A rare case of bilateral frontal lobe lesions due to thyroid storm.

Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 µIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.

A rare case of bilateral frontal lobe lesions due to thyroid storm

SUMMARY Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 μIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.

Secretory leukocyte peptidase inhibitor inhibits the inflammatory response and apoptosis of lipopolysaccharide-induced human proximal renal tubular cells / 中华危重病急救医学

Objective:To screen out the potential key genes of sepsis-associated acute kidney injury (AKI), and provide theoretical and experimental evidence for the treatment of sepsis-associated AKI.Methods:① Bioinformatics analysis: two gene expression datasets (GSE30718 and GSE53773) were downloaded for bioinformatics analysis from the Gene Expression Omnibus (GEO). These two datasets recorded mRNA microarray data from kidney biopsies before and after kidney transplantation, and a subset of patients developed AKI after kidney transplantation. Differential analysis was conducted, and the genes with the same differential expression and a higher area under the receiver operator characteristic curve (AUC) in both databases were used as the target gene for subsequent cell experiments. ② Cell validation experiment: human proximal renal tubular cells HK2 were cultured in vitro, and lipopolysaccharide (LPS) was used for establishing LPS-HK2 cell model (LPS 10 mg/L for 6 hours, LPS model group), and the blank control group was set. Then, small interfering RNA (siRNA) technology was used to knock down the target gene obtained by bioinformatics analysis in LPS-HK2 cells (gene knockdown group), and a gene negative control group was set. The real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-qPCR) technique was used to detect the expression of the target gene in HK2 cells. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory factors in the cell supernatants. Western blotting was used to detect the expressions of key apoptosis proteins. Results:① Results of bioinformatics analysis: 325 genes in the two datasets showed the same expression trend, of which 144 were significantly down-regulated and 181 were significantly up-regulated, while the expression difference of secretory leukocyte protease inhibitor (SLPI) in the two datasets was both statistically significant. Further receiver operator characteristic curve (ROC curve) analysis confirmed that the SLPI expression in GSE30718 and GSE53773 datasets had a high diagnostic efficiency for AKI, with AUC of 0.83 and 0.92, respectively. Therefore, SLPI was selected as the target gene for subsequent cell validation experiment. ② Cell validation experiment: the RT-qPCR analysis showed that the expression of SLPI in LPS-HK2 cells of the LPS model group was significantly higher than that of the blank control group (2 -ΔΔCT: 1.80±0.14 vs. 1.00±0.11, P < 0.01), and the change trend was the same with the results of bioinformatics analysis. Furthermore, knockdown SLPI gene analysis showed that the levels of inflammatory factors in LPS-HK2 cells supernatants in the gene knockdown group were significantly higher than those in the negative control group [Interleukin-6 (IL-6, ng/L): 509.58±27.08 vs. 253.87±75.83, IL-1β (ng/L): 490.99±49.52 vs. 239.67±26.97, tumor necrosis factor-α (TNF-α, ng/L): 755.22±48.66 vs. 502.06±10.92, all P < 0.01]. The above results indicated that SLPI could inhibit the inflammatory response of HK2 cells induced by LPS. The expressions of key apoptosis proteins Bax and caspase-3 in LPS-HK2 cells in the gene knockdown group were significantly higher than those in the negative control group [Bax protein (Bax/GAPDH): 1.38±0.12 vs. 1.00±0.10, caspase-3 protein (caspase-3/GAPDH): 1.44±0.15 vs. 1.00±0.11, both P < 0.05], and Bcl-2 expression was significantly decreased (Bcl-2/GAPDH: 0.83±0.08 vs. 1.00±0.05, P < 0.05), the above results indicated that SLPI could inhibit the apoptosis of cells in the inflammatory response. Conclusion:SLPI can inhibit the inflammatory response and apoptosis of HK2 cells induced by LPS, which may be involved in the protective mechanism of renal tubular cells in the response to sepsis, and is a potential target for the treatment of sepsis-associated AKI.

Nystagmus following acute avermectins poisoning.

BACKGROUND: Acute pesticide poisoning is a major public health problem in the world. Most pesticides are toxic to human beings, because of diverse components resulting in different reaction. OBJECTIVE: As clinicians identify various symptoms due to pesticide poisoning, it is necessary for the diagnosis and treatment for treating such toxins. Accidents associated with acute avermectins poisoning are rarely reported, especially self-induced nystagmus. In the present study, a case of human abamectin poisoning with relevant toxic effects has been reported. CONCLUSIONS: Acute avermectins poisoning-induced nystagmus may be affected due to the vestibular cerebellar system, but the exact mechanism and pharmacological basis is still worthy of further study.

