No abstract available.
Candidiasis* ; Fluconazole* ; Humans

Heparin, a widely used anticoagulant, is currently the anticoagulant of choice in long-term hemodialysis (HD). Heparin-induced thrombocytopenia (HIT) is one of the most serious side effects of heparin which can cause arterial or venous thromboembolism associated with substantial morbidity and mortality. We experienced two patients who had thrombocytopenia and vascular access occlusion during the induction period of HD with the use of unfractionated heparin. Thrombocytopenia was improved after discontinuation of heparin. HIT was confirmed with anti-heparin/platelet factor 4 antibody test. HD was conducted and arteriovenous fistula was created successfully after switch of heparin to argatroban (Novastan(R)) or nafamostat mesilate (Futhan(R)). Nephrologist should rule out HIT first when thrombocytopenia and thromboembolic complications occur after use of heparin, especially during the induction period of HD. For suspicious patients, immediate cessation of heparin and switch to alternative anticoagulant is very important to avoid serious complications.
Arteriovenous Fistula ; Heparin ; Humans ; Mesylates ; Mortality ; Renal Dialysis* ; Thrombocytopenia* ; Venous Thromboembolism

BACKGROUND/AIMS: Although several studies have claimed that Helicobacter pylori (H. pylori) infection is related to cardiovascular disease, it is still uncertain whether it is related to the acute process or the chronic inflammatory atherosclerotic changes. The aim of our study was to confirm the impact of active H. pylori infection on coronary heart disease, acute inflammatory factors, and the coagulation factors. METHODS: A total of 94 patients completed questionnaires about occupation, smoking, past medical history, and socio-economic status. The serum of the subjects was drawn for a low density lipoprotein test, white blood cell count, C reactive protein, fibrinogen, homocysteine, prothrombin time, activated partial thrombin time, plasminogen activator inhibitor type-1, and tissue-type plasminogen test. All of the subjects underwent a coronary angiography and an upper gastrointestinal endoscopy for the diagnosis of coronary heart disease and H. pylori infection, respectively. RESULTS: There was no significant difference in acute inflammatory factors, coagulation factors, atheromatous burden score, and Jeopardy score between the H. pylori-infected group and non-infected group. Odds ratio of H. pylori infection on coronary heart disease was 2.59 (95% CI, 0.80-6.17), but it diminished below 1.0 (95% CI, 0.14-1.36) after adjusting for conventional risk factors such as age, gender, diabetes, hypertension, smoking, body mass index and socio-economic status. CONCLUSIONS: H. pylori infection is not an independent risk factor for coronary heart disease, and it does not alter the coagulation system or evoke the systemic inflammatory response.
Aged ; Coronary Disease/blood/*microbiology ; Female ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Risk Factors

Liddle's syndrome was described in 1963 by Liddle, et al., as the disease featuring a hypertension and hypokalemia but with negligible secretion of aldosterone. This syndrome, which morphologically belongs to an abnormal intrinsic tubular disorder with normal renal function, is characterized by hypokalemia, metabolic alkalosis, and hypertension due to the abnormal increase in excretion of potassium in distal tubules or collecting duct and the increase in reabsorption of sodium in distal tubules. This syndrome, which is rare disease, is observed with the low level of plasma and urinary aldosterone and suppressed plasma renin level and is known as dominant mode of inheritance with a family background. The authors paid attention to a 79-year-old man who showed a high blood pressure of 210/130mmHg as well as musle weakness, especially lower extremities due to metabolic alkalosis featuring a hypokalemia level of 2.0mEq/L when he was admitted to our hospital, Because his serum potassium were not improved with the medication of intravenous potassium supply, and his blood pressure continued to be high without the improvement of muscle weakness, we prescribed 300mg of spironolactone for two weeks. His symptom, however, was not cured. Then, instead of spironolactone, we prescribed 150mg of triamterene and a low salt diet which finally improved his symptoms. Because there has been no reported case in the Korean medical literature, we report a case of successfully treated Liddle's syndrome due to triamterene administration.
Aged ; Aldosterone ; Alkalosis ; Blood Pressure ; Diet ; Humans ; Hypertension ; Hypokalemia ; Lower Extremity ; Muscle Weakness* ; Plasma ; Potassium ; Rare Diseases ; Renin ; Sodium ; Spironolactone ; Triamterene ; Wills

