RESUMO
We have previously reported the high levels of glutamic acid decarboxylase 65 autoantibodies (GAD65A) in patients with type 1 diabetes and autoimmune thyroid disease. Here we describe a 32-year-old Japanese female with a thirteen-year history of type 1 diabetes whose levels of GAD65A were elevated just after the emergence of anti-thyroid autoimmunity. At 19 years of age, she developed diabetic ketoacidosis and was diagnosed with type 1 diabetes. She had GAD65A, insulinoma-associated antigen-2 autoantibodies (IA-2A), and zinc transporter-8 autoantibodies (ZnT8A), but was negative for antibodies to thyroid peroxidase (TPOAb) and thyroglobulin (TGAb) at disease onset. ZnT8A and IA-2A turned negative 2-3 years after the onset, whereas GAD65A were persistently positive at lower level (approximately 40 U/mL). However, just after the emergence of TGAb at disease duration of 12.5 years, GAD65A levels were reelevated up to 5717 U/mL in the absence of ZnT8A and IA-2A. Her thyroid function was normal and TPOAb were consistently negative. She has a HLA-DRB1*03:01/*04:01-DQB1*02:01/*03:02 genotype. Persistent positivity for GAD65A might be associated with increased risk to develop anti-thyroid autoimmunity.
RESUMO
Au-framed Ag nanocubes were prepared by site-selective electrochemical deposition of Au onto the edges and vertices of Ag nanocubes modified with a self-assembled monolayer (SAM) of 1-octanethiol, and further chemical etching of the Ag cubes used as a template produced Au nanoframes.
RESUMO
We present here a case of dorsal column degeneration in a female patient with multiple myeloma following exposure to bortezomib. Two days after intravenous administration of a first course of bortezomib 1 mg/m(2), the patient developed rapidly-progressive numbness, pain and muscle weakness in the bilateral upper and lower limbs. Following gancyclovir treatment of subsequent cytomegalovirus viremia, the patient went on to receive a course of EPOCH (etoposide 50 mg/m(2)/day on days 1-4, vincristine 0.4 mg/m(2)/day on days 1-4, doxorubicin 10 mg/m(2)/day on days 1-4, cyclophosphamide 750 mg/m(2)/day on day 6, and prednisolone 60 mg/m(2)/day on days 1-6). Shortly thereafter, the patient developed bilateral Aspergillus pneumonia. Despite treatment with appropriate antifungal agents, the patient died from respiratory failure due to bilateral diffuse alveolar damage of the lungs and without recovery of severe sensory and motor neuropathy prior to her death. Post mortem examination revealed spongy degeneration of the dorsal column from the medulla oblongata to the cervical spinal cord. Bortezomib-associated peripheral neuropathy in patients with multiple myeloma has been commonly reported but appears to resolve in a majority of these patients after dose reduction or discontinuation. We believe this to be the first report of spinal cord abnormalities in a patient with multiple myeloma treated with bortezomib. Further investigation is required to ascertain the exact mechanism of this central neurotoxic effect and to identify appropriate neuroprotective strategies.
RESUMO
Clinical assays are very important for the diagnosis and management of clinical disorders. Each assay system consists of a specific method to detect and/or quantify a substance of interest in the clinical specimen. However, clinical assays can be unfavorably influenced by non-specific activities concomitantly present in the specimen, which may mislead clinical decisions. Thus, it is very important to know how each assay works, and how and when the assay is non-specifically influenced. Here, we report three cases shown clinical data of thyroid function influenced by new type of assay interference.
