Patient: Female, 88Final Diagnosis: Adult onset still’s diseaseSymptoms: Fever • rashMedication: —Clinical Procedure: —Specialty: RhaumatologyObjective:Unusual clinical courseBackground:Adult-onset Still’s disease (AOSD) is a rare multi-systemic inflammatory disorder of unknown etiology characterized by spiking fever, characteristic rash, and arthritis. It often associates with high serum ferritin levels.Case Report:An 88-year-old woman had fever of over 39°C without response to extended-spectrum antibiotics for 6 days. She had non-specific erythema with infiltration on her trunk. She had leukocytosis with neutrophilia of 80%, mild hepatic dysfunction, normal level of rheumatoid factor and antinuclear antibody, thrombocytopenia, elevated d-dimer and soluble interleukin2 receptor, extremely high serum ferritin (78 662 ng/mL), and splenomegaly. Although she had no arthritis or specific erythema, we made the diagnosis of AOSD according to Yamaguchi’s criteria with disseminated intravascular coagulation (DIC) and hemophagocytic syndrome (HPS) after ruling out infections, malignancies, or other connective tissue diseases. Twelve percent of AOSD patients have HPS. The mean serum ferritin of AOSD with HPS was reported at 18 179 ng/mL, which supported the diagnosis of AOSD because only a few other diseases could show such extremely high serum ferritin. Although she was treated with prednisolone (30 mg/day), her condition deteriorated and her left pleural effusion increased. Therefore, methylprednisolone 500 mg/day for 3 days was started followed by prednisolone 30 mg/day and immunosuppressive agent (Cyclosporine 50 mg/day), which improved her general condition, elevated C-reactive protein levels, and extremely high serum ferritin levels.Conclusions:We report the case of an elderly patient with severe AOSD, who developed HPS and DIC, whose extremely high serum ferritin level was useful in diagnosis.
Cephaloridine (CER) is a classical beta-lactam antibiotic that has long served as a model drug for the study of cephalosporin antibiotic-induced acute tubular necrosis. In the present study, we analyzed gene expression profiles in the kidney of rats given subtoxic and toxic doses of CER to identify gene expression alterations closely associated with CER-induced nephrotoxicity. Male Fischer 344 rats were intravenously injected with CER at three different dose levels (150, 300, and 600 mg/kg) and sacrificed after 24 h. Only the high dose (600 mg/kg) caused mild proximal tubular necrosis and slight renal dysfunction. Microarray analysis identified hundreds of genes differentially expressed in the renal cortex following CER exposure, which could be classified into two main groups that were deregulated in dose-dependent and high dose-specific manners. The genes upregulated dose dependently mainly included those involved in detoxification and antioxidant defense, which was considered to be associated with CER-induced oxidative stress. In contrast, the genes showing high dose-specific (lesion-specific) induction included a number of genes related to cell proliferation, which appeared to reflect a compensatory response to CER injury. Of the genes modulated in both manners, we found many genes reported to be associated with renal toxicity by other nephrotoxicants. We could also predict potential transcription regulators responsible for the observed gene expression alterations, such as Nrf2 and the E2F family. Among the candidate gene biomarkers, kidney injury molecule 1 was markedly upregulated at the mildly toxic dose, suggesting that this gene can be used as an early and sensitive indicator for cephalosporin nephrotoxicity. In conclusion, our transcriptomic data revealed several characteristic expression patterns of genes associated with specific cellular processes, including oxidative stress response and proliferative response, upon exposure to CER, which may enhance our understanding of the molecular mechanisms behind cephalosporin antibiotic-induced nephrotoxicity.
Background/Aims: In this study, investigations were carried out to ascertain whether soft coagulation hemostasis for non-variceal upper gastrointestinal bleeding (UGIB) has ever been performed in a time-dependent manner. Methods: Medical records of 502 patients who had undergone emergency endoscopic hemostasis for non-variceal UGIB from 2003 to 2014 were checked and the modalities were used to achieve hemostasis compared between the first period from 2003 to 2008 (197 patients) and the second period from 2009 to 2014 (305 patients). Results: Endoscopic hemostasis was successfully achieved in 96.0% of study patients. Peptic ulcers were the main cause of bleeding (89.4%). Endoscopic hemostasis was performed by soft coagulation significantly more frequently during the second (71.1%) than the first period (11.7%; p < 0.001). Endoscopic hemostasis was mainly achieved by trainees during the second period (76.1%); these trainees comprised a significantly greater proportion of endoscopists than during the first period (56.3%; p < 0.001). Endoscopic-related complications did not differ between the 2 periods. The only risk factor for rebleeding after hemostasis was Helicobacter pylori infection; the use of soft coagulation and the fact that endoscopists were just trainees were not risk factors. Conclusion: Our findings suggest that using soft coagulation to achieve endoscopic hemostasis for non-variceal UGIB is safe and effective, even when it is performed by trainees.
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