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Background: Thoracic paravertebral block (TPVB) is the technique of injecting local anesthetic alongside the thoracic vertebra close to where the spinal nerves emerge from the intervertebral foramen leading to unilateral, segmental, somatic, and sympathetic nerve block of ipsilateral dermatoma, which is effective for anesthesia and in treating acute and chronic pain of unilateral origin from the chest and abdomen. The most common indications for TPVB are rib fractures, refractory angina pectoris, neuralgia of the thoracic wall and also cancer pain. Today’s understanding of the use and efficacy of TPVB increased interest in using the technique not only for analgesia but also for surgical anesthesia. The most common surgical indications are breast surgery, thoracic wall surgery and unilateral abdominal wall surgery. The introduction of ultrasound in the practice of regional anesthesia has led to the recognition of the need to increase consistency of TPVB. Methods: Preparation of the patient for TPVB begins with monitoring the patient's vital functions, reading the ECG, measuring arterial pressure, pulse oximetry, setting the venous pathway alongside with sedation with midazolam. The patient is seated, with a TPVB level by placing an ultrasound probe in craniocaudal orientation about 5 cm lateral to the median line, visualizing the ribs and transverse extensions of the vertebrae, bone transverse ligaments, and pleura between which the paravertebral space is located. The needle is introduced by the in-plain technique thus visualizing the needle as a whole ; by entering the tip of the needle into the PVS, a local anesthetic is applied to fill the paravertebral space, which is seen as a pleural drop. The local anesthetic used in practice is levobupivacaine 0.5% in a dose of 20 ml and the duration of anesthesia is 4-6 hours and analgesia 12-16 hours. Conclusion: In 2019, the University Hospital for Tumors, Sestre milosrdnice University Hospital Center started with the application of TPBV technique. The advantage of TPVB block under ultrasound control is an effective perioperative analgesia, non-induction of general anesthesia, as well as lower financial cost compared to general anesthesia. The reason for insufficient application in everyday practice is organizationally and time-consuming preparation and procedure. To achieve the highest possible application and success rate without the development of complications, it is necessary to educate the performance of TPVB technique in anesthesia.

Cancer pain is not a homogenous and clearly understood pathological process. The best treatment is a combination of drug and non-drug measures. Pain is divided into visceral, bone or neuropathic pain and has characteristics of continuous or intermittent pain. Cancer bone pain therapy remains centered on strong opioid, radiotherapy and bisphosphonates. Invasive procedures are aimed to improve neurological function, ambulation and pain relief. Solid tumors often demand surgery. Treatment of acute postoperative pain is crucial for the prevention of chronic pain. Chemotherapy and radiation sometimes also cause pain. The management of cancer pain has improved because of rapid diagnosis and treatment, understanding of analgesics and the cooperation of patients and their family. The presence of special pain centers in hospitals also raise standard of cancer pain management. Drug therapy with non-opioid, opioid and adjuvant drugs is the base of such management. The side effects must be monitored and timely treated. Methods of regional nerve blockade in pain control are numerous. Placement of epidural, intrathecal and subcutaneous catheters, conductive nerve blocks with continuous delivery of mixed local anesthetics are very successful for selected patients. Conventional physical therapy involving lymphatic drainage is useful. Acupuncture, psychotherapy and similar methods are also applicable., Karcinomska bol nije homogen i potpuno razjašnjen patološki proces. Najbolja terapija je kombinacija medikamentozne terapije i nemedikametoznih postupaka. Možemo je podijeliti na visceralnu, koštanu i neuropatsku bol i ima karakteristike kontinuirane ili povremene boli. Terapija koštane boli fokusirana je na jake opioide, radioterapiju i bifosfonate. Cilj invazivnih metoda liječenja boli je poboljšati neurološku funkciju, pokretljivost i olakšanje boli. Solidni tumori često zahtjevaju operaciju. Liječenje akutne poslijeoperacijske boli je od iznimne važnosti u prevenciji nastanka kronične boli. Kemoterapija i radioterapija ponekad također uzrokuju bol. Liječenje karcinomske boli je poboljšano bržom dijagnostikom i terapijom, boljim poznavanjem analgetika i suradnjom s pacijentom i njegovom obitelji. Postojanje specijaliziranih centara za bol u bolnicama također je podiglo standard u liječenju boli. Liječenje boli medikamentozno neopioidima, opioidima i drugim pomoćnim lijekovima je osnova liječenja boli. Nuspojave lijekova moraju se neprestano pratiti i na vrijeme liječiti. Metode regionalne nervne blokade u liječenju boli su brojne. Plasiranje epiduralnih, intratekalnih i supkutanih katetera s kontinuiranom isporukom mješavine lokalnih anestetika veoma su uspješne kod određenih bolesnika. Fizikalna terapija s limfnom drenažom je korisna. Akupunktura, psihoterapija i slične metode su također primjenjive.

