Suchergebnisse

Tuan Dinh Le,1,2,* Nga Phi Thi Nguyen,2 Hoa Thanh Thi Tran,3 Thuc Luong Cong,4,* Lan Ho Thi Nguyen,5 Binh Do Nhu,6 Son Tien Nguyen,2 Manh Van Ngo,7 Hoa Trung Dinh,8 Hien Thi Nguyen,9 Kien Trung Nguyen,10 Duc-Cuong Le7,11,* 1Center of Emergency, Critical Care Medicine and Clinical Toxicology, Military Hospital 103, Vietnam Military Medical University, Ha Noi, Vietnam; 2Department of Rheumatology and Endocrinology, Military Hospital 103, Vietnam Military Medical University, Ha Noi, Vietnam; 3National Hospital of Endocrinology, Hanoi, Vietnam; 4Department of Cardiology, Military Hospital 103, Vietnam Military Medical University, Hanoi, Vietnam; 5Department of General Internal Medicine, National Hospital of Endocrinology, Ha Noi, Vietnam; 6Division of Military Science, Military Hospital 103, Vietnam Military Medical University, Ha Noi, Vietnam; 7Postgraduate Training Management Department, Thai Binh University of Medicine and Pharmacy, Thai Binh, Vietnam; 8Department of Requested Treatment, National Hospital of Endocrinology, Ha Noi, Vietnam; 9Department of Physiology, Thai Binh University of Medicine and Pharmacy, Thai Binh, Vietnam; 10Department of Science Management, Thai Binh University of Medicine and Pharmacy, Thai Binh, Vietnam; 11Epidemiology-Faculty of Public Health, Thai Binh University of Medicine and Pharmacy, Thai Binh, Vietnam*These authors contributed equally to this workCorrespondence: Tuan Dinh LeCenter of Emergency, Critical Care Medicine and Clinical Toxicology, Department of Rheumatology and Endocrinology, Military Hospital 103, Vietnam Military Medical University, 261 Phung Hung Street, Phuc La Ward, Ha Dong District, Ha Noi, VietnamTel +840388166078Email letuan985@gmail.comDuc-Cuong LePostgraduate Training Management Department; Epidemiology-Faculty of Public Health, Thai Binh University of Medicine and Pharmacy, 373 Ly Bon Street, Ky Ba Ward, Thai Binh, VietnamTel +84 93 8042 668Email cuongldvn@gmail.comPurpose: This study was aimed at the prevalence, cardiovascular risk factors of diabetic peripheral neuropathy (DPN), and the relationship between DPN and fasting glucagon-like peptide-1 (fGLP-1) concentrations in newly diagnosed patients with type 2 diabetes mellitus (nT2D).Methods: A cross-sectional descriptive study was conducted from 2015 to 2020 with a population of 473 nT2D. Screening for DPN was based on the United Kingdom screening test. fGLP-1 was measured by enzyme-linked immunosorbent assay.Results: The prevalence of DPN was 26.6%, in which mild grade was 17.3%, moderate grade was 8.2% and severe grade was 1.1% in total. Age (OR = 1.73, 95% CI 1.12– 2.67, p = 0.012), smoking (OR = 1.64, 95% CI 1.03– 2.62, p = 0.037), poor control HbA1c (OR = 2.66, 95% CI 1.23– 5.76, p = 0.01), 24-h urinary albumin (24hUA) (OR = 2.49, 95% CI 1.26– 4.94, p = 0.007), and diabetic retinopathy (OR = 3.17, 95% CI 1.46– 6.89, p = 0.002) significantly increased the risk for DPN. In multivariate logistic regression analysis, hypertension (OR = 2.96, 95% CI 1.16– 7.55, p = 0.023), triglyceride (OR = 1.50, 95% CI 1.11– 2.03, p = 0.009), albumin (OR = 0.85, 95% CI 0.75– 0.95, p = 0.005), and fGLP-1 (OR = 0.79, 95% CI 0.67– 0.93, p = 0.005) correlated with DPN. The fGLP-1 concentrations were reduced significantly in DPN (p < 0.001). In particular, male patients with DPN had a significantly lower fGLP-1 levels than those without DPN (p < 0.001).Conclusion: The prevalence of DPN among nT2D was 26.6%. Age, smoking, hypertension, HbA1c control, triglyceride, albumin, 24hUA, diabetic retinopathy were the associated risk factors of DPN, and fGLP-1 was negatively correlated with DPN (OR = 0.79, 95% CI 0.67– 0.93, p = 0.005).Keywords: newly diagnosed type 2 diabetes mellitus, diabetic peripheral neuropathy, cardiovascular risk factors, glucagon-like peptide-1 concentrations

