The significance of masticatory muscle's relaxation in the treatment of the temporomandibular disorders - Review article.

Temporomandibular disorder (TMD) is a disease of multifactorial etiology and a complex of symptoms, related to disorders of the masticatory muscles, temporomandibular joints and the surrounding orofacial structures. One of the main problems in the course of TMD disorders is the systematic increase in the tension of the masticatory muscles (masseter muscles, temporalis and medial and lateral pterygoid muscles), what is the cause of many damages and the development of pathological conditions in the stomatognathic system. The article discusses the differences in the structure of the masticatory and skeletal muscles, as well as the different nature and isoforms of myosin, which determines the much faster generation of contraction in the masticatory muscles and consequently easier generation of excessive, harmful tensions in the masticatory muscles. The article describes the causes of increased tension in the masticatory muscles and methods of their relaxation used in the basic and supportive treatment of temporomandibular disorders. The use of occlusal splints, physiotherapeutic procedures and TMD treatment with botulinum toxin type A were characterized. A role of psychological support and the methods used for patients with TMD were emphasized.

Administration of Warfarin Inhibits the Development of Cerulein-Induced Edematous Acute Pancreatitis in Rats.

Acute pancreatitis (AP) is a severe disease with high morbidity and mortality in which inflammation and coagulation play crucial roles. The development of inflammation leads to vascular injury, endothelium and leukocytes stimulation, and an increased level of tissue factor, which results in the activation of the coagulation process. For this reason, anticoagulants may be considered as a therapeutic option in AP. Previous studies have shown that pretreatment with heparin, low-molecular-weight heparin (LMWH), or acenocoumarol inhibits the development of AP. The aim of the present study was to check if pretreatment with warfarin affects the development of edematous pancreatitis evoked by cerulein. Warfarin (90, 180, or 270 µg/kg/dose) or saline were administered intragastrically once a day for 7 days consecutively before the induction of AP. AP was evoked by the intraperitoneal administration of cerulein. The pre-administration of warfarin at doses of 90 or 180 µg/kg/dose reduced the histological signs of pancreatic damage in animals with the induction of AP. Additionally, other parameters of AP, such as an increase in the serum activity of lipase and amylase, the plasma concentration of D-dimer, and interleukin-1ß, were decreased. In addition, pretreatment with warfarin administered at doses of 90 or 180 µg/kg/dose reversed the limitation of pancreatic blood flow evoked by AP development. Warfarin administered at a dose of 270 µg/kg/dose did not exhibit a preventive effect in cerulein-induced AP. Conclusion: Pretreatment with low doses of warfarin inhibits the development of AP evoked by the intraperitoneal administration of cerulein.

Analysis of biochemical parameters in an experimental model of chronic pancreatitis in rats.

BACKGROUND: Despite advanced research and great progress in understanding the chronic pancreatitis (CP) pathogenesis, no current causal treatment for the condition is available. For preclinical studies, the existence of a well-characterized CP animal model is essential. The aim of the study was to assess the impact of chronic pancreatitis on the antioxidant enzymes activity in rat blood serum and on the level of glutathione (intracellular antioxidant) in rat pancreas. METHODS: The experiments were carried out on the Wistar Kyoto rats in two groups: control and study group (CP), in which chemical induction of pancreatitis with dibutyl dichloride was performed. Serum enzyme activities of amylase, lipase, catalase and superoxide dismutase were analyzed. The levels of the following biochemical parameters were also investigated: total protein, albumin, calcium, magnesium, and triglycerides. Levels of low-molecular-weight thiols: reduced (GSH) and oxidized (GSSG) glutathione, were determined in pancreatic homogenates. RESULTS: Histopathological imaging of rat pancreatic parenchyma with induced inflammation confirmed focal lymphocytic interstitial chronic pancreatitis with fibrosis features and mild parenchymal atrophy, as well as pancreatic islets degeneration. In the CP group, we observed a statistically significant decrease in serum amylase and lipase activities and in total protein/albumin levels. Also, the elevated catalase activity was registered. In CP rats' tissues, we observed a 15-fold reduction in GSH levels. The other examined parameters remained unchanged. Clinically relevant are hypoalbuminemia and a moderate decrease in lipase activity. The described changes are most probably indicative of the impaired exocrine pancreas function, however without organ failure features.

