Hye-Ryoun Kim

Impact of Changing Trends in Medical Therapy on Surgery for Benign Prostatic Hyperplasia Over Two Decades

Purpose Following the introduction of medical therapy for benign prostatic hyperplasia (BPH), we determined the effect of the change in trends in medical therapy on the indication and outcome of surgical intervention for BPH. Materials and Methods We compared the basic characteristics of, weight of resected tissue of, transfusions in, and postoperative complications of patients who underwent surgery between 1985 and 1989 (before the advent of medical therapy for BPH), between 1995 and 1999 (when medical therapy was developed and became widely used as alternative treatment), and between 2005 and 2009 (when medical therapy superseded surgical intervention to become first-line treatment and when combination therapy became widely adopted). Results At our institution, the mean age and BMI of patients increased over the past two decades (p<0.001). Hypertension, operation history, and other comorbidities also increased significantly (p<0.001, p=0.005, and p<0.001, respectively). The indications for surgery in 1985 to 1989, 1995 to 1999, and 2005 to 2009 were as follows: acute urinary retention in 34.7%, 20.2%, and 15.1% of patients and symptomatic deterioration in 61.1%, 72.3%, and 73.0% of patients, respectively. Prostate volume and the weight of resected tissue increased from 34.4±14.5 ml to 61.3±32.4 ml and from 7.2±6.4 g to 10.8±7.6 g, respectively, over two decades. Patients who underwent surgery in 2005 to 2009 had their catheters removed earlier (p<0.001). Secondary hemorrhage within four postoperative weeks and repeat transurethral resection of the prostate within 1 year decreased significantly (p=0.03 and p=0.003, respectively). No statistically significant change in impaired detrusor contractility was found (p=0.523). Conclusions Although patients who underwent surgery were older after widespread use of medical therapy for BPH, advancements in surgical techniques have benefitted these patients.

Variants in the HEPSIN gene are associated with susceptibility to prostate cancer

Background:HEPSIN (HPN) gene is one of the most consistently overexpressed genes in patients with prostate cancer; furthermore, there is some evidence supporting an association between HPN gene variants and the risk of developing prostate cancer. In this study, sequence variants in the HPN gene were investigated to determine whether they were associated with prostate cancer risk in a Korean study cohort.Methods:We evaluated the association of 17 single-nucleotide polymorphisms (SNPs) in the HPN gene with prostate cancer risk and clinical characteristics (Gleason score and tumor stage) in Korean men (240 case subjects and 223 control subjects) using unconditional logistic regression.Results:The statistical analysis suggested that three SNPs (rs45512696, rs2305745, rs2305747) were significantly associated with the risk of prostate cancer (odds ratio (OR)=2.22, P=0.04; OR=0.73, P=0.03; OR=0.76, P=0.05, respectively).Conclusions:The results of this study suggest that, in Korean men, some polymorphisms in the HPN gene might be associated with the risk of developing prostate cancer.

Neutropenia and neutrophil-to-lymphocyte ratio in a healthy Korean population: race and sex should be considered.

We evaluated the prevalence and severity of asymptomatic neutropenia in a healthy Korean population according to sex and age. We explored normal neutrophil‐to‐lymphocyte ratio (NLR) and platelet‐to‐lymphocyte ratio (PLR) in an asymptomatic Korean population and the association of these ratios with biomarkers related to inflammation, rheumatoid disease, and glucose metabolism.

Reduction of natural killer and natural killer T cells is not protective in cisplatin-induced acute renal failure in mice

Aims:  A recent report showed that fractalkine (CX3CL1), which functions as both a potent chemoattractant and adhesion molecule for monocytes and natural killer (NK) cells was significantly increased in cisplatin‐induced acute renal failure (CisARF) in mice. Therefore, we developed the hypothesis that increased CX3CL1 expression in CisARF initiates NK cell infiltration in the kidney. The aim of the present study was to determine the role of NK cells in CisARF in mice.

Probable novel PSEN2 Val214Leu mutation in Alzheimer’s disease supported by structural prediction

BackgroundPSEN2 mutations are rare variants, and fewer than 30 different PSEN2 mutations have been found. So far, it has not been reported in Asia.Case presentationPSEN2 mutation at codon 214 for predicting a valine to leucine substitution was found in a 70-year-old woman, who showed a dementia of the Alzheimer type. We did not find the mutation in 614 control chromosomes. We also predicted the structures of presenilin 2 protein with native Val 214 residue and Leu 214 mutation, which revealed significant structural changes in the region.ConclusionIt could be a novel mutation verified with structural prediction in a patient with Alzheimer’s disease.