Inhibition and aging of neuropathy target esterase (NTE) by exposure to neuropathic organophosphorus compounds (OPs) can result in OP-induced delayed neuropathy (OPIDN). In the present study we aimed to build a model of OPIDN in adult zebrafish. First, inhibition and aging of zebrafish NTE activity were characterized in the brain by using the prototypic neuropathic compounds cresyl saligenin phosphate (CBDP) and diisopropylphosphorofluoridate (DFP). Our results show that, as in other animal models, zebrafish NTE is inhibited and aged by both neuropathic OPs. Then, a neuropathic concentration inhibiting NTE activity by at least 70% for at least 24 h was selected for each compound to analyze changes in phosphatidylcholines (PCs), lysophosphatidylcholines (LPCs) and glycerolphosphocholine (GPC) profiles. In spite to the strong inhibition of the NTE activity found for both compounds, only a mild increase in the LPCs level was found after 48 h of the exposure to DFP, and no effect were observed by CBDP. Moreover, histopathological evaluation and motor function outcome analyses failed to find any neurological abnormalities in the exposed fish. Thus, our results strongly suggest that zebrafish is not a suitable species for the development of an experimental model of human OPIDN. © 2018 The Author(s). ; This study was funded by the NATO SfP project MD.SFPP 984777 (D.R.), the European Research Council under European Union's Seven Framework Programme (FP/2007–2013)/ERC Grant Agreement n. 320737, and the Spanish Government (CTM2017-83242-R; D.R.). M.F. acknowledges the financial support from the Government of Catalonia through a Beatriu de Pinos fellowship (2016 BP-B 00233). I.F. was supported by the Ministry of Economy and Competitivity of Spain (FPI grant BES-2015-075023). The authors thank Mr. Marc Mañas for his valuable assistance building the Open Field Test setup. ; Peer reviewed

Postural orthostatic tachycardia syndrome is a condition characterized by imbalance in autonomic reactivity leading to exaggerated heart rate and other symptoms of orthostatic intolerance. In adolescents, it is characterized either by a continuous increase in heart rate of ≥40 bpm as compared to basal heart rate or sustained basal rate of ≥130 bpm. The objective of the research was to compare the characteristics of adolescent diabetics with postural orthostatic tachycardia syndrome with the controls. Methods. Seventy adolescents diagnosed with type 1 diabetes mellitus who were treated at the department of Endocrinology, Government Medical College and Shri Maharaja Hari Singh hospital, Srinagar, J&K, India were selected for the study. Lying to standing test was performed. Heart rate was recorded at the 2nd, 3rd, 5th and 10th minutes. Based on the results of lying to standing test, there were selected 25 diabetic adolescents with postural orthostatic tachycardia syndrome. Their characteristics were compared with age- and sex-matched adolescents using unpaired T test. P< 0.05 was considered significant. Results. We observed a significantly lower body mass index (p=0.027), as well as a significantly higher fasting blood glucose level (p<0.0001) in diabetics with postural orthostatic tachycardia syndrome. Conclusion. It may be concluded that lower body mass index and higher fasting blood glucose level may lead to the development of postural orthostatic tachycardia syndrome in adolescents.

Background: This study was designed to explore whether participant-driven patient education in group sessions, compared to the provision of standard information, will contribute to a statistically significant reduction in new ulceration during 20 months in patients with diabetes and high risk of ulceration. Methods and Material: This is a six-month interim assessment. The CONSORT guidelines were used to construct a randomized controlled trial. Age 34–78 years old, diabetes mellitus, sensory neuropathy, and a healed foot ulcer below the ankle were the inclusion criteria; 526 individuals (both male and female) were screened in order. Results: The research involved a total of 125 patients. Because of concerns regarding the patients' capacity to complete the trial according to protocol, an interim analysis of 85 participants was conducted after six months. After six months, 44.70 percent of the participants had acquired a new foot ulcer, with no statistical difference between the two groups. The number of patients was insufficient to draw any statistical conclusions about the intervention's effectiveness. Plantar stress ulcers and external trauma were the most common causes of ulcer formation.Conclusions: It was concluded that patients with diabetes and a healed foot ulcer develop foot ulcers despite participant-driven group education as this high-risk patient group has external risk factors that are beyond this form of education. The educational method should be evaluated in patients with a lower risk of ulceration.

