ABSTRACT
A 53-year-old man with adult-onset Still's disease developed severe streptococcal toxic shock syndrome (STSS) due to Streptococcus dysgalactiae subsp. equisimilis (SDSE), following retroperitoneal panniculitis. He was receiving tocilizumab (TCZ), an interleukin-6 receptor inhibitor. The modifying effect of TCZ on the immune response and the pathophysiology of SDSE infection may have led to retroperitoneal panniculitis and atypical STSS with delayed shock and flare of soft tissue inflammation.
Subject(s)
Panniculitis , Shock, Septic , Streptococcal Infections , Streptococcus , Humans , Shock, Septic/etiology , Shock, Septic/drug therapy , Shock, Septic/diagnosis , Shock, Septic/microbiology , Male , Middle Aged , Streptococcal Infections/diagnosis , Streptococcal Infections/drug therapy , Streptococcal Infections/complications , Streptococcal Infections/microbiology , Panniculitis/diagnosis , Panniculitis/etiology , Panniculitis/microbiology , Panniculitis/drug therapy , Streptococcus/immunology , Antibodies, Monoclonal, Humanized/therapeutic use , Antibodies, Monoclonal, Humanized/adverse effects , Still's Disease, Adult-Onset/diagnosis , Still's Disease, Adult-Onset/complications , Still's Disease, Adult-Onset/drug therapy , Receptors, Interleukin-6/antagonists & inhibitors , Treatment Outcome , Retroperitoneal SpaceABSTRACT
OBJECTIVES: Recently, the involvement of basophils and IgE-type autoantibodies in the pathogenesis of SLE has been elucidated using mouse models; however, few studies have been conducted in humans. In this study, the role of basophils and anti-double-stranded DNA (dsDNA) IgE in SLE was examined using human samples. METHODS: The correlation between disease activity and serum levels of anti-dsDNA IgE in SLE was evaluated using enzyme-linked immunosorbent assay. Cytokines produced by IgE-stimulated basophils from healthy subjects were assessed using RNA sequences. The interaction of basophils and B cells to promote B cell differentiation was investigated using a co-culture system. The ability of basophils from patients with SLE with anti-dsDNA IgE to create cytokines that may be involved in B cell differentiation in response to dsDNA was examined using real-time PCR. RESULTS: Anti-dsDNA IgE levels in the serum of patients with SLE correlated with disease activity. Healthy donor basophils produced IL-3, IL-4 and TGF-ß1 after anti-IgE stimulation. Co-culture of B cells with anti-IgE-stimulated basophils increased plasmablasts which were cancelled by neutralizing IL-4. After encountering the antigen, basophils released IL-4 more quickly than follicular helper T cells. Basophils isolated from patients with anti-dsDNA IgE promoted IL-4 expression by adding dsDNA. CONCLUSIONS: These results suggest that basophils contribute to the pathogenesis of SLE by promoting B cell differentiation via dsDNA-specific IgE in patients similar to the process described in mouse models.
Subject(s)
Basophils , Lupus Erythematosus, Systemic , Mice , Animals , Humans , Basophils/metabolism , Interleukin-4 , Cytokines/metabolism , DNA , Immunoglobulin E , Cell DifferentiationABSTRACT
Two veterinary personnel in Japan were infected with severe fever with thrombocytopenia syndrome virus (SFTSV) while handling a sick cat. Whole-genome sequences of SFTSV isolated from the personnel and the cat were 100% identical. These results identified a nosocomial outbreak of SFTSV infection in an animal hospital without a tick as a vector.
Subject(s)
Bunyaviridae Infections , Phlebovirus , Severe Fever with Thrombocytopenia Syndrome , Ticks , Animals , Bunyaviridae Infections/epidemiology , Bunyaviridae Infections/veterinary , Cats , Japan/epidemiology , Phlebovirus/genetics , Veterinarians , ZoonosesABSTRACT
Clozapine is the most effective antipsychotic medication for refractory schizophrenia, but it has many possible serious side effects, including antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). However, the rare case reports available have not presented sufficient characteristic features of drug-induced AAV. Herein, we report a case of a 48-year-old Japanese woman with schizophrenia who presented with fever, arthralgia, myalgia and skin rash after 2 years of clozapine treatment. Her C-reactive protein (CRP) level increased, myeloperoxidase ANCA was positive and skin biopsy revealed leukocytoclastic vasculitis. Initially, steroid administration achieved remission, but her symptoms and high CRP levels relapsed every time the steroid dosage was tapered down. Upon discontinuation of clozapine, her symptoms and elevated CRP level immediately improved and the steroid was successfully tapered and discontinued. This outcome suggested that clozapine was the main cause of AAV.
Subject(s)
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/diagnosis , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/etiology , Antibodies, Antineutrophil Cytoplasmic/immunology , Antipsychotic Agents/adverse effects , Clozapine/adverse effects , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/therapy , Biomarkers , Biopsy , Female , Humans , Middle Aged , Steroids/administration & dosage , Symptom Assessment , Treatment OutcomeABSTRACT
Individuals with spinal cord injuries often experience thermoregulation disorders as well as sensory and motor disabilities. In order to prevent such individuals from becoming hyperthermic, we developed a body heat removal system (BHRS) with thermoelectric devices. Our BHRS comprises four Peltier devices mounted on a wheelchair backrest and continuously transfers body heat through the contacting interface to the external environment. Here, we characterized thermophysiological responses induced by this novel contact-type cooling system. A cooling experiment in a hot environment with five able-bodied subjects demonstrated that sweating and systolic blood pressure in the back-cooling (BC) trial were significantly suppressed compared with those in no-cooling (NC) trial, while no difference was found in oral and skin temperatures. A correlation was observed between chest skin temperature and blood flow in the NC trial; this was not observed in the BC trial. These results suggest that BHRS modulates normal thermoregulatory responses, including sweating and vascular dilation and has the capability to partly replace these functions.
