Guillain-Barre Syndrome Publications (8467)
Guillain-Barre Syndrome Publications
The preliminary results of a portable and low-cost molecular diagnostics system for ZIKV infection are reported here. In less than 15 minutes, this low-cost platform can automatically perform high quality RNA extraction from up to 12 ZIKV-spiked urine samples simultaneously. It can also perform reverse transcription recombinase polymerase amplification reaction (RT-RPA) in ≤15 minutes. The fluorescent signal produced from probe-based RT-RPA or RT-PCR assays can be monitored using LEDs and a smartphone camera. In addition, the RT-RPA and RT-PCR assays do not cross-react with dengue and chikungunya viral RNA. This low-cost system lacks complicated, sensitive and high cost components, making it suitable for resource-limited settings. It has the potential to offer simple sample-to-answer molecular diagnostics and can inform healthcare workers of patients' diagnosis promptly.
Although a causal relationship between Guillain-Barré syndrome and TNF-α antagonist therapy cannot be proven, this report emphasizes the need to monitor for neurologic signs and symptoms in patients with inflammatory bowel diseases, with or without biological therapy, to avoid severe and irreversible complications associated with demyelinating diseases.
Prevailing models suggest entry into neuronal stem cells through transmembrane receptors, hijacking cellular signaling to interfere with neurogenesis and cell survival. Mechanisms of adult neurological disease are unknown, but recent evidence suggests propensity for infection of adult neural stem cells. Efforts focused on mechanisms of pathogenesis, vulnerabilities, and treatments are urgently needed.
We report a case of acute-onset CIDP that was initially diagnosed as GBS.
A 44-year-old male logger complained of acute quadriplegia and dyspnea. Mechanical ventilation was initiated. He was an HBV carrier with mild elevation of hepatic enzyme, and positive for hantavirus antibody. He was diagnosed with GBS and immunoglobulin therapy was administered.
After 8 months, quadriplegia and hypesthesia recurred. Immunoglobulin therapy at this time had no effect, but steroid therapy had some effect.
A diagnosis of CIDP was made. After 2 months, severe extremity pain and dyspnea developed again, and steroid pulse therapy was initiated.
Besides GBS, acute-onset CIDP can occur with hantavirus and HBV coinfection. Patients with this coinfection in whom GBS has been initially diagnosed should be followed up for a long time, because of the possibility of relapse or deterioration, and acute-onset CIDP should always be considered.
Subsequently, eligibility was expanded to pregnant women with sexual partners with similar travel history. Serum and urine collected within four weeks of symptom onset or six weeks of travel were tested with real-time RT-PCR assays targeting the ZKV envelope and NS2B genes. In this review of lessons learned from the first 80 positive cases in NYS, ZKV RNA was detected in urine only in 50 patients, serum only in 19 patients and both samples concurrently in 11 patients, with average viral loads in urine a log higher than in serum. Among 93 positive samples from the 80 patients, 41 were positive on both gene assays, 52 on the envelope only, and none on the NS2B only. Of the 80 infected patients, 74 (93%) would have been resulted as 'not detected' or 'equivocal', if the "two target positive requirement" in initial federal guidance to public health laboratories was enforced, urine was not tested, or extended eligibility time for molecular testing was not implemented. These changes facilitated more extensive molecular diagnosis of ZKV, reducing reliance on time-consuming and potentially inconclusive serology.
Typically, the soleus H-reflex is absent and a body-sway analysis using posturography shows a 1-Hz peak, which indicates proprioception dysfunction. Sensory nerve action potentials and somatosensory-evoked potentials are abnormal in approximately 30% of FS patients, indicating the occasional involvement of cutaneous (group 2) afferents. During the disease course, approximately 15% of FS patients suffer an overlap of axonal GBS with nerve conduction abnormalities that reflect axonal dysfunction. This review summarizes electrophysiological abnormalities and their clinical significance in FS.
To address this critical gap, we sought to test whether a cell-based assay that measures protection from the ZIKV-induced cytopathic effect could serve as a high-throughput screen assay for discovering novel anti-ZIKV inhibitors. Employing this approach, we tested the anti-ZIKV activity of previously known broad-spectrum antiviral compounds and discovered several compounds (e.g., NITD008, SaliPhe, and CID 91632869) with anti-ZIKV activity. Interestingly, while GTP synthesis inhibitors (e.g., ribavirin or mycophenolic acid) were too toxic or showed no anti-ZIKV activity (EC50 > 50 μM), ZIKV was highly susceptible to pyrimidine synthesis inhibitors (e.g., brequinar) in the assay. We amended the assay into a high-throughput screen (HTS)-compatible 384-well format and then screened the NIH Clinical Compound Collection library, which includes a total of 727 compounds organized, using an 8-point dose response format with two Zika virus strains (MR766 and PRVABC59, a recent human isolate). The screen discovered 6-azauridine and finasteride as potential anti-ZIKV inhibitors with EC50 levels of 3.18 and 9.85 μM for MR766, respectively. We further characterized the anti-ZIKV activity of 6-azauridine and several pyrimidine synthesis inhibitors such as brequinar in various secondary assays including an antiviral spectrum test within flaviviruses and alphaviruses, Western blot (protein), real-time PCR (RNA), and plaque reduction assays (progeny virus). From these assays, we discovered that brequinar has potent anti-ZIKV activity. Our results show that a broad anti-ZIKV screen of compound libraries with our CPE-based HTS assay will reveal multiple chemotypes that could be pursued as lead compounds for therapies to treat ZIKV-associated diseases or as molecular probes to study the biology of the ZIKV replication mechanism.
The Japan GBS outcome study (J-GOS) has been conducted to identify clinical or biological markers that predict the prognosis of Japanese GBS patients at an early stage. In the future, we expect to provide intractable patients so predicted with novel therapy, including molecular target drugs.