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This retrospective study aimed to evaluate the levels of coagulation factors and presence of disseminated intravascular coagulation (DIC) in patients with scrub typhus. We included patients confirmed to have scrub typhus at the Chosun University Hospital between September 2004 and December 2009. The DIC scores were evaluated in 365 patients and 36 healthy controls. The median concentrations of fibrinogen, d-dimer, and fibrin/fibrinogen degradation products (FDP) were compared between patients and healthy controls (p

악성 빈혈은 위점막의 위축 혹은 위벽세포의 자가면역성손상으로 내인자가 결핍되며 비타민 B12의 흡수 장애가 일어나 거대적혈모구빈혈이 발생한 것을 의미한다. 악성 빈혈의 치료는 비타민 B12 근육주사나 스테로이드의 투여이나, 저자들은 악성 빈혈로 진단된 후 특별한 치료 없이 자연적으로 호전된 악성 빈혈의 증례를 경험하였기에 이를 보고하는 바이다.

Tumor lysis syndrome is a well-described, serious complication of chemotherapy administered to treat malignancies. However, a very rare event resulting in the spontaneous necrosis of a tumor prior to therapy can also occur, which is termed spontaneous tumor lysis syndrome (STLS). We present a case of a 27-year-old male who presented to the hospital with epistaxis, dyspnea, and cervical lymphadenopathy. Laboratory findings included progressive pancytopenia, hyperuricemia, and acute renal failure. Bone marrow biopsy showed a T cell lymphoid neoplasm that had entirely infiltrated the marrow stroma. The patient was diagnosed with STLS in the setting of a T cell lymphoma with bone marrow infiltration. The patient was immediately treated with a blood transfusion and hemodialysis. After this urgent treatment, the patient's pancytopenia resolved and the lymphadenopathy disappeared spontaneously. One month post-treatment, the patient's cervical lymphadenopathy recurred and peripheral T cell lymphoma, not otherwise specified, was confirmed. STLS has previously been reported, however, most known cases of STLS did not show a decreased tumor burden resulting from massive tumor cell death. We present a rare case of STLS with resolution of pancytopenia and disappearance of lymphadenopathy in a patient with peripheral T cell lymphoma not otherwise specified.

OBJECTIVES The present study was attempted to investigate the effects of pentobarbital-Na, one of the barbiturates which are known to depress excitatory synaptic transmission in the central nervous system at concentrations similar to those required for the induction and maintenance of anesthesia, on catecholamines (CA) secretion evoked by cholinergic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland, and to clarify the mechanism of its action. METHODS Mature male Sprague-Dawley rats were anesthetized with thiopenal-Na (40 mg/kg, s.c.). The adrenal gland was isolated by the methods of Wakade. A cannula used for perfusion of the adrenal gland was inserted into the distal end of the renal vein. The adrenal gland was carefully removed from the animal and placed on a platform of a leucite chamber. RESULTS The perfusion of pentobarbital-Na(30-300 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh(5.32 mM), DMPP(100 uM for 1 min), McN-A-343(200 uM for 2 min), Bay-K-8644(10 uM) and high potassium(56 mM), while it did not affect the CA secretion of cyclopiazonic acid(10 uM). Also, in the presence of thiopental-Na (100 uM), CA secretory responses evoked by ACh, DMPP, McN-A-343 and high K+ were markedly depressed. Moreover, in adrenal glands preloaded with ketamine(100 uM for 20 min), which is known to be a dissociative anesthetic, CA secretion evoked by ACh, DMPP, McN-A-343 and high K+ were significantly attenuated. CONCLUSION Taken together, these experimental results suggest that pentobarbital-Na depresses CA release evoked by both cholinergic stimulation and membrane-depolarization from the isolated rat adrenal medulla and that this inhibitory activity may be due to the result of the direct inhibition of Ca++ influx into the chromaffin cells without any effect on the calcium mobilization from the intracellular store.

We performed time-kill studies of antimicrobial combinations that included minocycline, cefotaxime, and ciprofloxacin with Vibrio vulnificus ATCC 27562. Cefotaxime-plus-ciprofloxacin combinations acted synergistically against V. vulnificus in vitro, and this combination regimen can be a good choice as the empirical treatment for suspected necrotizing fasciitis due to V. vulnificus .