Disseminated Mycobacterium avium Complex Infection in a Non-HIV-infected Patient Undergoing Continuous Ambulatory Peritoneal Dialysis

Isolated bone marrow infection by nontuberculous mycobacteria (NTM) is extremely rare. Recently, we encountered a case of bone marrow Mycobacterium avium complex (MAC) infection, which presented as a fever of unknown origin shortly after starting continuous ambulatory peritoneal dialysis (CAPD). The patient was diagnosed with MAC infection on the basis of PCR-restriction fragment length polymorphism analysis and sequencing of DNA obtained from bone marrow specimens. Although this was a case of severe MAC infection, there was no evidence of infection of other organs. End-stage renal disease (ESRD) patients undergoing dialysis can be considered immunodeficient; therefore, when these patients present with fever of unknown origin, opportunistic infections such as NTM infection should be considered in the differential diagnosis.

11 C-PIB PET imaging reveals that amyloid deposition in cases with early-onset Alzheimer’s disease in the absence of known mutations retains higher levels of PIB in the basal ganglia

Purpose Early-onset Alzheimer’s disease (EOAD) has a different pathologic burden and clinical features compared with late-onset Alzheimer’s disease (LOAD). We examined the effects of age at onset on the burden and distribution of β-amyloid in patients with EOAD, in whom well-characterized mutations associated with Alzheimer’s disease were absent. Methods We genotyped ApoE, APP, PSEN1 and PSEN2 in the patients with Alzheimer’s disease: 9 patients with EOAD (age <65), 11 with LOAD (age >70) and 8 normal controls (NCs), all of whom had undergone 11C-labeled Pittsburgh compound B-positron emission tomography imaging. Results Patients with EOAD exhibited higher z scores and larger cluster sizes, and retained higher levels of Pittsburgh compound B in the bilateral thalamus and in some parts of the globus pallidus (P<0.05, false discovery rate). Conclusion Distribution of amyloid deposition in EOAD outside the context of genetic mutations topographically showed some differences from that in LOAD.

RHABDOMYOLYSIS AFTER A REGULAR EXERCISE SESSION IN A PATIENT WITH GRAVES' DISEASE

Clinically significant exertional rhabdomyolysis can be caused by strenuous, prolonged, and repetitive exercise. A few cases of rhabdomyolysis have been associated with hyperthyroidism, mainly in patients with thyroid storm. Recently, we experienced a patient with Graves’ disease who developed rhabdomyolysis after 40 minutes of his regular weight-lifting routine. A 23-year-old male college student, who is not a weighttrainer, a body-builder or an athlete, but who lifts weights regularly for fitness, presented to our outpatient clinic with bilateral pain in the flank area. Information provided by family members revealed that the symptoms started one day after a 40-minute weight-lifting session. On admission, He had bilateral flank pain and tenderness in the costovertebral area and palpitation (pulse rate 110/min) with sweating. He was not dehydrated. He did not take any protein supplementation/statins and heavy carbohydrate meal before exercise. The laboratory findings were as follows: serum creatinine phosphokinase, 36 640 (38–174) IU/L; urine myoglobin, 214.1 (1.4–4.1) ng/mL; and a urine dipstick test positive for blood with no demonstrable red blood cells upon microscopic assessment. Probably secondary to tubular damage caused by myoglobinuria or metabolism of creatine from muscle breakdown, his serum creatinine level slightly rose to 1.5 (0.6–1.3) mg/dL. Thyroid hormones were found to be elevated T3: 2.40 (0.60–1.81) ng/mL, free T4: 2.96 (0.89–1.76) ng/mL, TSH: <0.01 (0.35–5.5) mIU/mL. His serum potassium and phosphorous levels were 4.8 (3.5–5.3) mEq/L and 3.7 (1.9–4.4) mg/dL, respectively. Thyroid ultrasonography revealed a diffusely enlarged gland. The patient received a diagnosis of Graves’ disease with hyperthyroidism, positive antithyroglobulin (137.20 [0–60] U/mL]) and anti-microsomal (2090.29 [0–60] U/mL) antibody tests, and high thyrotrophin binding-inhibiting immunoglobulin (TBII) (1.98 [0.0– 1.75] IU/L). However, the patient did not meet the criteria for thyroid crisis such as confusion, agitation and headache. The overall findings suggested rhabdomyolysis secondary to a single bout of regular exercise in a hyperthyroid state. To look for muscle necrosis by radiolabelled phosphate uptake, we performed a bone scan using Tc99m-MDP, which revealed abnormal isotope uptake bilaterally in the flank muscles (Fig. 1). Rhabdomyolysis in hyperthyroidism is extremely rare. A few cases of rhabdomyolysis have been associated with hyperthyroidism, mainly in patients with thyroid storm. However, hyperthyroidism without thyroid storm may theoretically cause rhabdomyolysis by increasing energy consumption and thus depleting muscle energy stores and substrates. From this it seems plausible that even regular weight-lifting might trigger rhabdomyolysis in a hyperthyroid patient such as ours. We investigated other possible triggers, including common viral infections and metabolic disorders, but detected none. Hence, we present our patient