Background and purpose:Chronic postsurgical pain (CPSP) occurs in approximately 10% of surgical patients and is a common complication after breast cancer surgery. Research on prevention of CPSP suggests that the perioperative use of intravenous lidocaine may decrease the incidence of CPSP three and six months after breast surgery. Materials and methods: We investigated the results from controlled randomised trials in the last five years. These trials included 514 patients and assessed the incidence of CPSP after breast cancer surgery in women receiving intravenous lidocaine or placebo. Patients were randomized into two groups ; lidocaine (1.5 mg/kg bolus of intravenous lidocaine followed by 2mg/kg/hr infusion) or control group (saline). One recent pilot study tested further subcutaneous administration of lidocaine postoperatively for up to 12h (1, 33mg/kg/h). In the trials different tools for pain scoring were used, for instance Numerical Rating Scale (rest/movement ), yes/no scoring, Brief Pain Inventory, Neuropathic Pain Questionnaire, SF-MPQ- II. Results: After three months, more than half of the patients reported CPSP. Lidocaine decreased the development of CPSP (63% vs 43, 1%). The incidence of any pain or discomfort related to the surgical wound was lower in the lidocaine group than with placebo: 20% vs. 25% at 3 months, and 27% vs. 30% at 6 months, while moderate or severe CPSP was not significally reduced: 13% vs. 9% at 3 months and 12% vs. 12% at 6 months. Patients with moderate or severe CPSP reported severer neuropathic disorders than those with mild CPSP. One study showed reduction of pain at rest at 6 months in the lidocaine group vs placebo. Conclusions: Analyzing clinical trials, we conclude that intravenous perioperative lidocaine affects the development of CPSP after breast cancer surgery. Lidocaine has a positive impact on acute postoperative recovery, therefore surely preventing CPSP. More data by testing preventive administration of lidocaine alone or as a part of multimodal analgesia during and after breast cancer surgery should be collected. To evaluate CPSP by intensity, pain character and life quality modified neuropathic pain scales could be used.

