Although the worldwide prevalence of Helicobacter pylori (H. pylori) infection has decreased, peptic ulcer disease (PUD) remains prevalent due to increased usage of non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin. In recent years, the prevalence of H. pylori infection in PUD cases and the distribution of PUD have changed in Korea. The incidence of idiopathic H. pylori-negative ulcers has increased, and research is needed to determine the cause of these idiopathic ulcers. The eradication of H. pylori infection decreases PUD recurrence, and plays a crucial role in the treatment of PUD. The H. pylori test and-treat strategy is beneficial for patients starting NSAIDs and long-term aspirin users with a history of bleeding ulcers. Although the H. pylori eradication rate is declining steadily due to antibiotic resistance, especially to clarithromycin, current guidelines still recommend standard triple therapy, including a proton pump inhibitor, amoxicillin, and clarithromycin, as a first-line therapy. Recently, various treatment regimens, including sequential or concomitant therapies, have been developed in an attempt to overcome the low eradication rate observed with standard triple therapy. The aim of this article is to review recent trends in H. pylori-related PUD, focusing on epidemiology and treatment strategies. (Korean J Med 2014;86:655-663)

Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic, antipyretic, and anti-inflammatory properties and are widely used for treating musculoskeletal and cardiovascular diseases. Notwithstanding these therapeutic efficacies, gastrointestinal toxicity is the major health problem associated with NSAID use. NSAID-related peptic ulcers are a well known complication due to direct mucosal injury and cyclooxygenase inhibition. Risk factors for NSAID-related peptic ulcers include a prior history of peptic ulcer; age > 65 years; high-dose NSAID therapy; and concurrent use of aspirin (including low dose), corticosteroids, or anticoagulants. In addition, Helicobacter pylori infection is an independent risk factor; therefore, eradication therapy is recommended in high-risk patients using NSAIDs. Currently, misoprostol, H2-receptor antagonists, proton pump inhibitors, and COX-2 selective inhibitors are used to prevent and treat NSAID-related peptic ulcers. Further, strategic approaches are required through appropriate NSAID use and risk factor stratification to prevent NSAID-related peptic ulcers and associated complications. (Korean J Med 2014;86:664-672)

Antiplatelet therapies have been widely used to prevent cardiovascular diseases. However, antiplatelet agents cause gastrointestinal (GI) damage and are associated with a greater risk of gastroduodenal ulcers and life-threatening ulcer complications. The first step to reduce the GI risk of antiplatelet therapy is to assess whether the patient requires continuous antiplatelet therapy. The second step is to eliminate risk factors that may place the patient at greater GI risk such as Helicobacter pylori infection, NSAID use, steroid ingestion, and smoking. Continuous aspirin therapy plus a powerful proton pump inhibitor (PPI) is the choice of treatment for antiplatelet-related peptic ulcers. The risk of cardiovascular complications and risk of gastric complication using antiplatelet agents should be evaluated individually. (Korean J Med 2014;86:673-677)

Non-Helicobacter pylori, non-NSAID peptic ulcer disease, termed idiopathic peptic ulcer disease (IPUD), is being increasingly recognized. Current data suggest that the relative proportion of patients with IPUD among those with peptic ulcers has been increasing for the past decade in both the West and East, while the prevalence of H. pylori ulcers has decreased. Potential causative or risk factors of IPUD include cigarette smoking, genetic predisposition, psychological factors, infections other than H. pylori, non-NSAID drugs or toxins, systemic inflammatory disease, and local mucosal defects. Diagnosis is made after confident exclusion of H. pylori infection by at least two different standard tests and accurate exclusion of unrecognized or surreptitious NSAID use by careful history taking and serologic assay. IPUD is characterized by higher complication and recurrence rates than other forms of peptic ulcer disease and has become a main cause of refractory ulcer disease. Maintenance therapy using proton pump inhibitors may be required at higher doses and for longer durations than in H. pylori- or NSAID-associated peptic ulcer diseases. Well designed nationwide epidemiologic studies are required to fully elucidate this emerging condition. (Korean J Med 2014;86: 678-685)