Acute Changes in Serum Creatinine and Kinetic Glomerular Filtration Rate Estimation in Early Phase of Acute Pancreatitis.

In patients with acutely changing kidney function, equations used to estimate glomerular filtration rate (eGFR) must be adjusted for dynamic changes in the concentrations of filtration markers (kinetic eGFR, KeGFR). The aim of our study was to evaluate serum creatinine-based KeGFR in patients in the early phase of acute pancreatitis (AP) as a marker of changing renal function and as a predictor of AP severity. We retrospectively calculated KeGFR on day 2 and 3 of the hospital stay in a group of 147 adult patients admitted within 24 h from the onset of AP symptoms and treated in two secondary-care hospitals. In 34 (23%) patients, changes in serum creatinine during days 1-3 of the hospital stay exceeded 26.5 µmol/L; KeGFR values almost completely differentiated those with increasing and decreasing serum creatinine (area under receiver operating characteristic curve, AUROC: 0.990 on day 3). In twelve (8%) patients, renal failure was diagnosed during the first three days of the hospital stay according to the modified Marshall scoring system, which was associated with significantly lower KeGFR values. KeGFR offered good diagnostic accuracy for renal failure (area under receiver operating characteristic-AUROC: 0.942 and 0.950 on days 2 and 3). Fourteen (10%) patients developed severe AP. KeGFR enabled prediction of severe AP with moderate diagnostic accuracy (AUROC: 0.788 and 0.769 on days 2 and 3), independently of age, sex, comorbidities and study center. Lower KeGFR values were significantly associated with mortality. Significant dynamic changes in renal function are common in the early phase of AP. KeGFR may be useful in the assessment of kidney function in AP and the prediction of AP severity.

Soluble Complement Component 1q Receptor 1 (sCD93) Is Associated with Graft Function in Kidney Transplant Recipients.

Cluster of differentiation 93 (CD93), also known as complement component 1q receptor 1 is a transmembrane glycoprotein expressed in endothelial and hematopoietic cells and associated with phagocytosis, cell adhesion, angiogenesis and inflammation. The extracellular part, soluble CD93 (sCD93), is released to body fluids in inflammation. Data on sCD93 in kidney diseases are limited. Our aim was to evaluate serum sCD93 in long-term kidney transplant recipients as a marker of inflammation and endothelial dysfunction that may be potentially useful in early recognition of graft dysfunction. Seventy-eight adult patients with functioning kidney graft and stable clinical state were examined at least one year after kidney transplantation. Serum sCD93 was measured by enzyme immunosorbent assay. Estimated glomerular filtration rate (eGFR) and albuminuria or proteinuria were assessed at baseline and over one-year follow-up. Increased sCD93 was associated with lower baseline eGFR independently of the confounders. Moreover, sCD93 was negatively associated with eGFR during one-year follow-up in simple analysis; however, this was not confirmed after adjustment for confounders. Baseline sCD93 was positively associated with baseline albuminuria and with increased proteinuria during the follow-up. Serum sCD93 was not correlated with other studied inflammatory markers (interleukin 6, C-reactive protein, procalcitonin and C3 and C4 complement components). To the best of our knowledge, this is the first report regarding the concentrations of sCD93 in kidney transplant recipients and one of the first reports showing the inverse association between sCD93 and renal function. Serum sCD93 should be further evaluated as a diagnostic and prognostic marker in renal transplantation.

α1-Acid Glycoprotein and Dietary Intake in End-Stage Renal Disease Patients.