Background and Objective There is no agreement on the gold standard for detection and grading of chemotherapy-induced peripheral neurotoxicity (CIPN) in clinical trials. The objective is to perform an observational prospective study to assess and compare patient-based and physician-based methods for detection and grading of CIPN. Methods Consecutive patients, aged 18 years or older, candidates for neurotoxic chemotherapy, were enrolled in the United States, European Union, or Australia. A trained investigator performed physician-based scales (Total Neuropathy Score-clinical [TNSc], used to calculate Total Neuropathy Score-nurse [TNSn]) and supervised the patient-completed questionnaire (Functional Assessment of Cancer Treatment/Gynecologic Oncology Group-Neurotoxicity [FACT/GOG-NTX]). Evaluations were performed before and at the end of chemotherapy. On participants without neuropathy at baseline, we assessed the association between TNSc, TNSn, and FACT/GOG-NTX. Considering a previously established minimal clinically important difference (MCID) for FACT/GOG-NTX, we identified participants with and without a clinically important deterioration according to this scale. Then, we calculated the MCID for TNSc and TNSn as the difference in the mean change score of these scales between the 2 groups. Results Data from 254 participants were available: 180 (71%) had normal neurologic status at baseline. At the end of the study, 88% of participants developed any grade of neuropathy. TNSc, TNSn, and FACT/GOG-NTX showed good responsiveness (standardized mean change from baseline to end of chemotherapy >1 for all scales). On the 153 participants without neuropathy at baseline and treated with a known neurotoxic chemotherapy regimen, we verified a moderate correlation in both TNSc and TNSn scores with FACT/GOG-NTX (Spearman correlation index r = 0.6). On the same sample, considering as clinically important a change in the FACT/GOG-NTX score of at least 3.3 points, the MCID was 3.7 for TNSc and 2.8 for the TNSn. Conclusions ...

Background: The increased incidence of diabetes rapidly globally at an alarming rate. The presence of microvascular complications has been shown to have a negative impact on patient's quality of life. There are few clinical studies in this direction but most of them lack sufficient power and are focused only towards one specific complication. Subjects and Methods: An observational single arm cross sectional study done in 100 cases of type 2 diabetes mellitus in department of medicine, Government Medical College Bharatpur, Rajasthan. Each subject underwent detailed history and complete clinical examination. Diabetes was diagnosed according to American Diabetes Association (ADA) revised criteria. Blood glucose level estimation was done by glucose oxidase method in venous blood. Glycosylated haemoglobin (HbA1C) was measured by ion-exchange chromatography method. Results: The overall male to female ratio was approx 1:1 in our study. Our study showed that the maximum patients were suffering from retinopathy 12 (66.66%) in more than 10 years duration of diabetes. Mostly patients suffering from diabetic neuropathy 28 (90.32%) were occurred in more than 10 years & 5-10 years of duration of diabetes. Maximum cases of nephropathy 21 (50%) were seen in 5-10 years of duration of diabetes. So proportion of neuropathy, retinopathy & nephropathy significantly increases, when duration of diabetes increased in our results. Conclusion: Duration of diabetes was found to be a main culprit of micro vascular complication. Screening with some simple test such as ECG, fundoscopy, biothesiometer and biochemical tests namely, lipid, protein and fat profile for all cases of diabetes is essential to identify the complications at an early age.

Hannu Laaksovirta konsortion jäsenenä. ; IMPORTANCE Juvenile amyotrophic lateral sclerosis (ALS) is a rare form of ALS characterized by age of symptom onset less than 25 years and a variable presentation. OBJECTIVE To identify the genetic variants associated with juvenile ALS. DESIGN, SETTING, AND PARTICIPANTS In this multicenter family-based genetic study, trio whole-exome sequencing was performed to identify the disease-associated gene in a case series of unrelated patients diagnosed with juvenile ALS and severe growth retardation. The patients and their family members were enrolled at academic hospitals and a government research facility between March 1, 2016, and March 13, 2020, and were observed until October 1, 2020. Whole-exome sequencing was also performed in a series of patients with juvenile ALS. A total of 66 patients with juvenile ALS and 6258 adult patients with ALS participated in the study. Patients were selected for the study based on their diagnosis, and all eligible participants were enrolled in the study. None of the participants had a family history of neurological disorders, suggesting de novo variants as the underlying genetic mechanism. MAIN OUTCOMES AND MEASURES De novo variants present only in the index case and not in unaffected family members. RESULTS Trio whole-exome sequencing was performed in 3 patients diagnosed with juvenile ALS and their parents. An additional 63 patients with juvenile ALS and 6258 adult patients with ALS were subsequently screened for variants in the SPTLC1 gene. De novo variants in SPTLC1 (p. Ala20Ser in 2 patients and p.Ser331Tyr in 1 patient) were identified in 3 unrelated patients diagnosed with juvenile ALS and failure to thrive. A fourth variant (p.Leu39del) was identified in a patient with juvenile ALS where parental DNA was unavailable. Variants in this gene have been previously shown to be associated with autosomal-dominant hereditary sensory autonomic neuropathy, type 1A, by disrupting an essential enzyme complex in the sphingolipid synthesis pathway. CONCLUSIONS AND RELEVANCE These data broaden the phenotype associated with SPTLC1 and suggest that patients presenting with juvenile ALS should be screened for variants in this gene. ; Peer reviewed