Mozak je ciljni organ djelovanja inhalacijskih anestetika. Osjetljivost mozga na oksidacijski stres povezana je sa njegovom izraženom metaboličkom aktivnošću, proizvodnjom ROSa (engl. reactive oxygen species, ROS), velikim brojem mitohondrija i smanjenom enzimskom antioksidativnom aktivnošću. Inhalacijski anestetici, poput Isoflurana i Sevoflurana, utječu na jačanje osjetljivosti mozga na oštećenja oksidativnim stresom te na povećanje aktivnost beta-sekretaze (BACE), enzima koji formira beta-amiloidne plakove i izaziva beta-amiloidnu ovisnu apoptozu živčanih stanica. Nadalje, beta-amiloidni plakovi, kao patološki produkt amiloidnog prekursorskog proteina (APP), predstavljaju važnu značajku za razvoj neurodegenerativnih promjena povezanih sa nastankom Alzheimerove bolesti. Istraživanje prooksidativnih, upalnih i neurotoksičnih učinaka inhalacijskih anestetika, te praćenje razine oksidativnog stresa u moždanom tkivu i nastalih patohistoloških promjena na mozgu štakora vezanih za neurodegenerativna oštećenja i upalu možemo povezati sa dugotrajnim izlaganjem inhalacijskim anesteticima, narušavanjem oksidacijsko/antioksidacijske homeostaze i stvaranje beta-amiloidnih plakova. Razumijevanjem povezanosti izloženosti inhalacijskim anesteticima i nastanku ireverzibilnih neurodegenerativnih promjena sugeriralo bi se poštednijim korištenjem inhalacijskih anestetika utjecati na ograničavanje neurodegenerativnihpromjena vezanih za nastanak Alzheimerove bolesti., Main target of inhalation anesthetics is the brain. The sensitivity of the brain to oxidative stress is associated with its pronounced metabolic activity, production of ROS (reactive oxygen species), large number of mitochondria and reduced enzymatic antioxidant activity. Inhaled anesthetics, such as Isoflurane and Sevoflurane, increase the sensitivity of the brain to oxidative stress damage and increase the activity of beta-secretase (BACE), an enzyme that forms beta-amyloid plaques and causes beta-amyloid-dependent apoptosis of nerve cells. Furthermore, beta-amyloid plaques, pathological product of amyloid precursor protein (APP), represent an important feature for the development of neurodegenerative changes associated with the development of Alzheimer’s disease. By investigation of prooxidative, inflammatory and neurotoxic effects of inhaled anesthetics and analyzing the parameters of oxidative stress levels in brain tissue and pathohistological changes in rat brain related to neurodegenerative damage and inflammation, connection with long-term exposure to inhaled anesthetics disruption of oxidative/antioxidant homeostasis and formation of beta amyloid plaques can be made. By understanding the relationship between exposure to inhaled anesthetics and the occurrence of irreversible neurodegenerative changes it could be suggested to reduce using inhaled anesthetics to limit the neurodegenerative changes associated with the development of Alzheimer’s disease.

Inhalacijski anestetici normalno se smatraju nereaktivnim, ali pod odgovarajućim uvjetima metaboliziraju se u reaktivne slobodne radikale i stupaju u reakcije s dijelovima stanica pri čemu dovode do oštećenja. U mozgu željezo igra važnu ulogu u proizvodnji mijelina, metabolizmu monoaminskih transmitera i sintezi gama-aminomaslačne kiseline (GABA). S druge strane, nakupljanje željeza u mozgu mijenja metabolizam stanica mozga i vodi povećanju oksidacijskog stresa te neurodegeneraciji. Cilj rada bio je istražiti mogući antioksidativni/pro-oksidativni učinak izoflurana i željezo-dekstrana, kao i njihovo zajedničko djelovanje na uzorcima tkiva mozga štakora: a) procjenom razine neuroupale, mjerenjem relativne težine mozga u odnosu na zdravu kontrolu ; b) promjene u oksidacijsko-redukcijskom statusu mjerenjem razine malondialdehida(MDA, krajnjeg produkta lipidne peroksidacije) i glutationa(GSH), te aktivnosti katalaze(CAT)i superoksid dismutaze(SOD) ; c) analizom promjene hematoloških pokazatelja krvi, te osmotske fragilnosti eritrocita. Rezultati ukazuju da izofluran u kombinaciji s Fe-dekstranom uzrokuje oksidacijski stres koji potiče nastanak neurodegeneracijskih promjena. Fe-dekstran uzrokuje povećanu lipidnu peroksidaciju i neuroupalu. Izofluran i kombinacija izoflurana i Fe-dekstrana uzrokuje porast razine eritrocita te pad svih ostalih hematoloških parametara, dok sam Fe-dekstran uzrokuje pad svih hematoloških parametara.