Management of end-stage renal disease (ESRD) patients requires monitoring each of the components of malnutrition-inflammation-atherosclerosis (MIA) syndrome. Restrictive diet can negatively affect nutritional status and inflammation. An acute-phase protein-α1-acid glycoprotein (AGP), has been associated with energy metabolism in animal and human studies. The aim of our study was to look for a relationship between serum AGP concentrations, laboratory parameters, and nutrient intake in ESRD patients. The study included 59 patients treated with maintenance hemodialysis. A 24 h recall assessed dietary intake during four non-consecutive days-two days in the post-summer period, and two post-winter. Selected laboratory tests were performed: complete blood count, serum iron, total iron biding capacity (TIBC) and unsaturated iron biding capacity (UIBC), vitamin D, AGP, C-reactive protein (CRP), albumin, prealbumin, and phosphate-calcium metabolism markers (intact parathyroid hormone, calcium, phosphate). Recorded dietary intake was highly deficient. A majority of patients did not meet recommended daily requirements for energy, protein, fiber, iron, magnesium, folate, and vitamin D. AGP correlated positively with CRP (R = 0.66), platelets (R = 0.29), and negatively with iron (R = -0.27) and TIBC (R = -0.30). AGP correlated negatively with the dietary intake of plant protein (R = -0.40), potassium (R = -0.27), copper (R = -0.30), vitamin B6 (R = -0.27), and folates (R = -0.27), p < 0.05. However, in multiple regression adjusted for confounders, only CRP was significantly associated with AGP. Our results indicate that in hemodialyzed patients, serum AGP is weakly associated with dietary intake of several nutrients, including plant protein.

Protective and Healing Effects of Ghrelin and Risk of Cancer in the Digestive System.

Ghrelin is an endogenous ligand for the ghrelin receptor, previously known as the growth hormone secretagogue receptor. This hormone is mainly produced by endocrine cells present in the gastric mucosa. The ghrelin-producing cells are also present in other organs of the body, mainly in the digestive system, but in much smaller amount. Ghrelin exhibits a broad spectrum of physiological effects, such as stimulation of growth hormone secretion, gastric secretion, gastrointestinal motility, and food intake, as well as regulation of glucose homeostasis and bone formation, and inhibition of inflammatory processes. This review summarizes the recent findings concerning animal and human data showing protective and therapeutic effects of ghrelin in the gut, and also presents the role of growth hormone and insulin-like growth factor-1 in these effects. In addition, the current data on the possible influence of ghrelin on the carcinogenesis, its importance in predicting the risk of developing gastrointestinal malignances, as well as the potential usefulness of ghrelin in the treatment of cancer, have been presented.

Vertigo as One of the Symptoms of Lyme Disease.

OBJECTIVES: The aim of the study was to evaluate the frequency of vertigo symptoms and potential labyrinth damage in patients with diagnosed Lyme disease (LD). LD can affect the vestibulocochlear nerve, leading to hearing loss and vertigo/dizziness. MATERIAL AND METHODS: The study included a group of 38 patients between the ages of 20 and 77, who were hospitalized due to vertigo/dizziness between 2018 and 2019. All of the patients underwent a detailed medical interview and an otolaryngological and neurological examination, including video electronystagmography (VENG), in addition to audiological and diagnostic tests. Additionally, ELISA and Western blot tests were performed to confirm the diagnosis of LD. RESULTS: In 20 patients (53%), the Romberg trial was positive (p < 0.001). The degree of vestibular dysfunction as shown by the VENG test was associated with the rate of hearing loss as confirmed by the Auditory Brainstem Response (ABR) test (p = 0.011), and it mainly concerned high-frequency sounds (p = 0.014). CONCLUSION: Vertigo can be a symptom of LD. It is often associated with labyrinth and hearing-organ damage, which can imply that the inner ear or nerve VIII is dysfunctional in the course of this disease. Antibiotic therapy is effective in reducing otoneurological symptoms.

Complement Components in the Diagnosis and Treatment after Kidney Transplantation-Is There a Missing Link?

Currently, kidney transplantation is widely accepted as the renal replacement therapy allowing for the best quality of life and longest survival of patients developing end-stage renal disease. However, chronic transplant rejection, recurrence of previous kidney disease or newly acquired conditions, or immunosuppressive drug toxicity often lead to a deterioration of kidney allograft function over time. Complement components play an important role in the pathogenesis of kidney allograft impairment. Most studies on the role of complement in kidney graft function focus on humoral rejection; however, complement has also been associated with cell mediated rejection, post-transplant thrombotic microangiopathy, the recurrence of several glomerulopathies in the transplanted kidney, and transplant tolerance. Better understanding of the complement involvement in the transplanted kidney damage has led to the development of novel therapies that inhibit complement components and improve graft survival. The analysis of functional complotypes, based on the genotype of both graft recipient and donor, may become a valuable tool for assessing the risk of acute transplant rejection. The review summarizes current knowledge on the pathomechanisms of complement activation following kidney transplantation and the resulting diagnostic and therapeutic possibilities.