Hyponatremia results from a relative excess of total body water compared with the sodium content. Except for primary polydipsia, vasopressin activation plays a major role in pathogenesis of water retention. Consequently, the increase of solute-free water clearance by inactivating vasopressin action would be a more reasonable therapeutic approach than the addition of sodium. The V2 vasopressin receptor is mainly localized to the collecting ducts in the kidney and causes water reabsorption via water channels. Selective V2 receptor antagonists or vaptans were recently introduced to clinical practices and may be useful for correcting dilutional hyponatremia. Clinical trials have shown that vaptans are effective in increasing the serum sodium concentration in patients with syndrome of inappropriate anti-diuresis and congestive heart failure and that they might be safe as long as patients are allowed free accesses to water. However, the indications for using vaptans need to be more refined, and the question of their long-term cost-effectiveness should be answered. In addition, the potential roles of vaptans in ameliorating the growth of cysts in polycystic kidney disease, saving diuretics in edematous disorders, and retarding the progression of chronic kidney disease are being explored. (Korean J Med 2013;85:686-694)

Irritable bowel syndrome (IBS) is one of the most prevalent functional gastrointestinal disorders. It is a multi-factorial disorder due to abnormal gastrointestinal motility, low-grade inflammation, visceral hypersensitivity, and communication between the gut-brain axis. IBS is traditionally treated with dietary and lifestyle modifications, fiber supplementation, and psychological and pharmacological therapies. Diet therapy including the low FODMAP diet and excluding certain food constituents is often used. Antispasmodics plus stool consistency modifiers to treat the major symptoms and defecation are first-line drug treatments. 5-Hydroxytryptamine (5-HT) receptors in the gastrointestinal tract, particularly 5-HT3 and 5-HT4 receptors are involved not only in modulating gut motility but in visceral sensory pathways. Drugs that act on both receptor classes appear to reduce visceral sensitivity and have inhibitory effects on motor activity in the distal intestine. 5-HT4 agonists may improve constipation predominant IBS by normalizing bowel habits and thereby reduce abdominal pain. IBS continues to be a therapeutic challenge because of its diverse symptomatology and lack of a single pathophysiological target for drug intervention. (Korean J Med 2014;86:695-697)

Fenofibrate is one of PPAR-α (peroxisome proliferator activated receptor alpha) agonists. Fenofibrate decreases effectively triglyceride and increases high density lipoprotein cholesterol level through the effect on lipoprotein lipase, hepatic production and degradation of lipoproteins. Fenofibrate was recommended as the drug for hypertriglyceridemia treatment in European guideline released in 2011. But American heart association guideline in 2013 did not recommend non-statin therapy including fibrate for the prevention of atherosclerotic cardiovascular disease. But fenofibrate is still considered as the important drug for the management of atherogenic dyslipidemia especially in patients with metabolic syndrome and diabetes to reduce the residual risk after statin therapy from the evidence of many studies. Fibrates including bezafibrate, gemfibrozil, and fenofibrate increased serum creatinine level in several studies. But the mechanism of change in renal function is not clear till now. And the reversibility of renal function with drug discontinuation is dependent on the kinds of fibrate. Fenofibrate increased serum creatinine level, decreased albuminuria and renal function was reversible with the drug discontinuation in large clinical trials. In these days renal function change with fenofibrate therapy in Korean patients with hypertriglyceridemia was investigated. Fenofibrate treatment for 2 months increased serum creatinine level significantly and old age was associated with the change of renal function in multivariate analysis. Short term therapy significantly increased serum creatinine level even within normal range, and this change may be important in some groups especially old age. (Korean J Med 2014;86:698-701)

목적: 고중성지방혈증 환자에서 단기간 fenofibrate를 투여하였을 때에 혈중 크레아티닌 농도의 변화와 이에 영향을 미치는 인자들을 관찰해 보고자 하였다. 방법: 혈중 중성지방 농도가 200 mg/dL 이상인 86명의 고중성지방혈증 환자를 대상으로 하였다. 이들을 micronized fenofibrate 160 mg을 투여한 Fenofibrate 투여군과 대조군으로 나누었다. 혈중 지질농도와 신기능을 나타내는 인자들을 치료 전과 치료 후 2개월에 측정하였다. 결과: 추정 사구체여과율은 Fenofibrate군에서 감소한 반면에(p < 0.001), 대조군에서는 변화가 없었다(p = 0.80). 이것의 백분율 변화는 각각 -18.6 ± 8.6%와 0.9 ± 9.6%로 두 군사이에 차이가 있었다(p < 0.001). 크레아티닌 농도는 Fenofibrate군에서 증가한 반면에(p < 0.001), 대조군은 변화가 없었다(p = 0.37). 크레아티닌 농도의 백분율 변화는 Fenofibrate 군에서 대조군에 비해 유의하게 더 많이 증가하였다(p < 0.001). 전체 환자(n = 86)에서 크레아티닌 농도의 백분율 증가는 fenofibrate 투여(r = 0.71, p < 0.001)와 고령(r = 0.27, p < 0.05) 과 독립적 연관이 있었다. Fenofibrate군에서 크레아티닌 농도의 백분율 증가는 고령(r = 0.51, p < 0.001), 비흡연(r = 0.42, p < 0.005)과 독립적 연관이 있었다. 전체 환자에서 크레아티닌 농도의 증가가 20% 이상인 군(n = 21)과 20% 미만인 군(n =65)으로 나누었을 때에, 20% 이상의 증가는 다변수 로지스틱 회귀분석에서 fenofibrate 투여(p < 0.001)와 고령(p < 0.005)과 연관이 있었다. Fenofibrate군에서는 단지 고령(p < 0.001)과 연관이 있었다. 결론: 고중성지방을 가진 한국인 환자에서 단기간의 fenofibrate의 투여는 크레아티닌 농도를 의미 있게 증가시키며 이러한 증가는 고령에서 더 뚜렷하였다. 따라서 fenofibrate를 투여할 때에는 신기능의 추적관찰이 특히 고령에서 투약 초기에 필요할 것으로 생각된다.

