Povezanost leptina i adiponektina sa smrtnošću tijekom prve godine nakon osteoporotskog prijeloma proksimalnog femura [Association of leptin and adiponectin with one year mortality after osteoporotic fracture of the proximal femur]

Osteoporotic fracture of the proximal femur is a serious injury that results in significant impairment of functional status and decreased life expectancy. Leptin and adiponectin are a part of a adipocytokines family - which are hormones secreted by adipocytes. Numerous studies have examined their impact on mortality both in general and specific populations, but none of them was conducted in patients with hip fracture. The aim of this study was to determine the influence of leptin and adiponectin, as well as routine laboratory and antropomethric parameters on mortality during the first year after osteoporotic fractures of the proximal femur. A total of 236 consecutive patients (59 males) with hip fractures were followed over a one-year period. Patient age, gender, type of fracture, type of treatment, time from admission to surgery, type of anaesthesia, body mass index (BMI), and electrocardiograms were recorded. Routine preoperative laboratory tests including osteocalcin and beta-crosslaps were masured at admission. On the last day of hospitalization, the blood sample was taken and serum was separated and stored at -80 ° C. Later, that serum was used to determine adiponectin, insulin and leptin concentrations. One year after the fracture mortality rate was 28.4%. Older patients had higher mortality regardless of other parameters (HR 1.111, 95% CI 1:07 to 1:16, P <0.001). Male gender was a risk factor for mortality (OR 2.88, 95% CI 1:35 to 6:11, P = 0.006). Low albumin levels (P=0.46, HR 0,949, 95% CI 0,902-0,999), high adiponectin (P=0,022, HR 1,063, 95 % CI 1.009-1.120) and high β-cross laps levels (P=0,001, HR 4,632, 95%CI 1.874-11.452) were independent predictors of mortality within the first year after the fracture. There was no correlation between leptin and one-year mortality. In summary, gender, age, albumin, adiponectin and beta-crosslaps are independent predictors of one-year mortality in patients with fractures of the proximal femur

Hiperkalijemija izazvana nebivololom: prikaz slučaja

In this article, we document a conclusive case of nebivolol-induced hyperkalemia for the first time in the known medical literature. Hyperkalemia is associated with serious conditions such as cardiac arrhythmias and sudden cardiac death. Nebivolol was not known to cause hyperkalemia, and this event is not listed in its summary of product characteristics (SmPC). For older beta blockers, hyperkalemia is recognized as a rare adverse event linked to cytochrome P450 2D6 (CYP2D6) polymorphism and poor drug degradation. Our patient, a 47-year-old woman taking nebivolol for hypertension developed persistent hyperkalemia, with serum potassium levels up to 6.4 mmol/L. After extensive diagnostic evaluation and exclusion of other known conditions leading to hyperkalemia, its cause remained occult. Since hyperkalemia coincided with increased doses of nebivolol, dose reduction and discontinuation were attempted, resulting in normalized serum potassium. Poor drug metabolism could not explain this adverse effect, since pharmacogenetic testing showed no relevant aberrations. In conclusion, hyperkalemia is a harmful adverse event with possible lethal outcome, and it may be caused by nebivolol. Therefore, medical professionals have to be aware of this side effect and hyperkalemia should be listed as an adverse event in nebivolol SmPC.U ovom članku je po prvi put u poznatoj medicinskoj literaturi dokumentiran slučaj hiperkalijemije izazvane nebivololom. Hiperkalijemija je povezana s ozbiljnim stanjima kao što su srčane aritmije i iznenadna srčana smrt. Za nebivolol dosad nije bilo poznato da može uzrokovati hiperkalijemiju pa ona nije navedena u sažetku opisa svojstava lijeka. Za starije beta blokatore hiperkalijemija je poznata kao rijetka nuspojava lijeka vezana uz polimorfizam citokroma P450 2D6 (CYP2D6) i slabiju razgradnju lijeka. Nebivolol je uzimala i naša 47-godišnja bolesnica zbog hipertenzije, s posljedičnim razvojem refraktorne hiperkalijemije, s razinama serumskog kalija do 6,4 mmol/L. Nakon opsežne dijagnostičke evaluacije i isključenja drugih poznatih uvjeta koji dovode do hiperkalijemije njen uzrok nije razjašnjen. Pojava hiperkalijemije se podudarala s povećanjem doze nebivolola, a smanjenje doze i prekid terapije doveli su do normalizacije serumskog kalija. Ova nuspojava nije se mogla objasniti usporenim metabolizmom lijeka budući da farmakogenetičko testiranje nije pokazalo relevantnih aberacija. U zaključku napominjemo da je hiperkalijemija štetan događaj s mogućim smrtnim ishodom koja može biti uzrokovana nebivololom. Stoga liječnici moraju biti svjesni ove nuspojave i hiperkalijemija treba biti navedena kao moguća nuspojava u sažetku opisa svojstava ovoga lijeka