OBJECTIVE The purpose of this study was to investigate the quality of life among cancer survivors compared with individuals without a history of cancer (noncancer controls) using the Korea National Health and Nutrition Examination Survey. METHODS The study subjects were 783 adult cancer survivors and 36 456 noncancer controls who participated in the third, fourth and fifth Korea National Health and Nutrition Examination Survey. Demographic factors, health-related behavior, clinical characteristics and health-related quality of life were assessed with self-reported questionnaires. The EuroQoL-5Dimension was used to evaluate health-related quality of life. Descriptive statistics and multiple regression analysis were used to compare health-related quality of life between cancer survivors and noncancer controls. RESULTS About 67% were women and the mean age of the cancer survivors was 60.9 ± 12.4 years. About 52% of survivors were diagnosed with cancer between 45 and 64 years, and more than half of cancer survivors were diagnosed 5 years or less before the interview. The pain/discomfort dimension was the highest reported problem: 43.6% for cancer survivors. The proportion of any reported problem was significantly higher among cancer survivors compared with noncancer controls in terms of mobility (adjusted odds ratio (aOR), 1.56, 95% confidence interval, 1.24-1.97), usual activities (aOR, 1.45, 95% confidence interval, 1.11-1.89), pain/discomfort (aOR, 1.26, 95% confidence interval, 1.04-1.52) and anxiety/depression (aOR, 1.61, 95% confidence interval, 1.29-2.01). CONCLUSIONS Cancer survivors had a significantly lower quality of life compared with noncancer controls. The pain/discomfort dimension was the highest reported problem in cancer survivors.

There are no effective conventional systemic cytotoxic therapies for patients with unresectable or advanced hepatocellar carcinoma (HCC). Sorafenib, an oral multi-targeted tyrosine kinase inhibitor, was recently approved for the treatment of patients with HCC. Sorafenib is generally well tolerated and has an acceptable toxicity profile. Gastrointestinal perforation is a rare adverse event. We present a case of transverse colon perforation during sorafenib therapy for advanced HCC. A 68-year-old woman with advanced HCC was treated with sorafenib. Eight weeks later the patient presented with the sudden onset of sharp abdominal pain. Emergency surgery was performed for panperitonitis and a perforation involving the transverse colon.

The present study was conducted to investigate the influence of arachidonic acid, which is known to be an important unsaturated fatty acid component of membrane phospholipids and to be liberated by phospholipase A2 action, on secretion of catecholamines (CA) from the isolated perfused rat adrenal glands and to clarify the mechanism of its action. Arachidonic acid (10 uM) perfused into an adrenal gland of the rat for 20 min caused a significant inhibition of CA secretion evoked by ACh (5.32 x 10(-3) M), DMPP (10(-4) M) and muscarine (10(-4) M) while it did not affect that induced by excess K+ (5.6 x 10(-2) M). Arachidonic acid, in the presence of ouabain (100 uM), an inhibitor of Na+, K(+) -ATPase, also produced a marked inhibitory effect of CA secretion evoked by ACh, DMPP and muscarine but did not modify the secretory effect of excess K+. The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh, DMPP and muscarine while it did not influence that by excess K+. Prostaglandin F2 alpha perfused in a retrograde direction for 20 min inhibited greatly the CA secretion evoked by DMPP but did not affect the effect evoked by excess K+. All of arachidonic acid, ouabain, indomethacin and prostaglandin F2 alpha used in the present study did not affect the spontaneous basal release of CA in the perfused rat adrenal glands. Taken together, these experimental results suggest that arachidonic acid, as well as prostaglandin F2 alpha, cause the inhibitory action of CA secretion evoked by cholinergic receptor-mediated stimulation, but not by membrane depolarization, and also play a modulatory role in regulating CA secretion from the rat adrenal medulla.

The release of potassium from platelets is a well-known cause of pseudohyperkalemia in thrombocytosis. In predicting the magnitude of pseudohyperkalemia associated with thrombocytosis, previous investigations considered only the amount of potassium released from platelets during blood clotting, although the increment in serum potassium during blood clotting depends on the quantity of potassium released from platelets as well as the volume of distribution of the released potassium, which is inversely proportionate to the hematocrit. The present study proposes a new mathematical formula to predict the magnitude of increase in serum potassium during blood clotting, and accuracy of this formula has been tested in a patient with thrombocytosis.

Disseminated intravascular coagulation (DIC) is an acquired coagulation disorder that occurs when the normal hemostatic balance is disturbed, primarily by excessive thrombin formation. Moreover, while DIC is a rare complication of aortic dissecting aneurysm, it is also a well-recognized one. We reported a case of DIC associated with aortic dissecting aneurysm in a 55-year-old woman who was transferred from another hospital because of chest pain radiating to her back and thrombocytopenia. Laboratory findings showed DIC with severe thrombocytopenia, and she was diagnosed as having an acute aortic dissection and DIC. After medical treatment on the aortic dissecting aneurysm, her DIC profile recovered.

