Effects of a 980 nm Diode Laser as an Adjunct to Nonsurgical Periodontal Therapy on Periodontal Status and Inflammatory Markers in Patients After Myocardial Infarction: A Randomized Controlled Trial.

Objective: The aim of this study was to evaluate the efficacy of diode laser (DL) therapy as an adjunct to nonsurgical periodontal therapy in the treatment of periodontitis in patients after myocardial infarction (MI). Methods: After given permission by Ethics Commission of the Pomeranian Medical University (KB-0012/06/12), 36 patients <65 years of age (mean: 56.3 ± 7.9) with periodontitis, 6 weeks to 6 months after MI were enrolled for the study. The control group (n = 18) received nonsurgical periodontal therapy, whereas the test group (n = 18) received nonsurgical periodontal therapy followed by laser therapy of the periodontal pockets with 980 nm DL, 1 W, continuous wave mode, and 20 sec per tooth side. Procedures were repeated twice at 5-7 day intervals. Clinical periodontal parameters and inflammatory markers in gingival crevicular fluid (GCF) [elastase, aspartate transaminase (AST), alanine transaminase (ALT) and interleukin (IL)-6, proteins], bloodstream [fibrinogen, high-sensitivity CRP (hs-CRP), IL-6, AST and ALT], and lipid fractions (triglycerides, high-density lipoprotein, low-density lipoprotein, and total cholesterol) were measured before treatment, 2 weeks, and 3 months after treatment. Results: The difference between groups in the reduction of periodontal pocket depth (PPD) in pockets ≥7 mm was found to be significant in the test group (p < 0.05). There was also a statistically significant reduction in the volume of GCF and hs-CRP concentration in blood 2 weeks after the completion of treatment in the test group (p < 0.05). Conclusions: Within the limits of this study, it can be concluded that in the nonsurgical treatment of periodontitis with patients after MI, the additional use of DL enables greater reduction of PPD in pockets ≥7 mm. In addition, a faster reduction of GCF volume and hs-CRP was noted in the laser group.

Can metabolic disorders in aging men contribute to prostatic hyperplasia eligible for transurethral resection of the prostate (TURP)?

PURPOSE: The aim of this study was to evaluate the incidence and severity of metabolic disorders occurring in the metabolic syndrome in patients with benign prostatic hyperplasia eligible for surgical treatment. METHODS: The study group consisted men with diagnosed benign prostatic hyperplasia. The control group consisted patients recruited from basic health care units. Abdominal circumference, body weight and blood serum metabolic parameters were determined in the experimental and control groups. The concentrations of glucose were determined, as well as total cholesterol (ChT), low-density lipoprotein (LDL), high density lipoprotein (HDL) and triglycerides (TAG), by spectrophotometric method using reagent kits. RESULTS: In the study group 91 (60.3%) cases of metabolic syndrome (MetS) were diagnosed, while in the control group 71 (46.1%) men met the diagnostic criteria for this syndrome (p=0.018). The analysis shows a relationship between MetS in patients with BPH and concentration glucose, ChT, LDL, HDL, systolic blood pressure and diastolic blood pressure. We found no significant statistical relationship between body weight, abdominal circumference and concentration TAG, hypertension in patients and controls. CONCLUSIONS: in the study presented in this article, statistically significant relationships between BPH and the diagnostic parameters of the metabolic syndrome were demonstrated. These results indicate to the necessity of the modification of the lifestyle, taking preventive measures in diabetes, and evaluation of lipid metabolism disorders. It is recommended to assess symptoms that may suggest BPH (as a manifestation of LUTS) in men over 50 years of age with diagnoses of metabolic disorders (including MetS), and provide them with specialist urological care in order to prevent surgical treatment of the prostate.

[Dihydropirymidine dehydrogenase (DPD)--a toxicity marker for 5-fluorouracil?]. / Dehydrogenaza dihydopirymidynowa (DPD)--marker toksycznosci 5-fluorouracylu?

In proceedings relating to patients suffering from cancer, an important step is predicting response and toxicity to treatment. Depending on the type of cancer, physicians use the generally accepted schema of treatment, for example pharmacotherapy. 5-fluorouracil (5-FU) is the most widely used anticancer drug in chemotherapy for colon, breast, and head and neck cancer. Patients with dihydropyrimidine dehydrogenase (DPD) deficiency, which is responsible for the metabolism of 5-FU, may experience severe side effects during treatment, and even death. In many publications the need for determining the activity of DPD is discussed, which would protect the patient from the numerous side effects of treatment. However, in practice these assays are not done routinely, despite the high demand. In most cases, a genetic test is used to detect changes in the gene encoding DPD (such as in the USA), but because of the large number of mutations the genetic test cannot be used as a screening test. Dihydropyrimidine dehydrogenase activity has been shown to have high variability among the general population, with an estimated proportion of at least 3-5% of individuals showing low or deficient DPD activity. In this publication we presents data about average dihydropirymidine dehydrogenase activity in various populations of the world (e.g. Japan, Ghana, Great Britain) including gender differences and collected information about the possibility of determination of DPD activity in different countries. Detection of reduced DPD activity in patients with planned chemotherapy will allow a lower dosage of 5-FU or alternative treatment without exposing them to adverse reactions.