Chronic kidney disease mineral bone disorder

Chronic kidney disease – mineral bone disease (CKD-MBD) is a syndrome defined as a systemic mineral metabolic disorder associated with CKD. The term renal osteodystrophy, as a part of CKD-MBD, indicates a pathomorphological concept of bone lesions. High morbidity and mortality of CKD patients is a consequence of CKD-MBD. The pathogenesis of this syndrome is not completely understood, but undoubtedly the development of mineral and bone disorder begins in the earliest stages of CKD. The diagnosis is made by non-invasive methods (biochemistry, x-ray, ultrasound, etc.) and bone biopsy as an invasive method. In addition to new drugs, e.g. non-calcium phosphate binders, vitamin D analogs, calcimimetics, prevention and treatment is still a major challenge for the nephrologist. In this article we will briefly discuss the pathophysiology, diagnosis, prevention and treatment of CKD-MBD

Cytotoxicity of Selected Pyridinium Oximes in Human SH-SY5Y Neuroblastoma Cell Line

Pyridinium oximes are pharmacologically important nucleophylic agents acting as effective antidotes against poisoning by organophosphorus compounds that inhibit acetylcholinesterase (AChE; EC 3.1.1.7.). In this study, the cytotoxicity of 1-phenacylpyridinium-4-aldoxime chloride (FEPA-4) was analyzed in human SH-SY5Y neuroblastoma cell line highly expressing acetylcholinesterase. The concentrations of 0.5, 1, 2 and 4 mmol dm–3 and time-dependent effects at 1, 3, 6, 12 and 24 hours were tested in comparison with non-treated cells. In addition, neuroblastoma cells were treated with a well known antidote 1,1\u27-bis(pyridinium-4-aldoxime)trimethylene dibromide (TMB-4) at the concentration of 0.8 mmol dm–3, the highest studied concentration which in several non-neural cellular models induced no cytotoxicity. Cytotoxic effects i.e. altered cellular morphology and decreased cellular volume density quantified by stereological method were observed in FEPA-4 treated cells, while no cytotoxic effect was observed for 0.8 mmol dm–3 TMB-4. Possible mechanisms of observed FEPA-4 cytotoxicity in neuroblastoma cells are discussed

Chronic kidney disease mineral bone disorder

Chronic kidney disease – mineral bone disease (CKD-MBD) is a syndrome defined as a systemic mineral metabolic disorder associated with CKD. The term renal osteodystrophy, as a part of CKD-MBD, indicates a pathomorphological concept of bone lesions. High morbidity and mortality of CKD patients is a consequence of CKD-MBD. The pathogenesis of this syndrome is not completely understood, but undoubtedly the development of mineral and bone disorder begins in the earliest stages of CKD. The diagnosis is made by non-invasive methods (biochemistry, x-ray, ultrasound, etc.) and bone biopsy as an invasive method. In addition to new drugs, e.g. non-calcium phosphate binders, vitamin D analogs, calcimimetics, prevention and treatment is still a major challenge for the nephrologist. In this article we will briefly discuss the pathophysiology, diagnosis, prevention and treatment of CKD-MBD