Background/Aims: Recently, many cases of vitamin K-dependent coagulopathy of unknown origin have been reported. Such patients lack any relevant family history and have no systemic disease, raising suspicion of superwarfarin intoxication. We evaluated individual risk factors causing coagulopathy and hemorrhagic symptoms in patients with suspected superwarfarin intoxication. In addition, we determined how to effectively treat vitamin K-dependent coagulopathy caused by suspected superwarfarin intoxication. Methods: Seven patients with suspected superwarfarin intoxication who lacked any definitive history of rodenticide ingestion were included. Thirty-one patients initially diagnosed with rodenticide poisoning were also included. We performed a retrospective chart review of all subjects and examined clinical data including patient demographics and medical histories. Results: Patients initially diagnosed with rodenticide poisoning were divided into two groups, one of which had a laboratory abnormality (prothrombin time [PT] > 13 seconds) and another group with PTs in the normal range. There was no significant difference between the two groups in any of age, gender, the extent of chronic alcohol consumption, the causative rodenticide, psychiatric problems, ingestion of drugs interacting with warfarin, the extent of intoxication, or the type of ingestion attempt. The albumin level of the former group was significantly lower than that of the latter group (p = 0.014). Furthermore, a significant differ ence between the two groups was evident in terms of simultaneous ingestion of rodenticide and alcohol (p = 0.023). Conclusions: Most patients with superwarfarin poisoning did not exhibit any complication. When such complications were evident, they were associated with serum albumin level and coingestion of rodenticide and alcohol.

Background/Aims: For many years, conventional treatment for multiple myeloma (MM) not ineligible for high-dose therapy has been the combination of oral melphalan and prednisone (MP). However, melphalan-based regimens are associated with numerous complications. Another alkylating agent, cyclophosphamide, has similar effects on MM and is associated with fewer reports of complications. Therefore, cyclophosphamide-based regimens have usually been used as salvage therapy in patients with refractory or relapsed MM, despite the development of newer drugs. The purpose of this report was to evaluate the efficacy and tolerability of cyclophosphamide and prednisone as a first-line therapy for MM. Methods: For the period January 2002 to June 2012, we retrospectively analyzed 29 patients newly diagnosed with MM who underwent a treatment regimen consisting of intravenous cyclophosphamide (1,000 mg/kg) for 1 day and prednisone (100 mg) for 4 days. Results: The rate of response to this regimen was 31.1 percent. The median progression-free survival (PFS) was 5.5 months and the median overall survival (OS) was 47.3 months. The regimen was well tolerated. Adverse effects of grades above III were as follows: anemia in seven patients (24.1%), neutropenia in five patients (17.2%), and thrombocytopenia in two patients (6.8%). These adverse effects were easily adjusted. No one developed a secondary malignancy or hemorrhagic cystitis. Conclusions: Although PFS was less than for the MP regimen, median OS was better than for the MP regimen. Furthermore, the cyclophosphamide-prednisone regimen was well tolerated, and the adverse effects that did occur were easily adjusted. The cyclophosphamide-prednisone combination regimen may represent an effective and well tolerated first-line therapy for non-transplant candidates with MM. (Korean J Med 2013;84:690-697)

The prognosis of patients with end-stage renal disease has improved with advances in hemodialysis techniques. However, many patients who undergo hemodialysis suffer from various types of cancer. Limited data is available to guide clinical management of these patients who may have impaired renal function. Here, we report our experience with the use of irinotecan for the treatment of a hemodialysis patient with small-cell lung cancer and end-stage renal disease.

The presence of lupus anticoagulant is associated with an elevated risk of venous and arterial thrombosis, and recurrent miscarriages as well. For some cases, this disease can present with bleeding as a consequence of lupus anticoagulant hypoprothrombinemia (LAHPS). LAHPS is a rare disease and it is reported to be most frequent in young females with/without systemic lupus erythematosus or in healthy children who are suffering with a viral infection. In such cases, steroid therapy is usually effective in normalizing the biological abnormalities and controlling the bleeding problems. A 34-year-old previously healthy man was admitted to our department because of his prolonged coagulation times; these abnormalities were discovered before performing orthopedic surgery. The prothrombin time (PT) was 15.2 sec, and the activated partial thromboplastin time (APTT) was 37.7 sec. A 1:1 dilution of patient plasma with normal plasma nearly corrected the PT, but this failed to correct the APTT. Evaluation of the clotting factors revealed decreased levels of factors II, V, VIII, IX and XI. The presence of LA was demonstrated by the dRVVT test, and the patient was diagnosed with LAHPS. He was successfully treated with corticosteroid before performing the orthopedic surgery.

Up to 5% of all small cell carcinomas develop at extrapulmonary sites. Primary small cell carcinomas originating in the kidney are extremely rare neoplasms. Here we report a case of primary small cell carcinoma of the kidney. A nephrectomy was performed on a 52-year-old female patient to remove a large tumor located in the right kidney. The histology and immunohistochemistry of the resected tumor revealed a pure small cell carcinoma with invasion into the renal capsule. The patient received postoperative adjuvant chemotherapy with etoposide and cisplatin. The patient has been monitored with regular check ups and remains stable with no recurrence at 28 months after the initial diagnosis.