Inhalacijski anestetici su lako hlapljive tekućine, a služe za uvod ili održavanje anestezije pri operativnim zahvatima nepredvidljivog trajanja. U ovom radu proučavan je utjecaj sevoflurana, samog ili združenog s željezo-dekstranom, na nastanak i razvoj neurodegenerativnih promjena na tkivu mozga štakora. Neurodegeneracija je mjerena: (i) promjenama oksidacijskog statusa mjerenjem razine malondialdehida (MDA), glutationa (GSH), te enzimatske aktivnosti katalaze (CAT) i superoksid dismutaze (SOD) ; (ii (anti)genotoksičnog odgovora u limfocitima štakora, pokazujući razinu oštećenja DNA ; (iii) procjenom razine neuroupale prema relativnoj težini mozga u odnosu na zdravu kontrolu ; (iv) procjenom toksičnog učinka na hematološke i biokemijske odrednice u krvi, te osmotsku fragilnost eritrocita. Rezultati pokazuju da željezo-dekstran uzrokuje značajnu neuroupalu, te povećanu razinu oksidacijskog stresa: povećava razinu MDA, mijenja aktivnosti antioksidativnih enzima (SOD, CAT) i snižava GSH. Sevofluran u kombinaciji sa Fe-dekstranom pokazuje izraženi gubitak moždanih stanica i prividno niske razine MDA te antioksidansa, kao i značajne toksične učinke na krvne odrednice. Komet test pokazuje najveća oštećenja DNA limfocita pri izlaganju sevofluranu združenim sa željezodekstranom. Temeljem rezultata može se zaključiti kako jaka neuroupala i pojava lipidne peroksidacije u mozgu životinja obrađenih Fe-dekstranom ukazuju na neurotoksičnost, dok kombinacija sa sevofluranom uzrokuje najteža oštećenja mozga i trajno narušava homeostazu organizma.

Anesthetics are types of medicines in a gaseous, liquid or other form, whose function is the introduction and/or maintenance of anesthesia with the aim of facilitating surgical and other painful interventions. Isoflurane has rapid pharmacological activity and absorbance, and stimulates rapid recovery after anesthesia. Long- term exposure to anesthetic acts negatively on peripheral organs and tissues, stimulates inflammation, oxidative stress, necrosis, and apoptosis leading to neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Iron is an indispensable part of the living organism and the disorder of its homeostasis produces redox active iron that affects the formation of ROS, tissue injury, cell growth disorder, and ultimately the appearance of oxidative stress. The aim of the study was to investigate the effect of isoflurane itself and/or the combination of iron dextran on the level of oxidative stress and consequent inflammation on liver, spleen and kidney tissues. The obtained results indicate that long-term use of isoflurane and iron-dextran alone or in combination increases the level of oxidative stress and inflammation in the liver, kidney and spleen cells and leads to their impairment, indicating an increase in biochemical parameters in serum and hemolysis of erythrocyte.

Chemotherapy is used to stop proliferation and spreading of cancer cells, as well as to initiate apoptosis in cancer cells. Due to its necrotic nature, chemotherapy usually causes damage to nearby healthy tissue. Flavonoids have shown their capability to fight cancer cells and to prevent some damage to healthy cells. In this research curcumin was tested in vitro for its effect on Ehrlich ascites tumor (EAT) cells, their proliferation and ability to initiate apoptosis/necrosis in the cells, and curcumins effect in interaction with bleomycin and hyperthermia. EAT was grown in Swiss albino mice, the cells were isolated on the 7th day, and were incubated in culture medium, and treated with curcumin, bleomycin and hyperthermia. The antiproliferative effect of the test components was confirmed by a colorimetry assay after a short incubation directly with bleomycin for 2 h and curcumin for 13. HBK 295 13th CBC the next 2 h at physiological or hyperthermal (43°C) conditions and after the treatment of cells for 24 hrs. The percentage of tumor cells in apoptosis and necrosis on the flow cytometer was analyzed and the genotoxic effect of the comet test was investigated. Curcumin demonstrated the potential to inhibit the proliferation of EAT cells in vitro, and to slightly increase the percentage of cells in apoptosis. The combination with cytostatic bleomycin and hyperthermia provides a better anti- proliferative effect which is based on the high percentage induction of necrosis and complete cell lysis.