Chronic kidney disease mineral bone disorder

Chronic kidney disease – mineral bone disease (CKD-MBD) is a syndrome defined as a systemic mineral metabolic disorder associated with CKD. The term renal osteodystrophy, as a part of CKD-MBD, indicates a pathomorphological concept of bone lesions. High morbidity and mortality of CKD patients is a consequence of CKD-MBD. The pathogenesis of this syndrome is not completely understood, but undoubtedly the development of mineral and bone disorder begins in the earliest stages of CKD. The diagnosis is made by non-invasive methods (biochemistry, x-ray, ultrasound, etc.) and bone biopsy as an invasive method. In addition to new drugs, e.g. non-calcium phosphate binders, vitamin D analogs, calcimimetics, prevention and treatment is still a major challenge for the nephrologist. In this article we will briefly discuss the pathophysiology, diagnosis, prevention and treatment of CKD-MBD

Chronic kidney disease mineral bone disorder

Chronic kidney disease – mineral bone disease (CKD-MBD) is a syndrome defined as a systemic mineral metabolic disorder associated with CKD. The term renal osteodystrophy, as a part of CKD-MBD, indicates a pathomorphological concept of bone lesions. High morbidity and mortality of CKD patients is a consequence of CKD-MBD. The pathogenesis of this syndrome is not completely understood, but undoubtedly the development of mineral and bone disorder begins in the earliest stages of CKD. The diagnosis is made by non-invasive methods (biochemistry, x-ray, ultrasound, etc.) and bone biopsy as an invasive method. In addition to new drugs, e.g. non-calcium phosphate binders, vitamin D analogs, calcimimetics, prevention and treatment is still a major challenge for the nephrologist. In this article we will briefly discuss the pathophysiology, diagnosis, prevention and treatment of CKD-MBD

Association of leptin and adiponectin with one year mortality after osteoporotic fracture of the proximal femur

Osteoporotska fraktura proksimalnog femura ozbiljna je ozljeda koja rezultira značajnim oštećenjem funkcionalnog statusa i smanjenjem očekivanog trajanja života. Podaci iz literature govore da smrtnost nakon prijeloma kuka unutar prve godine dana iznosi između 12-37%. S obzirom na opće starenje populacije, broj fraktura u budućnosti će se vjerojatno povećati. Leptin i adiponektin spadaju u skupinu adipocitokina - hormona koje luče adipociti. Do sada je utvrđeno da imaju značajnu ulogu u metabolizmu glukoze, lipida, kostiju, regulaciju upale kao i u patogenezi kardiovaskularnih bolesti. Brojne studije ispitivale su njihov utjecaj na smrtnost kako u općoj, tako i u specifičnim populacijama, međutim, dobiveni rezultati su kontradiktorni. Svrha ovog istraživanja bila je definirati utjecaj leptina i adiponektina, te ostalih rutinskih laboratorijskih i antropometrijskih parametara na mortalitet tijekom prve godine u bolesnika s osteoporotskim prijelomom proksimalnog femura. Provedena je prospektivna studija koja je obuhvatila ukupno 236 bolesnika neovisno o spolu i dobi s radiološki definiranim prijelomom proksimalnog femura. Glavni ishod istraživanja bila je smrtnost godinu dana nakon prijeloma. Prilikom primitka na odjel, bolesnicima su iz uzorka krvi određeni rutinski laboratorijski parametri (kompletna krvna slika, serumske vrijednosti elektrolita uključujući Ca i P, ureje, kreatinina, ukupnih proteina i albumina, C reaktivnog proteina, lipidogram, glukoza i HbA1c, osteokalcin i beta-crosslaps, urin mikroskopski i sediment urina), snimljen je EKG te izmjerena visina i težina iz čega je bio izračunat indeks tjelesne mase. Zadnji dan hospitalizacije bolesnicima je uzet uzorak krvi iz koje je odijeljen serum koji je pohranjen na -80 ºC iz kojeg su kasnije određene koncentracije adiponektina, inzulina i leptina. Mortalitet unutar godinu dana iznosio je 28.4%. Stariji ispitanici imali su veću smrtnost neovisno o drugim parametrima (HR 1.111, 95% CI 1.07 – 1.16, P<0.001). Muški spol bio je rizični faktor za smrtnost (OR 2.88, 95% CI 1.35-6.11, P=0.006). Dokazano je da su smanjene koncentracije albumina (P=0.46, HR 0,949, 95% CI 0,902-0,999) te povišene koncentracije adiponektina (P=0,022, HR 1,063, 95 % CI 1.009-1.120) i β-crosslaps-a (P=0,001, HR 4,632, 95%CI 1.874-11.452) nezavisni prediktori smrtnosti unutar prve godine dana od prijeloma. Nije dokazana ni povezanost leptina i jednogodišnjeg mortaliteta. U zaključku, istraživanje je pokazalo da su dob, muški spol, albumini, adiponektin i beta-crosslaps nezavisni prediktori jednogodišnje smrtnosti u bolesnika s prijelomom proksimalnog femura.Osteoporotic fracture of the proximal femur is a serious injury that results in significant impairment of functional status and decreased life expectancy. Leptin and adiponectin are a part of a adipocytokines family - which are hormones secreted by adipocytes. Numerous studies have examined their impact on mortality both in general and specific populations, but none of them was conducted in patients with hip fracture. The aim of this study was to determine the influence of leptin and adiponectin, as well as routine laboratory and antropomethric parameters on mortality during the first year after osteoporotic fractures of the proximal femur. A total of 236 consecutive patients (59 males) with hip fractures were followed over a one-year period. Patient age, gender, type of fracture, type of treatment, time from admission to surgery, type of anaesthesia, body mass index (BMI), and electrocardiograms were recorded. Routine preoperative laboratory tests including osteocalcin and beta-crosslaps were masured at admission. On the last day of hospitalization, the blood sample was taken and serum was separated and stored at -80 ° C. Later, that serum was used to determine adiponectin, insulin and leptin concentrations. One year after the fracture mortality rate was 28.4%. Older patients had higher mortality regardless of other parameters (HR 1.111, 95% CI 1:07 to 1:16, P <0.001). Male gender was a risk factor for mortality (OR 2.88, 95% CI 1:35 to 6:11, P = 0.006). Low albumin levels (P=0.46, HR 0,949, 95% CI 0,902-0,999), high adiponectin (P=0,022, HR 1,063, 95 % CI 1.009-1.120) and high β-cross laps levels (P=0,001, HR 4,632, 95%CI 1.874-11.452) were independent predictors of mortality within the first year after the fracture. There was no correlation between leptin and one-year mortality. In summary, gender, age, albumin, adiponectin and beta-crosslaps are independent predictors of one-year mortality in patients with fractures of the proximal femur