Association between Sudden Sensorineural Hearing Loss and Lyme Disease.

OBJECTIVES: Sudden sensorineural hearing loss (SSNHL) is defined as sensorineural hearing loss of 30 dB or more over at least three adjacent audiometric frequencies occurring within a 72-h period of time. One of the causes of SSNHL could be the progressive inflammatory state caused by an infection. The aim of this study was to assess the prevalence of SSNHL caused by various factors, most importantly those potentially related to Lyme disease. MATERIAL AND METHODS: The study includes a group of 86 patients between the ages of 20 and 70 who were hospitalized due to SSNHL between 2017 and 2018. All of these patients underwent a detailed medical interview and an otolaryngological examination, including audiological and diagnostic tests. Additionally, ELISA and Western blot tests were performed to confirm the diagnosis of Lyme disease. RESULTS: In this group of 86 patients, nine patients presented with positive antibodies toward Borrelia burgdorferi sensu lato. This group was treated with antibiotics and experienced partial or complete regression of their deafness. This may suggest a relationship between SSNHL and Lyme disease. CONCLUSION: Infections caused by Borrelia burgdorferi may contribute to the development of inflammatory and angiopathic lesions, which are a possible cause of SSNHL. The longer the duration of the infection, the greater the likelihood of permanent and irreversible changes in the vessels of the cochlea or auditory nerve. Therefore, serological tests for Borrelia burgdorferi should be performed during the diagnosis of SSNHL as a possible cause of this illness.

Urinary NGAL Measured after the First Year Post Kidney Transplantation Predicts Changes in Glomerular Filtration over One-Year Follow-Up.

Currently, serum creatinine and estimated glomerular filtration rate (eGFR) together with albuminuria or proteinuria are laboratory markers used in long-term monitoring of kidney transplant recipients. There is a need for more sensitive markers that could serve as early warning signs of graft dysfunction. Our aim was to assess the urinary concentrations of neutrophil gelatinase-associated lipocalin (NGAL) as a predictor of changes in kidney transplant function after the first year post-transplantation. We prospectively recruited 109 patients with functioning graft at least one year after the transplantation, with no acute conditions over the past three months, during their control visits in kidney transplant ambulatory. Urinary NGAL measured on recruitment was twice higher in patients with at least 10% decrease in eGFR over 1-year follow-up compared to those with stable or improving transplant function. Baseline NGAL significantly predicted the relative and absolute changes in eGFR and the mean eGFR during the follow-up independently of baseline eGFR and albuminuria. Moreover, baseline NGAL significantly predicted urinary tract infections during the follow-up, although the infections were not associated with decreasing eGFR. Additionally, we assessed urinary concentrations of matrix metalloproteinase 9-NGAL complex in a subgroup of 77 patients and found higher levels in patients who developed urinary tract infections during the follow-up but not in those with decreasing eGFR. High urinary NGAL in clinically stable kidney transplant recipients beyond the first year after transplantation may be interpreted as a warning and trigger the search for transient or chronic causes of graft dysfunction, or urinary tract infection.

Esophageal Peristalsis Disorders in ALS Patients with Dysphagia.

To detect the variations of esophageal peristalsis in amyotrophic lateral sclerosis (ALS) patients with predominantly bulbar or predominantly pseudobulbar clinical presentation by using esophageal manometry (EM). Fifteen ALS patients with pseudobulbar clinical presentation (PBP) and 13 patients with bulbar presentation (BP), fulfilling WFN Criteria, were studied. EM was performed in all subjects using a flexible catheter with solid-state transducers. Swallowing was initiated with 5 to 10 mL of water (wet swallows) and saliva (dry swallows) and repeated at 30 s intervals. The manometric parameters were measured automatically and visualized by the computer system. The tracings were analyzed using Synectics software. In PBP patients, an increase of resting pressure value in the upper esophageal sphincter (UES) >45 mmHg, a wave-like course of resting pressure, and toothed peristaltic waves were observed. In BP patients, a low amplitude of peristaltic waves <30 mmHg (mean: 17 ± 5) was recorded, without signs of esophageal motility disturbance at onset or during progression. EM procedure allows objectively distinguishing dysphagia in ALS patients due to bulbar syndrome from the dysphagia due to pseudobulbar syndrome. It is important to identify PBP patients because of their high risk of aspiration.