The aim of this study was to investigate possible antioxidant/prooxidative effect of sevoflurane on AlCl3-induced oxidative stress by monitoring:change in oxidoreduction status of the brain by changing the level of glutathione (GSH) and malondialdehyde (MDA) ; activity of catalase (CAT) and superoxide dismutase (SOD) in brain tissue ; evaluation of the neuro- inflammation, by measuring the relative weight of the brain compared to a healthy control group ; analyzing changes in haematological parameters and osmotic fragility of erythrocytes as indicators of the toxicity of AlCl3, sevoflurane and/or these combination. Results show that AlCl3 causes an increased level of oxidative stress ; significantly increases MDA levels and decreased GSH levels in the brain and changes to a lesser extent the activity of antioxidant enzymes compared to sevoflurane. Sevoflurane in combination with AlCl3 exhibits a stronger toxic effect ; MDA level was significantly increased as well as activity of antioxidant enzymes SOD and CAT. Increased neuro-inflammation is visible in group treated with AlCl3, while sevoflurane + AlCl3 cause decaying of brain cells and significant toxic effects on haematological parameters. Based on obtained results we can conclude that significantly increased level of lipid peroxidation in the brain and neuro- inflammation indicates neurotoxicity of AlCl3, while sevoflurane in combination with AlCl3 exhibits a higher toxic effect and a significant degradation of brain cells.

Temeljni cilj ovog rada bio je istražiti mogući antioksidativni/prooksidativni učinak sevoflurana na AlCl3 izazvani oksidacijski stres praćenjem: promjena u oksidoredukcijskom statusu mozga mjenjenjem razine glutationa (GSH) i malondialdehida (MDA, krajnjeg produkta lipidne peroksidacije), te aktivnosti katalaze (CAT) i superoksid dismutaze (SOD) u tkivu mozga ; procjenom razine neuroupale, mjerenjem relativne težine mozga u odnosu na zdravu kontrolnu skupinu ; analizom promjene hematoloških pokazatelja krvi te osmotsku fragilnost eritrocita kao pokazatelja toksičnosti AlCl3, sevoflurana ili njihove kombinacije. Rezultati pokazuju da AlCl3 uzrokuje povećanu razinu oksidacijskog stresa ; značajno povećava razinu MDA i snižava razinu GSH u mozgu te u manjoj mjeri mjenja aktivnosti antioksidativnih enzima u odnosu na sevofluran. Sevofluran u kombinaciji s AlCl3 pokazuje jači toksični učinak ; razina MDA je značajno povećana kao i aktivnost antioksidacijskih enzima SOD i CAT. Povećana neuroupala vidljiva je u skupini obrađenoj s AlCl3, dok sevofluran u kombinaciji s AlCl3 pokazuje propadanje moždanih stanica te značajne toksične učinke na hematološkim odrednicama. Temeljem dobivenih rezultata možemo zaključiti da značajno povećana razina lipidne peroksidacije u mozgu i neuroupale ukazuje na neurotoksičnost AlCl3 dok sevofluran u kombinaciji s AlCl3 pokazuje jači toksični učinak i značajno propadanje moždanih stanica.

Nutrition is important factor that influence bone metabolism, the endocrine and/or paracrine system, and bone-active mineral elements homeostasis. We studied antiosteoporetic effects of icariin and alendronate (ALN) in retinoic acid-induced (13cRA) bone loss in rats. Icariin has beneficial effects on bone health ; it improved the decrease in bone weight, the length and the diameter of the bone, calcium, and phosphorus content in bone ash, bone mineral density (BMD) and the biochemical markers of bone turnover and uterus atrophy induced by 13cRA. All result suggests that icariin reverses osteoporosis in 13cRA rats by stimulating bone formation or regulating bone resorption by its antioxidative and estrogenic-like activity without toxic-side effect observed in ALN treatment.

