTOR activation, which is quite a novel finding in the field of research on metabolic diseases and cognitive impairment. SGLT2i have a great potential to protect against atherosclerosis and cognitive impairment in patients with type 2 diabetes mellitus