We describe a scrub typhus patient with acute renal failure for whom a diagnosis was made based on serology as well as immunohistochemical (IHC) staining and an electron microscopic examination (EM) of a renal biopsy specimen. For our case, we demonstrated by IHC staining and EM that renal failure was caused by acute tubular necrosis due to a direct invasion of Orientia tsutsugamushi. CASE REPORTA healthy-looking, 33-year-old male patient received a drug treatment for a 2-week history of cough and sputum. One day before admission to our hospital, he complained of abdominal pain and nausea after he played football. He was suspected of having renal failure on examination at a local clinic and was transferred to Chosun University Hospital in Gwang-ju, South Korea. At the time of admission, his vital signs were a blood pressure of 120 over 80 mm Hg, a pulse rate of 72 times/min, a respiratory rate of 20 breaths/min, and a body temperature of 37.2°C. A urinalysis showed no gross hematuria, with a urine output of 50 ml/h. His mental status was alert. There was no skin rash or lymphadenopathy. The patient's complete blood count showed a white blood cell count of 11,630/mm 3 , a hemoglobin count of 14.5 g/dl, and a platelet count of 243,000/ mm 3 . An arterial blood gas analysis showed a pH of 7. , 120 meq/liter; blood urea nitrogen, 39.3 mg/dl; and creatinine, 5.0 mg/dl. The biochemistry results showed a total protein level of 6.73 g/dl, albumin at 3.78 g/dl, aspartate transaminase at 30 IU/liter, alanine aminotransferase at 18 IU/liter, creatine phosphokinase at 446 U/liter, lactate dehydrogenase at 565 U/liter, myoglobin at 168.4 ng/ml, fibrin degradation products at 1 mg/ml (range, 0 to ϳ5.0 mg/ml), and a D-dimer concentration of 143.6 ng/ml (range, 0 to ϳ255 ng/ml). On urinalysis, hematuria (score, ϩ3) and proteinuria (score, ϩ4) were shown to be present. A microscopic urinalysis revealed 10 to 19 red blood cells/high-power field (HPF), 2% dysmorphic red blood cells/HPF, 1 to 4 white blood cells/HPF, and no cast/HPF. A urinalysis using urine collected during 24 h detected selective proteinuria (albumin, 895 mg/day). Serologic tests were all negative for rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, and cold agglutinin, human immunodeficiency virus, hepatitis B virus, and hepatitis C virus antibodies, and the VDRL test was negative. Antistreptolysin O and complement levels were all normal.A self-employed person, our patient presented with no typical symptoms of scrub typhus, including rash, fever, and headache.

Background/AimsSerum procalcitonin (PCT) levels are low in healthy individuals but are elevated in patients with a serious bacterial infection or sepsis. In this study, we examined the ability of serum PCT concentration to diagnose infections in end-stage renal disease (ESRD) patients, and sought to determine an appropriate threshold level.MethodsSerum PCT levels were measured in ESRD patients on antibiotic therapy for a suspected bacterial infection (ESRD infection [iESRD] group, n = 21), and compared with those of ESRD patients on hemodialysis with no sign of infection (ESRD control [cESRD] group, n = 20).ResultsThe mean serum PCT concentration of the iESRD group was significantly higher than in the cESRD group (2.95 ± 3.67 ng/mL vs. 0.50 ± 0.49 ng/mL, p = 0.006), but serum PCT concentrations did not correlate with severity of infection. The optimized threshold level derived for serum PCT was 0.75 ng/mL, rather than the currently used 0.5 ng/mL; this threshold demonstrated a sensitivity and specificity of 76.2% and 80.0% for infection and 100% and 60.6% for systemic inflammatory response syndrome, respectively, compared with the cutoff of 0.5 ng/mL.ConclusionsThis study suggests that serum PCT at a cutoff value of 0.75 ng/mL is an appropriate indicator of infection in ESRD patients.