Osteoporosis is a skeletal disease characterized by the significant decrease in bone mineral density (BMD) and bone microarchitecture disorder. The risk of osteoporosis can be genetic or acquired. Contributing to acquire risk are numerous medications, including 13-cis retinoic acid (13cRA). The main effects of 13cRA that contribute to bone loss are: a) increased oxidative stress (OS) and the formation of reactive radicals, decreased activity of osteoblasts and increased osteoclast activity ; b) osteoblasts apoptosis ; c) decreased levels of estrogen and appearance of inflammatory cytokines, d) reducing the activity of vitamin D receptor, decrease of the absorption of Ca2+ in the intestine, increasing excretion of calcium through the kidneys ; d) the effects on parathyroid hormone. Epidemiological evidence has indicated a link between dietary intake of antioxidants such as grape seed proanthocyanidins and bone health. The present study investigates the antiosteoporotic effects of grape seed proanthocyanidins (GSPs), natural antioxidants, in a 13cRA-induced osteoporosis model of rats and healthy rats. Three month-old female rats of the Y59 strain were given GSPs (100 mg kg-1) or alendronate (AL ; 40 mg kg-1, a positive control) concomitant with 13cRA (80 mg kg-1) once daily for 14 days by a single intragastric (i.g.) application. Twenty four hours after the treatment, we analysed bone turnover serum biochemical markers, such as: osteocalcin (OC), C-terminal fragment of type I collagen (CTX), bone mineral density (BMD), bone ash contents, calcium (Ca) and phosphorus (P) content, geometrical and physical parameters of bone as well as oxidative stress parameters (glutathione levels and lipid peroxidation). 13cRA successfully induced osteoporosis-like changes in rats. The treatment with GSPs increased BMD, OC level, femoral geometric characteristics, Ca and P content (P=0.025 ; P=0.025) in 13cRA-induced bone loss model. In addition, GSPs-treated rats had significantly lower serum alkaline phosphatase activity (P

Introduction. Oxidative stress plays an important role in the etiology of diabetes mellitus and can produce damage on cellular macromolecules, such as DNA and lipids in cellular membrane, impair protein function, and trigger cell death. Many polyphenols, exert positive effects on diseases caused by oxidative stress. Curcumin and naringin differ in number and arrangement of the hydroxyl groups, as well as by the nature and extent of alkylation. They can act as reducing agents, free radical scavengers, metal chelators, and singlet oxygen quenchers. The antioxidant activity of curcumin and naringin in vitro are compared with some of their antidiabetic effect in vivo on molecular cellular and organism level. Aim. The aim of the present study was to assess whether naringin or curcumincan influence oxidative stress induced DNA damage in mice with alloxan-induced diabetes. Materials and methods. Diabetes was induced in Swiss albino mice with a single intravenous injection of alloxan at dose of 75 mg kg-1 body weight. Two days after alloxan injection, naringin or curcumin preparations (50 mg kg-1) were given intraperitoneally for 7 days. In order to evaluate the effectiveness of naringin and curcumin we used three assays which cover different aspects of antioxidant activity, observed changes in body weight and survival of mice and used the alkaline comet and micronucleus assays. Results. In vitro curcumin showed appreciable antioxidant properties, while naringin was much less effective. Naringin or curcumin administration to diabetic mice resulted in decreased DNA damage in lymphocytes and increased level of DNA damage in liver, kidney and reticulocytes. Administration of naringin and curcumin resulted in significant increase of the body weight and 100% survival of mice. Conclusion. Results suggests that antioxidant activity of naringin and curcumin leads to long time survival of diabetic mice and possible prevention of further oxidative damage, so they could be candidates for antidiabetic agent, but the precise targets of naringin and curcumin in diabetic mice are still to be clarified.