Brachial plexus neuropathy is often seen in the military population, especially due to pressure (backpack palsy, BPP) or idiopathic (neuralgic amyotrophy, NA). We aimed to gain insight in the disease characteristics of soldiers with brachial plexus neuropathies in the Dutch military population and to compare disease characteristics between patients with BPP and NA. In this retrospective chart review study we aimed to include all patients with brachial plexus neuropathy, who presented in the Joint Military Hospital between 1 January, 2011 and 31 December, 2016. We calculated the incidence of NA and BPP and Chi‐square tests or Student t tests were performed for differences in patient characteristics between NA and BPP. We included 127 patients, 63 with BPP, 45 with NA, 10 with traumatic brachial plexus neuropathy, and 9 with other plexopathy. The incidence of brachial plexus neuropathy was 50/100 000 person years overall, 25/100 000 person years for BPP, and 18/100 000 person years for NA. Patients in the BPP group differed from the NA with regard to pain (BPP 41% vs NA 93%, P = .000), atrophy (13% BPP vs 29% NA, P = .049), and sensory symptoms (83% BPP vs 44% NA, P = .000). In the BPP group 90% had incomplete recovery and in the NA group 78%. Our study showed a high incidence of BPP and NA in the military population and suggests recovery is not so benevolent as previously thought. Future research is necessary to improve insight and outcome of military patients with brachial plexus neuropathies.

Thi My Hanh Pham,1,2 Chien Thang Nguyen,1 Quoc Tung Mai,2 Thi Huong Giang Bui,2 Dung Hoa Do,2 Peter McCluskey,3 Trong Van Pham2 1Department of Ophthalmology, 103 Military Hospital, Hanoi, Vietnam; 2Department of Ophthalmology, Hanoi Medical University, Hanoi, Vietnam; 3Department of Ophthalmology, University of Sydney, Sydney, NSW, AustraliaCorrespondence: Quoc Tung MaiTung Department of Ophthalmology, Hanoi Medical University, 1 Ton That Tung Street, Hanoi, 100000, VietnamTel +84 915644181Email maiquoctung@hmu.edu.vnPurpose: To evaluate the efficacy and safety of endoscopic orbital decompression in patients with Graves' orbitopathy.Patients and Methods: This is a prospective study in Hanoi Medical University and a Military Hospital from December 2017 to December 2018. Twenty-eight orbits of fifteen patients were undergoing endoscopic orbital decompression for Graves' orbitopathy. Indications for surgery were proptosis in twenty-two orbits and compressive optic neuropathy in six orbits. The outcome measures were proptosis reduction, visual acuity, visual field test and diplopia. Post-operative complications including cerebrospinal fluid leakage, haemorrhage, lacrimal duct impairment, worsening diplopia, sinusitis and cellulitis were collected.Results: The mean proptosis reduction was 2.23 mm. Visual acuity and medium deviation in the Humphrey visual field were significantly improved in four of six eyes with compressive optic neuropathy. There was one patient with intra-operative excessive bleeding which resolved without affecting visual outcome. Post-operatively, two patients developed a new onset of diplopia and two others worsened diplopia; three have already undergone successful strabismus surgery and moderate proptosis reduction.Conclusion: Endoscopic orbital decompression surgery was effectively and safely to manage compressive optic neuropathy of Graves' orbitopathy and moderately reduce proptosis in a group of Vietnamese patients.Keywords: endoscopy, Graves' orbitopathy, decompression, optic neuropathy