목적: 스티븐스-존슨증후군(Stevens-Johnson syndrome, SJS), 독성표피괴사용해(toxic epidermal necrolysis, TEN) 그리고 호산구 증가증 및 전신 증상을 동반한 약물 반응(drug reaction with eosinophilia and systemic symptoms, DRESS)은 중증피부 유해반응(severe cutaneous adverse reactions, SCARs)에 속하는 질환으로 내부 장기를 침범하고 사망률이 높다. 국내에는 지금까지 SCARs에 대한 범국가적인 연구가 없었다. 방법: 2009년 6월부터 2010년 12월까지 약물감시사업단을 통해 수집된 의약품 유해사례보고 자료 중 SCARs에 해당되는 사례들을 분석하였다. 보고자 나이, 성별, 투약 경로, 의심 약물의 종류에 대하여 분석하였다. 아울러 기존에 국내에서 발표된 SCARs 사례를 분석하였다. 결과: SJS은 66건, TEN은 7건 그리고 DRESS는 27건으로 총 100건의 SCAR가 보고되었다. 환자군의 평균 연령은 54.1 ± 19.8였고, 남녀 비율은 1:0.88이었다. SJS 61가지, TEN 15가지, DRESS 29가지로 총 81가지의 약물이 보고되었다. 가장 빈번하게 보고된 의심 약물은 allopurinol (12건)이었다. SJS의 의심 약물로 allopurinol (8건)이 가장 빈번하였고 carbamazepine 이 5건으로 그 뒤를 따랐다. TEN에서는 levofloxacin이 2건으로 가장 많았다. DRESS에서 가장 빈번하게 보고된 의심 약물은 allopurinol (4건)과 vancomycin (4건)이었다. 가장 흔한 약물군은 전신적 항감염제(antiinfectives for systemic use, 75건, 46.6%)였다. 국내에서 보고된 증례에서 가장 빈번한 의심 약물은 carbamazepine이었다. 결론: 자발적 보고에서 가장 흔한 SCARs 원인은 개별약제로는 allopurinol, 약물군으로는 전신적 항감염제가 원인 약물이었다. 지금까지 국내에서 보고된 SCARs 증례를 분석한 결과 carbamazepine이 가장 높은 빈도를 차지하였다.

초음파 가이드를 이용한 고주파 열치료는 간세포암 치료에 있어 효과적이고 안전한 치료방법이다. 비록 간세포암의 최선의 치료법은 수술적 절제이나 고주파 열치료는 이러한 수술을 대체할 수 있는 대안으로 떠오르고 있다. 고주파 열치료의 잠재적 합병증으로 간농양, 복수, 흉수, 피부 화상, 저산소증, 기흉, 간피막하 혈종, 혈복강, 간부전, 종양 파종, 담도 병변 등이 있다. 본 증례에서는 매우 드문 합병증으로 간세포암에 대해 고주파 열치료 후 지연형으로 발생한 간농양-횡행결장 누공을 보고 하는 바이다. 환자는 경피적 농양배액술 및 항생제 치료 후 간의 부분절제와 결장을 포함한 누공의 절제를 통하여 성공적으로 치료되었다. 본 증례의 희소성으로 인하여 문헌고찰과 함께 보고하는 바이다.