Association of leptin and adiponectin with one year mortality after osteoporotic fracture of the proximal femur

Osteoporotska fraktura proksimalnog femura ozbiljna je ozljeda koja rezultira značajnim oštećenjem funkcionalnog statusa i smanjenjem očekivanog trajanja života. Podaci iz literature govore da smrtnost nakon prijeloma kuka unutar prve godine dana iznosi između 12-37%. S obzirom na opće starenje populacije, broj fraktura u budućnosti će se vjerojatno povećati. Leptin i adiponektin spadaju u skupinu adipocitokina - hormona koje luče adipociti. Do sada je utvrđeno da imaju značajnu ulogu u metabolizmu glukoze, lipida, kostiju, regulaciju upale kao i u patogenezi kardiovaskularnih bolesti. Brojne studije ispitivale su njihov utjecaj na smrtnost kako u općoj, tako i u specifičnim populacijama, međutim, dobiveni rezultati su kontradiktorni. Svrha ovog istraživanja bila je definirati utjecaj leptina i adiponektina, te ostalih rutinskih laboratorijskih i antropometrijskih parametara na mortalitet tijekom prve godine u bolesnika s osteoporotskim prijelomom proksimalnog femura. Provedena je prospektivna studija koja je obuhvatila ukupno 236 bolesnika neovisno o spolu i dobi s radiološki definiranim prijelomom proksimalnog femura. Glavni ishod istraživanja bila je smrtnost godinu dana nakon prijeloma. Prilikom primitka na odjel, bolesnicima su iz uzorka krvi određeni rutinski laboratorijski parametri (kompletna krvna slika, serumske vrijednosti elektrolita uključujući Ca i P, ureje, kreatinina, ukupnih proteina i albumina, C reaktivnog proteina, lipidogram, glukoza i HbA1c, osteokalcin i beta-crosslaps, urin mikroskopski i sediment urina), snimljen je EKG te izmjerena visina i težina iz čega je bio izračunat indeks tjelesne mase. Zadnji dan hospitalizacije bolesnicima je uzet uzorak krvi iz koje je odijeljen serum koji je pohranjen na -80 ºC iz kojeg su kasnije određene koncentracije adiponektina, inzulina i leptina. Mortalitet unutar godinu dana iznosio je 28.4%. Stariji ispitanici imali su veću smrtnost neovisno o drugim parametrima (HR 1.111, 95% CI 1.07 – 1.16, P<0.001). Muški spol bio je rizični faktor za smrtnost (OR 2.88, 95% CI 1.35-6.11, P=0.006). Dokazano je da su smanjene koncentracije albumina (P=0.46, HR 0,949, 95% CI 0,902-0,999) te povišene koncentracije adiponektina (P=0,022, HR 1,063, 95 % CI 1.009-1.120) i β-crosslaps-a (P=0,001, HR 4,632, 95%CI 1.874-11.452) nezavisni prediktori smrtnosti unutar prve godine dana od prijeloma. Nije dokazana ni povezanost leptina i jednogodišnjeg mortaliteta. U zaključku, istraživanje je pokazalo da su dob, muški spol, albumini, adiponektin i beta-crosslaps nezavisni prediktori jednogodišnje smrtnosti u bolesnika s prijelomom proksimalnog femura.Osteoporotic fracture of the proximal femur is a serious injury that results in significant impairment of functional status and decreased life expectancy. Leptin and adiponectin are a part of a adipocytokines family - which are hormones secreted by adipocytes. Numerous studies have examined their impact on mortality both in general and specific populations, but none of them was conducted in patients with hip fracture. The aim of this study was to determine the influence of leptin and adiponectin, as well as routine laboratory and antropomethric parameters on mortality during the first year after osteoporotic fractures of the proximal femur. A total of 236 consecutive patients (59 males) with hip fractures were followed over a one-year period. Patient age, gender, type of fracture, type of treatment, time from admission to surgery, type of anaesthesia, body mass index (BMI), and electrocardiograms were recorded. Routine preoperative laboratory tests including osteocalcin and beta-crosslaps were masured at admission. On the last day of hospitalization, the blood sample was taken and serum was separated and stored at -80 ° C. Later, that serum was used to determine adiponectin, insulin and leptin concentrations. One year after the fracture mortality rate was 28.4%. Older patients had higher mortality regardless of other parameters (HR 1.111, 95% CI 1:07 to 1:16, P <0.001). Male gender was a risk factor for mortality (OR 2.88, 95% CI 1:35 to 6:11, P = 0.006). Low albumin levels (P=0.46, HR 0,949, 95% CI 0,902-0,999), high adiponectin (P=0,022, HR 1,063, 95 % CI 1.009-1.120) and high β-cross laps levels (P=0,001, HR 4,632, 95%CI 1.874-11.452) were independent predictors of mortality within the first year after the fracture. There was no correlation between leptin and one-year mortality. In summary, gender, age, albumin, adiponectin and beta-crosslaps are independent predictors of one-year mortality in patients with fractures of the proximal femur

Association of leptin and adiponectin with one year mortality after osteoporotic fracture of the proximal femur

