ANCA-negative eosinophilic granulomatosis with polyangiitis complicated by peripheral nerve damage: A case report.

RATIONALE: Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare autoimmune disease that can affect multiple systems of the body and is characterized by asthma, blood and tissue eosinophilia, and small vascular inflammation. Eosinophilic tissue infiltration and extravascular granuloma formation can lead to any organ damage, but peripheral neuropathy is relatively rare. PATIENT CONCERNS: A 29-year-old male patient was admitted to the hospital due to fever and rash on both lower extremities for 18 days. The patient complained of muscle pain in both lower extremities, with nausea, anorexia, abdominal pain, and diarrhea. He had a 2-year history of asthma and bronchiectasis. The physical examination results were as follows: temperature, 37.8 °C; multiple patchy red rashes on both lower extremities; and no obvious abnormalities in other systems. The patient was negative for anti-neutrophil cytoplasmic antibody (ANCA). Chest computed tomography showed bilateral ground-glass opacities, small nodules, and bronchiectasis. Histopathology of rectal tissues revealed numerous eosinophilic infiltrations. One week after admission, the patient developed symptoms of peripheral nerve damage, presenting with distal weakness in both lower extremities, foot drop, cross-threshold gait, and hypoalgesia on the lateral sides of both lower legs. Electromyography showed that the motor sensory fibers of the lower extremities were damaged. DIAGNOSES: Referring to the diagnostic criteria of the American College of Rheumatology in 1990, the patient was diagnosed with systemic EGPA (vasculitic phase) with rare peripheral nerve damage. INTERVENTIONS: After diagnosis, the patient was administered oral prednisone (60 mg/d; 1.0 mg/kg/d), and cyclophosphamide (900 mg) was infused on the 5th and 18th days of hormone therapy. Prednisone was reduced to 50 mg/d 1 month thereafter. OUTCOMES: After 1+ months of treatment, most of the symptoms disappeared. Limb weakness did not improve. Currently, the patient is undergoing outpatient follow-up and is adhering to treatment. LESSONS: EGPA is a rare disease that can affect multiple systems and has diverse clinical manifestations, with no specific manifestations in the early stage. Diagnosis is difficult, and there is a high misdiagnosis rate. The rate of ANCA positivity for this disease is not high, and clinicians should consider the possibility of ANCA-negative EGPA.

CONSORT-epidural dexmedetomidine improves gastrointestinal motility after laparoscopic colonic resection compared with morphine.

BACKGROUND: We have previously shown that epidural dexmedetomidine, when used as an adjunct to levobupivacaine for control of postoperative pain after open colonic resection, improves recovery of gastrointestinal motility compared with morphine. METHODS: Sixty patients undergoing laparoscopic colonic resection were enrolled and allocated randomly to treatment with dexmedetomidine (group D) or morphine (group M). Group D received an epidural loading dose of dexmedetomidine (5 mL, 0.5 µg/kg), followed by continuous epidural administration of dexmedetomidine (80 µg) in 0.125% levobupivacaine (240 mL) at a rate of 5 mL/h for 2 days. Group M received an epidural loading dose of morphine (5 mL, 0.03 mg/kg) followed by continuous epidural administration of morphine (4.5 mg) in 0.125% levobupivacaine (240 mL) at a rate of 5 mL/h for 2 days. Verbal rating score (VRS) of pain, postoperative analgesic requirements, side effects related to analgesia, and time to postoperative first flatus (FFL) and first feces (FFE) were recorded. RESULTS: VRS and postoperative analgesic requirements were not significantly different between the treatment groups. In contrast, FFL and FFE were significant delayed in group M compared with group D (P < .05). Patients in group M also had a significantly higher incidence of nausea, vomiting, and pruritus (P < .05). No neurological deficits were observed in either group. CONCLUSIONS: Compared with morphine, epidural dexmedetomidine is a better adjunct to levobupivacaine for control of postoperative pain after laparoscopic colonic resection.

Effects of Dexmedetomidine combined with Dezocine on cognition function and hippocampal microglia activation of rats.