Effects of Biofeedback Training on Esophageal Peristalsis in Amyotrophic Lateral Sclerosis Patients with Dysphagia.

Esophageal manometry (EM) could serve as an objective method for the detection of esophageal peristalsis in patients with amyotrophic lateral sclerosis (ALS). In this group of patients, biofeedback training (BT) using the EM procedure is a promising method for the rehabilitation of swallowing function. A total of 20 ALS patients with clinical evidence of dysphagia and who met WFN criteria were recruited for this study. The standard transnasal EM with solid-state transducers was performed, and swallows with water and saliva were initiated in all subjects and repeated at 30-s intervals. The median upper esophageal contractile amplitude, duration, and velocity results during the wet and dry swallows were evaluated and compared in both the ALS and the control groups. In ALS patients, in contrast to the control, significant abnormalities in all EM parameters were recorded, which implies a specific pattern of esophageal peristalsis. Twelve months after BT, the body mass index (BMI) of ALS patients who underwent BT (ALSBT) was compared to the BMI of those who did not (ALS1)-compared to the ALS1 group, ALSBT patients showed a slightly smaller drop in BMI value. We presume that BT using EM can be a promising tool for the improvement of the swallowing mechanism in ALS patients.

The Marker of Tubular Injury, Kidney Injury Molecule-1 (KIM-1), in Acute Kidney Injury Complicating Acute Pancreatitis: A Preliminary Study.

Acute pancreatitis (AP) may be associated with severe inflammation and hypovolemia leading to organ complications including acute kidney injury (AKI). According to current guidelines, AKI diagnosis is based on dynamic increase in serum creatinine, however, creatinine increase may be influenced by nonrenal factor and appears late following kidney injury. Kidney injury molecule-1 (KIM-1) is a promising marker of renal tubular injury and it has not been studied in AP. Our aim was to assess if urinary KIM-1 may be used to diagnose AKI complicating the early stage of AP. We recruited 69 patients with mild to severe AP admitted to a secondary care hospital during the first 24 h from initial symptoms of AP. KIM-1 was measured in urine samples collected on the day of admission and two subsequent days of hospital stay. AKI was diagnosed based on creatinine increase according to Kidney Disease: Improving Global Outcomes 2012 guidelines. Urinary KIM-1 on study days 1 to 3 was not significantly higher in 10 patients who developed AKI as compared to those without AKI and did not correlate with serum creatinine or urea. On days 2 and 3, urinary KIM-1 correlated positively with urinary liver-type fatty acid-binding protein, another marker of tubular injury. On days 2 and 3, urinary KIM-1 was higher among patients with systemic inflammatory response syndrome, and several correlations between KIM-1 and inflammatory markers (procalcitonin, urokinase-type plasminogen activator receptor, C-reactive protein) were observed on days 1 to 3. With a limited number of patients, our study cannot exclude the diagnostic utility of KIM-1 in AP, however, our results do not support it. We hypothesize that the increase of KIM-1 in AKI complicating AP lasts a short time, and it may only be observed with more frequent monitoring of the marker. Moreover, urinary KIM-1 concentrations in AP are associated with inflammation severity.