Tinnitus is associated with increased social costs and reduced quality of life through sleep disorders or psychological distress. The pathophysiology of chronic subjective tinnitus, which accounts for most tinnitus, has not been clearly elucidated. This is because chronic subjective tinnitus is difficult to evaluate objectively, and there are no objective markers that represent the diagnosis or therapeutic effect of tinnitus. Based on the results of studies on patients with chronic subjective tinnitus, objective and measurable biomarkers that help to identify the pathophysiology of tinnitus have been summarized. A total of 271 studies in PubMed, 303 in EMBASE, and 45 in Cochrane Library were found on biomarkers related to chronic subjective tinnitus published until April 2021. Duplicate articles, articles not written in English, review articles, case reports, and articles that did not match our topic were excluded. A total of 49 studies were included. Three specimens, including blood, saliva, and urine, and a total of 58 biomarkers were used as indicators for diagnosis, evaluation, prognosis, and therapeutic effectiveness of tinnitus. Biomarkers were classified into eight categories comprising metabolic, hemostatic, inflammatory, endocrine, immunological, neurologic, and oxidative parameters. Biomarkers can help in the diagnosis, measure the severity, predict prognosis, and treatment outcome of tinnitus.

The prevalence of sensorineural hearing loss has increased along with increases in life expectancy and exposure to noisy environments. Metabolic syndrome (MetS) is a cluster of co-occurring conditions that increase the risk of heart disease, stroke and type 2 diabetes, along with other conditions that affect the blood vessels. Components of MetS include insulin resistance, body weight, lipid concentration, blood pressure, and blood glucose concentration, as well as other features of insulin resistance such as microalbuminuria. MetS has become a major public health problem affecting 20–30% of the global population. This study utilized health examination to investigate whether metabolic syndrome was related to hearing loss. Methods: A total of 94,223 people who underwent health check-ups, including hearing tests, from January 2010 to December 2020 were evaluated. Subjects were divided into two groups, with and without metabolic syndrome. In addition, Scopus, Embase, PubMed, and Cochrane libraries were systematically searched, using keywords such as “hearing loss” and “metabolic syndrome”, for studies that evaluated the relationship between the two. Results: Of the 94,223 subjects, 11,414 (12.1%) had metabolic syndrome and 82,809 did not. The mean ages of subjects in the two groups were 46.1 and 43.9 years, respectively. A comparison of hearing thresholds by age in subjects with and without metabolic syndrome showed that the average pure tone hearing thresholds were significantly higher in subjects with metabolic syndrome than in subjects without it in all age groups. (p < 0.001) Rates of hearing loss in subjects with 0, 1, 2, 3, 4, and 5 of the components of metabolic syndrome were 7.9%, 12.1%, 13.8%, 13.8%, 15.5% and 16.3%, respectively, indicating a significant association between the number of components of metabolic syndrome and the rate of hearing loss (p < 0.0001). The odds ratio of hearing loss was significantly higher in subjects with four components of metabolic syndrome: waist circumference, blood pressure, and triglyceride and fasting blood sugar concentrations (p < 0.0001). (4) Conclusions: The number of components of the metabolic syndrome is positively correlated with the rate of sensorineural hearing loss.

Otitis media is mainly caused by upper respiratory tract infection and eustachian tube dysfunction. If external upper respiratory tract infection is not detected early in the middle ear, or an appropriate immune response does not occur, otitis media can become a chronic state or complications may occur. Therefore, given the important role of Toll-like receptors (TLRs) in the early response to external antigens, we surveyed the role of TLRs in otitis media. To summarize the role of TLR in otitis media, we reviewed articles on the expression of TLRs in acute otitis media (AOM), otitis media with effusion (OME), chronic otitis media (COM) with cholesteatoma, and COM without cholesteatoma. Many studies showed that TLRs 1–10 are expressed in AOM, OME, COM with cholesteatoma, and COM without cholesteatoma. TLR expression in the normal middle ear mucosa is absent or weak, but is increased in inflammatory fluid of AOM, effusion of OME, and granulation tissue and cholesteatoma of COM. In addition, TLRs show increased or decreased expression depending on the presence or absence of bacteria, recurrence of disease, tissue type, and repeated surgery. In conclusion, expression of TLRs is associated with otitis media. Inappropriate TLR expression, or delayed or absent induction, are associated with the occurrence, recurrence, chronicization, and complications of otitis media. Therefore, TLRs are very important in otitis media and closely related to its etiology.