OBJECTIVE: This study aimed to investigate the effects of Dexmedetomidine combined with Dezocine on the cognition and hippocampal microglia activation of rats. METHODS: Laparotomy was successfully performed in 48 rats which were then divided into Dexmedetomidine+Dezocine group and Dezocine group. Rats in Dexmedetomidine+dezocine group were infused with Dexmedetomidine and dezocine via the tail vein after anesthesia; rats in Dezocine group were infused with dezocine via the tail vein. After surgery, rats underwent detection of learning and memory functions at 1, 3, and 7 days after surgery, and the neuroglobin and norepinephrine expression was detected in the hippocampal microglia at the same time points. RESULTS: 1, 3 and 7 days after surgery, the latency to escape in Dexmedetomidine+Dezocine group was significantly shorter than that in Dezocine group, and the number of cells positive for neuroglobin or norepinephrine in the CAL region of hippocampus of Dexmedetomidine+Dezocine group was also markedly higher than that of Dezocine group (P < 0.05). CONCLUSION: Surgery and anesthesia have influence on the cognition of rats to a certain degree, and dexmedetomidine combined with dezocine can effectively improve the impaired cognition due to surgery and anesthesia, which may be attributed to the increase in the protective neuroglobin and norepinephrine in the hippocampus.

Effects of electroacupuncture preconditioning on jugular vein glucose level and cerebral edema in rats undergoing cerebral ischemia reperfusion that induced injury.

OBJECTIVE: To determine the effects of electroacupuncture (EA) preconditioning on the blood glucose level in jugular vein and water content in brain tissues in rats undergoing cerebral ischemia reperfusion that induced injury. METHODS: 90 healthy male Wister rats were randomly assigned to 3 groups: sham-operation (SH) group, cerebral ischemia reperfusion (IR) group and electroacupuncture (EA) preconditioning plus IR group. EA group was pretreated with EA delivered to acupoints of "Baihui" (Du 20) and "Shuigou" (Du 26) 30 min before cerebral ischemia. RESULTS: No marked difference was observed in brain water content 2 h after procedure in IR group, SH group and EA group. Compared with SH group, the brain water contents in IR group and EA group were significantly higher 6 h after reperfusion and peaked at 48 h (P < 0.01). The blood glucose levels in EA and IR groups were significantly higher than that of SH group 2 h after reperfusion, which peaked at 6 h and tended to decline up to 24 h after reperfusion (P < 0.01). 2 h, 6 h, and 24 h after reperfusion, EA group had significantly lower blood glucose levels than IR group (P < 0.01). CONCLUSION: Electroacupuncture preconditioning can significantly inhibit the augmentation of the blood glucose level and attenuate cerebral edema induced by reperfusion, which leads to alleviation of injury caused by ischemia reperfusion.

Effects of mixture of lidocaine and ropivacaine at different concentrations on the central nervous system and cardiovascular toxicity in rats.

BACKGROUND: Lidocaine and ropivacaine are often combined in clinical practice to obtain a rapid onset and a prolonged duration of action. However, the systemic toxicity of their mixture at different concentrations is unclear. This study aimed to compare the systemic toxicity of the mixture of ropivacaine and lidocaine at different concentrations when administered intravenously in rats. METHODS: Forty-eight male Wistar rats were randomly divided into 4 groups (n = 12 each): 0.5% ropivacaine (group I); 1.0% ropivacaine and 1.0% lidocaine mixture (group II); 1.0% ropivacaine and 2.0% lidocaine mixture (group III); and 1.0% lidocaine (group IV). Local anesthetics were infused at a constant rate until cardiac arrest. Electrocardiogram, electroencephalogram and arterial blood pressure were continuously monitored. The onset of toxic manifestations (seizure, dysrhythmia, and cardiac arrest) was recorded, and then the doses of local anesthetics were calculated. Arterial blood samples were drawn for the determination of local anesthetics concentrations by high-performance liquid chromatography. RESULTS: The onset of dysrhythmia was later significantly in group IV than in group I, group II, and group III (P < 0.01), but there was no significant difference in these groups (P > 0.05). The onset of seizure, cardiac arrest in group I ((9.2 + or - 1.0) min, (37.0 + or - 3.0) min) was similar to that in group II ((9.1 + or - 0.9) min, (35.0 + or - 4.0) min) (P > 0.05), but both were later in group III ((7.5 + or - 0.7) min, (28.0 + or - 3.0) min) (P < 0.05). The onset of each toxic manifestation was significantly later in group IV than in group I (P < 0.01). The plasma concentrations of the lidocaine-alone group at the onset of dysrhythmia (DYS), cardiac arrest (CA) ((41.2 + or - 6.8) min, (59.0 + or - 9.0) min) were higher than those of the ropivacaine alone group ((20.5 + or - 3.8) min, (38.0 + or - 8.0) min) (P < 0.05). The plasma concentrations of ropivacaine inducing toxic manifestation were not significantly different among groups I, II, and III (P > 0.05). CONCLUSIONS: The systemic toxicity of the mixture of 1.0% ropivacaine and 2.0% lidocaine is the greatest while that of 1.0% lidocaine is the least. However, the systemic toxicity of the mixture of 1.0% ropivacaine and 1.0% lidocaine is similar to that of 0.5% ropivacaine alone.