Investigation and analysis of patients with severe pesticide poisoning in Tongling area of Anhui province / 中国中西医结合急救杂志

ObjectiveTo analyze the related data of patients with severe pesticide poisoning in Tongling area, put forward the countermeasures,and provide available basis to improve the level of prevention and treatment of the disease.Methods Forty patients with severe pesticide poisoning admitted to the Department of Critical Care Medicine of Tongling People's Hospital Affiliated to Wannan Medical College from August 2014 to November 2015 were analyzed retrospectively, the clinical data including distributions of sex, ages, kinds of poisoning drugs, causes of poisoning, time from intoxication to admission into a hospital, rescue therapy, prognosis etc.Results In the 40 patients, there were 12 males and 28 females, the ratio between male to female was 1∶2.33, and the number of women was significantly higher than that of men. Their ages ranged from 40 - 60 years, accounting for 37.5% (15/40). The toxic agent the most commonly seen was organic phosphorus pesticide (15 cases, accounting for 37.5%), and cases with mixed poisoning by taking two or more than two kinds of toxic material accounted for 25.0% (10/40). In addition, the cause of poisoning was mainly due to family quarrels (33 cases, accounting for 82.5%). In regard of time between taking toxic material to admission into a hospital, only did 3 cases admit into the hospital within 1 hour (7.5%), and the majority was within 3 hours (15 cases, accounting for 37.5%). The comprehensive treatments were as follows: clear means to clear the toxin,solution (to use antidote to detoxify), maintainance (to maintain the basic vital signs) and exclusion (to exclude other complications early); the curative effect of comprehensive treatments was satisfied, and 3 cases died, accounding for 7.5%.Conclusions The majority of patients with severe pesticide poisoning in Tongling city are adult females, the main cause of taking toxic material is due to family quarrels, and the toxic agent the most commonly seen is organic phosphorus pesticide. Directing to the above high risk factors, the prevention and treatment are carried out, anticipating the incidence, mortality and medical cost can be reduced significantly.

Effects of dexmedetomidine on outcomes following craniocerebral operation - a meta-analysis.

OBJECTIVE: To evaluate the effect of dexmedetomidine on outcomes following craniocerebral operation and provide evidence for individualized medication. METHODS: We searched the Cochrane Library, PubMed, Springer, CNKI, Wanfang Data Resource and other Chinese and foreign databases with electronic retrieval, within the period 1990-2013, for records relating to dexmedetomidine, brain pharmacokinetics and clinical randomized controlled studies. Records were assessed using the Cochrane system evaluation method for assessing the quality of research, using Revman 5.1 Meta-analysis software. RESULTS: After screening and removal of duplicate documents there were 22 English and 44 Chinese articles, among which there were eight describing clinical trials, with a total of 412 cases. Meta-analysis showed that dexmedetomidine on rate during craniocerebral operation (standardized mean difference=-8.32, 95% confidence interval [CI] -10.38 to 6.26, P<0.00001), and blood pressure (standardized mean difference=-3.37, 95% CI -5.36 to 1.38, P<0.00001). The study had good heterogeneity using random effects model analysis, and there was no publication bias. CONCLUSION: Dexmedetomidine can reduce the hemodynamic response and play a role in brain protection.

Effects of praeruptorin C on blood pressure and expression of phospholamban in spontaneously hypertensive rats.

BACKGROUND: The traditional Chinese medicine Praeruptorin c (Pra-c) has many physiological and pharmacological effects, including antagonistic effects on blood pressure and calcium levels, maintenance of cellular calcium homeostasis, and improved cardiac systolic and diastolic function. It is potentially a novel and versatile drug for the treatment and prevention of cardiovascular diseases. OBJECTIVE: To explore the possible impact of Pra-c on blood pressure in SHR and its mechanism of action. MATERIALS AND METHODS: Twenty SHR were randomly divided into a Pra-c group [Pra-c was administered intragastrically, 20 mg kg(-1) d(-1), n=10] or an untreated control group (n=10), containing 10 age-matched SD rats. Each group of rats was followed for 8 weeks. Before and during the treatment, tail artery systolic blood pressure was measured using a tail-cuff every 2 weeks. After 8 weeks, the rats were sacrificed and RNA was extracted from homogenates of cardiac tissue. Tissue from the left ventricle was fixed, sectioned and H&E stained to assess possible changes in myocardial cell structure and morphology. Semi-quantitative RT-PCR was used to assess changes in phospholamban gene expression in treated and untreated rats. RESULTS: SHR treated with Pra-c for 8 weeks had a lower systolic pressure than untreated SHR (p<0.05), two measures of cardiac damage, the heart mass index and left ventricle mass index (HMI and LVMI, respectively) were improved, and the level of PLB mRNA expression was lower in the untreated SHR group (p<0.05). DISCUSSION AND CONCLUSION: With continuous hypertension, SHR gradually formed or developed cardiac hypertrophy and fibrosis. Pra-c had a clear effect on blood pressure in SHR, and reversed SHR ventricular remodeling by upregulating the gene expression of sarcoplasmic reticulum PLB.