Pretreatment with Warfarin Attenuates the Development of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

In acute pancreatitis (AP), pancreatic damage leads to local vascular injury, manifesting as endothelial damage and activation, increased vascular permeability, leukocyte rolling, sticking and transmigration to pancreatic tissue as well as activation of coagulation. Previous studies have shown that pretreatment with heparin or acenocoumarol inhibits the development of AP. The aim of the present study was to check the impact of pretreatment with warfarin, an oral vitamin K antagonist, on the development of ischemia/reperfusion-induced AP in rats. AP was induced by pancreatic ischemia followed by reperfusion of the gland. Warfarin (90, 180 or 270 µg/kg/dose) or vehicle were administered intragastrically once a day for 7 days before induction of AP. The effect of warfarin on the severity of AP was assessed 6 h after pancreatic reperfusion. The assessment included histological, functional, and biochemical analyses. Pretreatment with warfarin given at a dose of 90 or 180 µg/kg/dose increased the international normalized ratio and reduced morphological signs of pancreatic damage such as pancreatic edema, vacuolization of acinar cells, necrosis and the number of hemorrhages. These effects were accompanied by an improvement of pancreatic blood flow and a decrease in serum level amylase, lipase, pro-inflammatory interleukin-1ß and plasma level of D-dimer. In contrast, pretreatment with warfarin given at a dose of 270 µg/kg/dose led to an increase in severity of pancreatic damage and biochemical indicators of AP. In addition, this dose of warfarin resulted in deaths in some animals. Pretreatment with low doses of warfarin inhibits the development of AP induced by pancreatic ischemia followed by reperfusion.

Acute Phase Proteins and Vitamin D Seasonal Variation in End-Stage Renal Disease Patients.

End-stage renal disease (ESRD) patients are vulnerable to vitamin D deficiency due to impaired renal hydroxylation, low dietary intake and inadequate sun exposure. Vitamin D plays a role in innate and adaptive immunity and its seasonal variation has been linked to mortality. ESRD is associated with inadequate removal of pro-inflammatory cytokines regulating acute phase protein (APP) synthesis. Our aim was to look for associations between lifestyle factors, diet, and vitamin D seasonal variation and their relationship with selected APPs and calcium-phosphate metabolism. The study included 59 ESRD patients treated with maintenance hemodialysis. A 24-hour dietary recall was conducted in the post-summer (November 2018, PS) and post-winter (February/March 2019, PW) period, and blood was collected for the measurements of serum total vitamin D, α1-acid glycoprotein (AGP), C-reactive protein (CRP), albumin, prealbumin (PRE), parathormone, calcium and phosphate. A self-constructed questionnaire gathered information on vitamin D supplementation, sun exposure and physical activity. Higher caloric intake was observed PW compared PS. Less than 15% of participants met the dietary recommendations for energy, protein, fiber, vitamin D and magnesium intake. Vitamin D supplementation was associated with higher serum vitamin D regardless of season. AGP, PRE, albumin, and vitamin D presented seasonal changes (higher values PS). In patients with serum vitamin D below 25 ng/mL, vitamin D seasonal change correlated with CRP and prealbumin change. Phosphate and Ca × P correlated positively with AGP. A low vitamin D serum level could impact the inflammatory process; however, more studies are needed to confirm the relationship.

Does Beta-Trace Protein (BTP) Outperform Cystatin C as a Diagnostic Marker of Acute Kidney Injury Complicating the Early Phase of Acute Pancreatitis?

Acute pancreatitis (AP) belongs to the commonest acute gastrointestinal conditions requiring hospitalization. Acute kidney injury (AKI) often complicates moderately severe and severe AP, leading to increased mortality. Among the laboratory markers proposed for early diagnosis of AKI, few have been studied in AP, including cystatin C and neutrophil gelatinase-associated lipocalin (NGAL). Beta-trace protein (BTP), a low-molecular-weight glycoprotein proposed as an early marker of decreased glomerular filtration, has never been studied in AP. We investigated the diagnostic usefulness of serum BTP for early diagnosis of AKI complicating AP in comparison to previously studied markers. BTP was measured in serum samples collected over the first three days of hospital stay from 73 adult patients admitted within 24 h of mild to severe AP. Thirteen patients (18%) developed AKI in the early phase of AP. Serum BTP was higher in patients who developed AKI, starting from the first day of hospitalization. Strong correlations were observed between BTP and serum cystatin C but not serum or urine NGAL. On admission, BTP positively correlated with endothelial dysfunction. The diagnostic usefulness of BTP for AKI was similar to cystatin C and lower than NGAL. Increased BTP is an early predictor of AKI complicating AP. However, it does not outperform cystatin C or NGAL.

Redox Balance Correlates with Nutritional Status among Patients with End-Stage Renal Disease Treated with Maintenance Hemodialysis.