Closed-globe injury can cause visual loss in military and civilian populations, with retinal cell death, including retinal ganglion cell (RGC) degeneration, leading to irreversible blindness. RGC and optic nerve (ON) degeneration after eye or head injury is termed traumatic optic neuropathy (TON). There are currently no treatments for RGC loss, therefore novel therapeutics to prevent RGC death or promote axonal regeneration are a priority. We investigated necroptotic signaling mechanisms in a rat blunt ocular injury model. After bilateral blunt trauma, protein expression and retinal localization of necroptosis pathway members (receptor interacting protein kinase 1, RIPK1 ; receptor interacting protein kinase 3, RIPK3 ; and mixed lineage kinase domain like pseudokinase, MLKL) were assessed by Western blot and immunohistochemistry (IHC), and potent necroptosis inhibitor Necrostatin-1s (Nec-1s) was delivered by intravitreal injection to one eye and vehicle to the contralateral eye. RGC and photoreceptor survival were assessed by cell counting and outer nuclear layer (ONL) thickness measurements on histology. The neuroprotective effects of Nec-1s were assessed in primary retinal culture by &beta ; III-tubulin+ RGC cell counts. MLKL protein expression were upregulated at 48 h after injury and MLKL immunolocalised to retinal binding protein with multiple splice (RBPMS)+ RGC, inner nuclear cells and ONL cells, specifically at the retinal injury site. RIPK3 expression did not increase but RIPK3 co-immunolocalised with RBPMS+ RGC in intact and injured retinae. In vitro, a Nec-1s concentration of 0.01 pg/µ ; L was RGC neuroprotective. In the blunt ocular injury rat model, Nec-1s prevented RGC death at the center of the impact site but did not protect against ONL thinning or provide functional restitution. RGC degeneration in our blunt ocular injury model is site-specific, with necroptosis driving death at the center of the focal impact site.

AIM: Type 2 diabetes mellitus (T2DM) is a risk factor for increased arterial stiffness. We evaluated associations between the cardio-ankle vascular index (CAVI) and carotid plaque, intima media thickness (IMT), and diabetic microvascular complications in Korean T2DM patients. METHODS: We conducted a retrospective, cross-sectional study of 320 Korean T2DM patients without a history of macrovascular disease or macroalbuminuria. We measured 24-hour urinary albumin excretion (UAE) levels and performed funduscopic and neuropathy examinations to assess the extent of diabetic microvascular complications. Arterial stiffness was assessed using CAVI. We also measured the ankle-brachial index (ABI), common carotid artery IMT, and carotid beta stiffness index. RESULTS: Among the 320 patients enrolled in this study, 64 (20%) had increased CAVI (�돟 9). We found that CAVI was correlated with systolic blood pressure, pulse pressure, IMT, carotid beta stiffness index, log-transformed UAE, and total cholesterol. In multiple logistic regression analysis, mean IMT and the presence of carotid plaque were independently associated with increased CAVI (�돟 9) (OR=5.77, P < 0.01; OR=5.36, P < 0.001, respectively). Furthermore, an increased CAVI was associated with peripheral neuropathy (OR=2.03, P = 0.03) and microalbuminuria (OR=2.47, P < 0.01) after adjusting for possible confounding variables. CONCLUSIONS: The results of this study suggest that increased CAVI is associated with the presence of arterial plaque, increased IMT, and microvascular complications, such as nephropathy and neuropathy, in T2DM patients. ; open

PURPOSE: To evaluate the efficacy and safety of endoscopic orbital decompression in patients with Graves' orbitopathy. PATIENTS AND METHODS: This is a prospective study in Hanoi Medical University and a Military Hospital from December 2017 to December 2018. Twenty-eight orbits of fifteen patients were undergoing endoscopic orbital decompression for Graves' orbitopathy. Indications for surgery were proptosis in twenty-two orbits and compressive optic neuropathy in six orbits. The outcome measures were proptosis reduction, visual acuity, visual field test and diplopia. Post-operative complications including cerebrospinal fluid leakage, haemorrhage, lacrimal duct impairment, worsening diplopia, sinusitis and cellulitis were collected. RESULTS: The mean proptosis reduction was 2.23 mm. Visual acuity and medium deviation in the Humphrey visual field were significantly improved in four of six eyes with compressive optic neuropathy. There was one patient with intra-operative excessive bleeding which resolved without affecting visual outcome. Post-operatively, two patients developed a new onset of diplopia and two others worsened diplopia; three have already undergone successful strabismus surgery and moderate proptosis reduction. CONCLUSION: Endoscopic orbital decompression surgery was effectively and safely to manage compressive optic neuropathy of Graves' orbitopathy and moderately reduce proptosis in a group of Vietnamese patients.