Background: It is well known that a large number of patients with diabetes also have dyslipidemia, which significantly increases the risk of cardiovascular disease (CVD). This study aimed to evaluate the efficacy and safety of combination drugs consisting of metformin and atorvastatin, widely used as therapeutic agents for diabetes and dyslipidemia. Methods: This randomized, double-blind, placebo-controlled, parallel-group and phase III multicenter study included adults with glycosylated hemoglobin (HbA1c) levels >7.0% and <10.0%, low-density lipoprotein cholesterol (LDL-C) >100 and <250 mg/dL. One hundred eighty-five eligible subjects were randomized to the combination group (metformin+atorvastatin), metformin group (metformin+atorvastatin placebo), and atorvastatin group (atorvastatin+metformin placebo). The primary efficacy endpoints were the percent changes in HbA1c and LDL-C levels from baseline at the end of the treatment. Results: After 16 weeks of treatment compared to baseline, HbA1c showed a significant difference of 0.94% compared to the atorvastatin group in the combination group (0.35% vs. −0.58%, respectively; P<0.0001), whereas the proportion of patients with increased HbA1c was also 62% and 15%, respectively, showing a significant difference (P<0.001). The combination group also showed a significant decrease in LDL-C levels compared to the metformin group (−55.20% vs. −7.69%, P<0.001) without previously unknown adverse drug events. Conclusion The addition of atorvastatin to metformin improved HbA1c and LDL-C levels to a significant extent compared to metformin or atorvastatin alone in diabetes and dyslipidemia patients. This study also suggested metformin’s preventive effect on the glucose-elevating potential of atorvastatin in patients with type 2 diabetes mellitus and dyslipidemia, insufficiently controlled with exercise and diet. Metformin and atorvastatin combination might be an effective treatment in reducing the CVD risk in patients with both diabetes and dyslipidemia because of its lowering effect on LDL-C and glucose.

Background: It is well known that a large number of patients with diabetes also have dyslipidemia, which significantly increases the risk of cardiovascular disease (CVD). This study aimed to evaluate the efficacy and safety of combination drugs consisting of metformin and atorvastatin, widely used as therapeutic agents for diabetes and dyslipidemia. Methods: This randomized, double-blind, placebo-controlled, parallel-group and phase III multicenter study included adults with glycosylated hemoglobin (HbA1c) levels >7.0% and <10.0%, low-density lipoprotein cholesterol (LDL-C) >100 and <250 mg/dL. One hundred eighty-five eligible subjects were randomized to the combination group (metformin+atorvastatin), metformin group (metformin+atorvastatin placebo), and atorvastatin group (atorvastatin+metformin placebo). The primary efficacy endpoints were the percent changes in HbA1c and LDL-C levels from baseline at the end of the treatment. Results: After 16 weeks of treatment compared to baseline, HbA1c showed a significant difference of 0.94% compared to the atorvastatin group in the combination group (0.35% vs. −0.58%, respectively; P<0.0001), whereas the proportion of patients with increased HbA1c was also 62% and 15%, respectively, showing a significant difference (P<0.001). The combination group also showed a significant decrease in LDL-C levels compared to the metformin group (−55.20% vs. −7.69%, P<0.001) without previously unknown adverse drug events. Conclusion The addition of atorvastatin to metformin improved HbA1c and LDL-C levels to a significant extent compared to metformin or atorvastatin alone in diabetes and dyslipidemia patients. This study also suggested metformin’s preventive effect on the glucose-elevating potential of atorvastatin in patients with type 2 diabetes mellitus and dyslipidemia, insufficiently controlled with exercise and diet. Metformin and atorvastatin combination might be an effective treatment in reducing the CVD risk in patients with both diabetes and dyslipidemia because of its lowering effect on LDL-C and glucose.

Background: It is well known that a large number of patients with diabetes also have dyslipidemia, which significantly increases the risk of cardiovascular disease (CVD). This study aimed to evaluate the efficacy and safety of combination drugs consisting of metformin and atorvastatin, widely used as therapeutic agents for diabetes and dyslipidemia. Methods: This randomized, double-blind, placebo-controlled, parallel-group and phase III multicenter study included adults with glycosylated hemoglobin (HbA1c) levels >7.0% and <10.0%, low-density lipoprotein cholesterol (LDL-C) >100 and <250 mg/dL. One hundred eighty-five eligible subjects were randomized to the combination group (metformin+atorvastatin), metformin group (metformin+atorvastatin placebo), and atorvastatin group (atorvastatin+metformin placebo). The primary efficacy endpoints were the percent changes in HbA1c and LDL-C levels from baseline at the end of the treatment. Results: After 16 weeks of treatment compared to baseline, HbA1c showed a significant difference of 0.94% compared to the atorvastatin group in the combination group (0.35% vs. −0.58%, respectively; P<0.0001), whereas the proportion of patients with increased HbA1c was also 62% and 15%, respectively, showing a significant difference (P<0.001). The combination group also showed a significant decrease in LDL-C levels compared to the metformin group (−55.20% vs. −7.69%, P<0.001) without previously unknown adverse drug events. Conclusion The addition of atorvastatin to metformin improved HbA1c and LDL-C levels to a significant extent compared to metformin or atorvastatin alone in diabetes and dyslipidemia patients. This study also suggested metformin’s preventive effect on the glucose-elevating potential of atorvastatin in patients with type 2 diabetes mellitus and dyslipidemia, insufficiently controlled with exercise and diet. Metformin and atorvastatin combination might be an effective treatment in reducing the CVD risk in patients with both diabetes and dyslipidemia because of its lowering effect on LDL-C and glucose.