Over 50% of end-stage renal disease (ESRD) patients die of cardiovascular disease. ESRD patients treated with maintenance hemodialysis are repeatedly exposed to oxidative stress. The aim of the study was to find the relationship between lifestyle factors, nutritional status, calcium-phosphate metabolism, and selected redox parameters such as glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), uric acid (UA), and total antioxidant capacity expressed as ferric reducing antioxidant power (FRAP). The study included 97 ESRD hemodialysis patients and 42 controls with no renal disease. Patients were asked to complete a questionnaire which gathered information on their physical activity, hours of sleep, smoking, and frequency of fruit and vegetable intake; the blood samples were then drawn before the midweek dialysis session. The ESRD patients had lower levels of GR, GPx, and SOD activity, a lower level of FRAP, and a higher UA concentration than the control group. The FRAP value decreased with age (ρ = -0.32, p = 0.001); smokers had a significantly lower SOD activity in comparison to nonsmokers (p = 0.03). In the ESRD patients, FRAP and UA correlated with both albumin (ρ = 0.26, p = 0.011; ρ = 0.41, p = 0.006, respectively) and prealbumin (ρ = 0.34, p ≤ 0.001; ρ = 0.28, p = 0.006, respectively), whereas UA, GR, GPx, and SOD correlated with calcium, UA, GR, and GPx with phosphate level. Based on the findings, there are weak associations between nutritional status and selected redox parameters in hemodialyzed patients. Further studies are needed to establish if diet modifications and adequate nutritional status can positively impact the antioxidant capacity in this group of patients.

Potential Prognostic Markers of Acute Kidney Injury in the Early Phase of Acute Pancreatitis.

Acute kidney injury (AKI) is a serious complication of acute pancreatitis (AP), which occurs in up to 70% of patients with severe AP and significantly increases the risk of mortality. At present, AKI is diagnosed based on dynamic increase in serum creatinine and decreased urine output; however, there is a need for earlier and more accurate biomarkers. The aim of the study was to review current evidence on the laboratory tests that were studied as the potential biomarkers of AKI in AP. We also briefly summarized the knowledge coming from the studies including sepsis or ICU patients since severe acute pancreatitis is associated with systemic inflammation and organ failure. Serum cystatin C and serum or urine NGAL have been shown to predict or diagnose AKI in AP; however, this evidence come from the single center studies of low number of patients. Other markers, such as urinary kidney injury molecule-1, cell cycle arrest biomarkers (tissue inhibitor metalloproteinase-2 and urine insulin-like growth factor-binding protein 7), interleukin-18, liver-type fatty acid-binding protein, or calprotectin have been studied in other populations suffering from systemic inflammatory states. In AP, the potential markers of AKI may be significantly influenced by either dehydration or inflammation, and the impact of these factors may be difficult to distinguish from kidney injury. The subject of AKI complicating AP is understudied. More studies are needed, for both exploratory (to choose the best markers) and clinical (to evaluate the diagnostic accuracy of the chosen markers in real clinical settings).

Right Heart Catheterization-Background, Physiological Basics, and Clinical Implications.

The idea of right heart catheterization (RHC) grew in the milieu of modern thinking about the cardiovascular system, influenced by the experiments of William Harvey, which were inspired by the treatises of Greek philosophers like Aristotle and Gallen, who made significant contributions to the subject. RHC was first discovered in the eighteenth century by William Hale and was subsequently systematically improved by outstanding experiments in the field of physiology, led by Cournand and Dickinson Richards, which finally resulted in the implementation of pulmonary artery catheters (PAC) into clinical practice by Jeremy Swan and William Ganz in the early 1970s. Despite its premature euphoric reception, some further analysis seemed not to share the early enthusiasm as far as the safety and effectiveness issues were concerned. Nonetheless, RHC kept its significant role in the diagnosis, prognostic evaluation, and decision-making of pulmonary hypertension and heart failure patients. Its role in the treatment of end-stage heart failure seems not to be fully understood, although it is promising. PAC-guided optimization of the treatment of patients with ventricular assist devices and its beneficial introduction into clinical practice remains a challenge for the near future.