Reactive oxygen species (ROS) play a role in a numbered of degenerative conditions including psoriasis. Psoriasis is a chronic inflammatory disease who’s the etiopathogenesis is not yet completely understood, and therefore there is no standardized therapeutical approach. Flavonoids, recognized as potent antioxidants, are multifunctional molecules that can act as anti- inflammatory and antiproliferative agents through the modulation of multiple signaling pathways. The present study was designed to investigate the protective role of flavonoids [quercetin, chrysin, curcumin or Epigallocatechin 3-gallate (EGCG)] against n- Hexyl salicylate (HXS)-induced oxidative stress and inflammation in skin. Anti-oxidative and anti-inflammatory effect of flavonoids is quantified by histopathological assessment of skin, measuring the levels of lipid peroxidation and glutathione (GSH) in the skin, total number of inflammatory cells in peritoneal cavity, macrophage spreading index, and hematological and biochemical parameters.Topically applied of n-Hexyl salicylate caused significant increase in lipid peroxidation and decrease in GSH, which is accompanied by an increase total number of inflammatory cells in skin and peritoneal cavity, functional activity of macrophages, and enzymatic activity of ALP and AST. In contrast, topically applied 5 % preparation of flavonoids (quercetin, chrysin, curcumin or EGCG) with HXS effectively prevented these alterations and maintained the antioxidant status. The results suggest that flavonoid preparations can serve as a potent antioxidant and anti-inflammatory agents in psoriatic-like skin lesions, without toxic effects.

The anti-aggregating effect of clopidogrel (75 mg/day) on platelet function was monitored in 33 solid tumor patients. Clopidogrel irreversibly blocks the platelet P2Y12 receptor and inhibits platelet aggregation induced by adenosine diphosphate (ADP). Whole blood aggregation was measured using a Siemens PFA-100 aggregometer including the Innovance PFA P2Y cartridge. The mean age of patients was 62 ± 13 years. Among them, there were 19 (58%) males and 14 (42%) females. The values of platelet aggregation >106 seconds and, Praćen je klopidogrelski (75 mg/dan) antiagregacijski učinak na trombocite u 33 bolesnika sa solidnim tumorima. Klopidogrel ireverzibilno blokira trombocitni receptor P2Y12 i sprječava trombocitnu agregaciju pokrenutu adenozin difosfatom(ADP). Agregacija je mjerena u punoj krvi agregometrom Siemens PFA-100 s uloškom Innovance PFA P2Y. Prosječnadob bolesnika bila je 62 ± 13 godine. Muškaraca je bilo 19 (58%); a žena 14 (42%). Vrijednost trombocitne agregacije >106 sekunda pokazala je klopidogrelski antiagregacijski učinak u 22 (67%) bolesnika; a vrijednost

The manufacture of albumin derived from human plasma started by Professor E. J. Cohn during World War II has expanded into international business over the past sixty years (1). In vital situations, albumin was used as a plasma expander. This is a biological preparation and always potentially dangerous. The manufacture of albumin is getting more and more expensive as the preparation has to meet standards ever higher. With the market abundant in artificial macro-molecular plasma expanders, improved parenteral nutrition, and studies questioning the effectiveness of albumin use, the administration of albumin has been reduced. Because of the nature of their disease and chemoradiotherapy treatment, patients with tumors are prone to having low protein levels. However, indications for albumin therapy are restricted, the same as that in other patient groups. With the quality parenteral and enteral nutrition available, the use of albumin to correct hypoalbuminemia is not justified., Proizvodnju albumina iz ljudske plazme započeo je profesor Cohn E. J. tijekom Drugog svjetskog rata; koja je u posljednjih šezdesetak godina prerasla je u internacionalni biznis (1). U vitalnim situacijama; albumin je upotrebljavan kao plazmaekspander. To je biološki preparat i uvijek je potencijalno opasan. Proizvodnja albumina sve je skuplja; jer preparat mora zadovoljavati sve više i više standarde. Uz bogato tržište umjetnih makromolekularnih plazmaekspandera; unaprijeđene intravenske prehrane i studije koje govore o upitnom djelovanju albumina; njegova primjena je u padu. Tumorski bolesnici; zbog prirode bolesti i liječenja kemoradioterapijom; skloni su nižim razinama proteina. Međutim; indikacije albuminske terapije su restriktivne; iste kao i kod ostalih skupina bolesnika. Uporaba albumina za korekciju hipoalbuminemije nije opravdana pored kvalitetne parenteralne i enteralne prehrane.