Osteoporotska fraktura proksimalnog femura ozbiljna je ozljeda koja rezultira značajnim oštećenjem funkcionalnog statusa i smanjenjem očekivanog trajanja života. Podaci iz literature govore da smrtnost nakon prijeloma kuka unutar prve godine dana iznosi između 12-37%. S obzirom na opće starenje populacije, broj fraktura u budućnosti će se vjerojatno povećati. Leptin i adiponektin spadaju u skupinu adipocitokina - hormona koje luče adipociti. Do sada je utvrđeno da imaju značajnu ulogu u metabolizmu glukoze, lipida, kostiju, regulaciju upale kao i u patogenezi kardiovaskularnih bolesti. Brojne studije ispitivale su njihov utjecaj na smrtnost kako u općoj, tako i u specifičnim populacijama, međutim, dobiveni rezultati su kontradiktorni. Svrha ovog istraživanja bila je definirati utjecaj leptina i adiponektina, te ostalih rutinskih laboratorijskih i antropometrijskih parametara na mortalitet tijekom prve godine u bolesnika s osteoporotskim prijelomom proksimalnog femura. Provedena je prospektivna studija koja je obuhvatila ukupno 236 bolesnika neovisno o spolu i dobi s radiološki definiranim prijelomom proksimalnog femura. Glavni ishod istraživanja bila je smrtnost godinu dana nakon prijeloma. Prilikom primitka na odjel, bolesnicima su iz uzorka krvi određeni rutinski laboratorijski parametri (kompletna krvna slika, serumske vrijednosti elektrolita uključujući Ca i P, ureje, kreatinina, ukupnih proteina i albumina, C reaktivnog proteina, lipidogram, glukoza i HbA1c, osteokalcin i beta-crosslaps, urin mikroskopski i sediment urina), snimljen je EKG te izmjerena visina i težina iz čega je bio izračunat indeks tjelesne mase. Zadnji dan hospitalizacije bolesnicima je uzet uzorak krvi iz koje je odijeljen serum koji je pohranjen na -80 ºC iz kojeg su kasnije određene koncentracije adiponektina, inzulina i leptina. Mortalitet unutar godinu dana iznosio je 28.4%. Stariji ispitanici imali su veću smrtnost neovisno o drugim parametrima (HR 1.111, 95% CI 1.07 – 1.16, P<0.001). Muški spol bio je rizični faktor za smrtnost (OR 2.88, 95% CI 1.35-6.11, P=0.006). Dokazano je da su smanjene koncentracije albumina (P=0.46, HR 0,949, 95% CI 0,902-0,999) te povišene koncentracije adiponektina (P=0,022, HR 1,063, 95 % CI 1.009-1.120) i β-crosslaps-a (P=0,001, HR 4,632, 95%CI 1.874-11.452) nezavisni prediktori smrtnosti unutar prve godine dana od prijeloma. Nije dokazana ni povezanost leptina i jednogodišnjeg mortaliteta. U zaključku, istraživanje je pokazalo da su dob, muški spol, albumini, adiponektin i beta-crosslaps nezavisni prediktori jednogodišnje smrtnosti u bolesnika s prijelomom proksimalnog femura.Osteoporotic fracture of the proximal femur is a serious injury that results in significant impairment of functional status and decreased life expectancy. Leptin and adiponectin are a part of a adipocytokines family - which are hormones secreted by adipocytes. Numerous studies have examined their impact on mortality both in general and specific populations, but none of them was conducted in patients with hip fracture. The aim of this study was to determine the influence of leptin and adiponectin, as well as routine laboratory and antropomethric parameters on mortality during the first year after osteoporotic fractures of the proximal femur. A total of 236 consecutive patients (59 males) with hip fractures were followed over a one-year period. Patient age, gender, type of fracture, type of treatment, time from admission to surgery, type of anaesthesia, body mass index (BMI), and electrocardiograms were recorded. Routine preoperative laboratory tests including osteocalcin and beta-crosslaps were masured at admission. On the last day of hospitalization, the blood sample was taken and serum was separated and stored at -80 ° C. Later, that serum was used to determine adiponectin, insulin and leptin concentrations. One year after the fracture mortality rate was 28.4%. Older patients had higher mortality regardless of other parameters (HR 1.111, 95% CI 1:07 to 1:16, P <0.001). Male gender was a risk factor for mortality (OR 2.88, 95% CI 1:35 to 6:11, P = 0.006). Low albumin levels (P=0.46, HR 0,949, 95% CI 0,902-0,999), high adiponectin (P=0,022, HR 1,063, 95 % CI 1.009-1.120) and high β-cross laps levels (P=0,001, HR 4,632, 95%CI 1.874-11.452) were independent predictors of mortality within the first year after the fracture. There was no correlation between leptin and one-year mortality. In summary, gender, age, albumin, adiponectin and beta-crosslaps are independent predictors of one-year mortality in patients with fractures of the proximal femur