The pathogenic mechanism of focal segmental glomerulosclerosis (FSGS) and aplastic anemia are associated with immunologic events which lead to glomerular cell injury or hematopoietic cell destruction. We present an extremely rare case of FSGS with aplastic anemia in a 30-yr-old woman. The laboratory examination showed hemoglobin 7.2 g/dL, white blood count of 4,200/ microL, platelet count 70,900/microL. Proteinuria (2+, 3.6 g/day) and microscopic hematuria were detected in urinalysis. The diagnosis of FSGS and aplastic anemia were confirmed by renal and bone marrow biopsy. She was treated with immunosuppressive therapy of prednisone 60 mg/day orally for 8 weeks and cyclosporine A 15 mg/kg/day orally. She responded with gradually improving her clinical manifestation and increasing peripheral blood cell counts. Prednisone was maintained at the adequate doses with tapering after 8 weeks and cyclosporine was given to achieve trough serum levels of 100-200 ng/mL. At review ten month after diagnosis and initial therapy, the patient was feeling well and her blood cell counts increased to near normal (Hb 9.5 g/dL, Hct 32%, WBC 8,300/microL, platelet 123,000/microL) and renal function maintains stable with normal range proteinuria (0.25 g/day).

Influence of Total Ginseng Saponin on Contractile Responses of Vasoconstrictors in the Isolated Rat Aorta Choon-Hae Chung, MD1, Soon-Pyo Hong, MD1, Seong-Ho Cho, MD2, Jang-Gwon Hong, MD2, Yong-Kyoon Lee, MD2, Geon-Han Lim, MD2, Won-Ho Yang, MD2, Ho-Jin You, MD2, Seong-Chang Woo, MD2, Cheol-Hee Choi, MD2 and Dong-Yoon Lim2, PhD Department of Internal Medicine and Pharmacology, College of Medicine, Chosun University, Kwangju, Korea

Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.

To assess the role and responses of lipoperoxide and superoxide dismutase in hypertensive disease, the serum and erythrocyte lipid peroxide and erythrocyte superoxide dismutase levels were measured in 65 normal persons and hypertensive patients. The results are summerized as follows: In normal persons, serum and erythrocyte lipoperoxide values showed an increase according to age, but the elevation was not statistically significant. In normal persons, the erythrocyte superoxide dismutase value did not change according to age. In hypertensive patients, the serum and erythrocyte lipoperoxide values showed increases of 10.8% and 26% respectively compared to those of the controls. In hypertensive patients, the erythrocyte superoxide dismutase value showed a decrease of 29.9% compared to that of the controls. Keywords: Lipoperoxides, Superoxide dismutase, Normal person, Hypertensive patients INTRODUCTION Glavid1) reported that lipoperoxide produced in vivo is related to atherosclerosis. We proposed to examine the relationship between the concentration of serum and tissue lipoperoxide with damage to tissue. Recently, it has been noticed that lipoperoxide induces various disease including atherosclerosis.2–5) These lipoperoxides are produced by a chain reaction between superoxide radicals and unsaturated fatty acids. Lipoperoxide inhibits production of prostaglandin l2 in vascular endothelium and causes cell membrane degeneration in smooth muscle cells by polymerization with protein. It is these actions that are thought to be the mechanism behind the development of atherosclerosis. We investigated the difference between serum and R.B.C. lipoperoxide and the degree of activation of superoxide dismutase in 38 normal controls who had no evidence of atherosclerosis, either symptomatically or by investigation, and 27 hypertensive patients admitted to the Dept. of Internal Medicine, College of Medicine, Chosun University. We report our experimental results with a review of the literature.

Introduction Hepatitis B virus (HBV) reactivation (so-called reverse seroconversion) is a rare but known complication of hematopoietic stem cell transplantation, immunosuppressive therapy, or high-dose chemotherapy plus rituximab. This event is linked to a treatment-related fall in titers of antibodies to hepatitis B surface antigen (HBsAb) below the protective threshold level. Case presentation A 77-year-old Korean man diagnosed with primary amyloidosis was started on melphalan/dexamethasone combination therapy. During treatment, laboratory indices of hepatic function suddenly deteriorated, and he developed acute hepatitis through reverse HBV seroconversion, becoming positive for hepatitis B surface antigen (HBsAg) and negative for HBsAb. HBV DNA was also detectable in serum to a profound extent. Normal liver function was gradually restored during the course of antiviral therapy (entecavir). Conclusions HBV reactivation may lead to fatal liver disease in a significant percentage of patients. As a result, physicians often screen for HBsAg and HBsAb prior to initiating chemotherapy, advising antiviral treatment in patients seropositive for HBsAg, even in the absence of hepatitis B e antigen. Here, a case of HBV reactivation is described, involving a patient given relatively low-dose chemotherapy (melphalan/dexamethasone) for primary amyloidosis.