Non-Aneurysmal Perimesencephalic Subarachnoid Hemorrhage: A Literature Review.

Spontaneous non-aneurysmal subarachnoid haemorrhage (NAPMSAH) (addressing point 1) is a relatively rare occurrence in clinical settings as it is rarely misdiagnosed and usually involves a significantly better prognosis than the classical aneurysmal pattern. We hereby focused on a comprehensive analysis of this distinct pathological entity with the purpose of analysing possible pathophysiological entities, outcomes and treatment options involving this diagnosis with a focus on demographical, epidemiological and clinical data. The clinical setting includes focal neurological signs related to the anatomical structures, while computer tomography followed by tomographic angiography are the most common diagnosis tools, with a typical hyperdense lesion involving the midbrain, fourth ventricle and subthalamic areas without an angiographic correspondent, such as an aneurysmal pathology. Further investigations can also be used to highlight this diagnosis, such as interventional angiography or magnetic resonance imaging. Given the rarity of this condition and its relatively better prognosis, treatment options usually remain conservative. In the present review, the main characteristics of NAPMSAH are discussed.

Natalizumab Changes the Peripheral Profile of the Th17 Panel in MS Patients: New Mechanisms of Action.

INTRODUCTION: Natalizumab (NAT) is an effective treatment for relapsing remitting multiple sclerosis (RRMS), as it makes the blood-brain-barrier impenetrable by binding to the α4integrin subunit. The objectives of our study were to find new peripheral mechanisms of action of NAT and new biomarkers of treatment response. MATERIAL AND METHODS: We prospectively assessed the serum levels of 15 cytokines from the Th17 Cytokine Panel using Bio-plex Pro Human in a group of 29 RRMS patients treated with NAT and 29 healthy subjects (HS) at inclusion and after 8 months of NAT treatment. For each patient, demographic data, number of relapses and Expanded Disability Status Scale (EDSS) were collected and compared with the initial and final values of each cytokine. Moreover, the Th17/Treg shift was assessed using the interleukine (IL)-17F/IL-10 ratio and the cytokine signature (the sum of all the cytokines). Advanced statistical analysis was used. RESULTS: RRMS patients had significantly lower serum levels of IL-23, IL-17F, IL-1ß and IL-31 compared to HS. Serum sCD40L, IL-17F, IL-31 and cytokine signature levels significantly decreased after 8 months of NAT treatment. Positively correlations were found between the relapse number and IL- 17F, IL-1ß, IL-31 serum levels and between EDSS and tumor necrotic factor-α, IL-1ß and IL-17/IL-10 serum levels. IL-10 serum levels correlated negatively with the EDSS score. CONCLUSION: In evaluating the mode of action of NAT, it is important to determine the value of each cytokine, the Th17/Treg shift and the cytokine signature. NAT significantly decreased peripheral serum levels of some pro-inflammatory cytokines as a novel mechanism of action. IL-17F, sCD40L and IL-31 were the best biomarkers to assess the effectiveness of NAT.

Influence of GSTM1, GSTT1, and GSTP1 Polymorphisms on Type 2 Diabetes Mellitus and Diabetic Sensorimotor Peripheral Neuropathy Risk.

BACKGROUND AND AIMS: Diabetic neuropathy is a frequent complication of type 2 diabetes mellitus (T2DM). Genetic susceptibility and oxidative stress may play a role in the appearance of T2DM and diabetic neuropathy. We investigated the relation between polymorphism in genes related to oxidative stress such as GSTM1, GSTT1, and GSTP1 and the presence of T2DM and diabetic neuropathy (DN). METHODS: Samples were collected from 84 patients with T2DM (42 patients with DN and 42 patients without DN) and 98 healthy controls and genotyped by using polymerase chain reaction and restriction fragment length polymorphism method. RESULTS: GSTP1 Ile105Val polymorphism was associated with the risk of developing T2DM (p = 0.05) but not with the risk of developing DN in diabetic cases. GSTM1 and GSTT1 gene polymorphisms were associated with neither the risk of developing T2DM nor the risk of DN occurrence in diabetic patients. No association was observed between the patients with T2DM and DSPN (diabetic sensorimotor peripheral neuropathy) and T2DM without DSPN regarding investigated polymorphism. CONCLUSION: Our data suggest that GSTP1 gene polymorphisms may contribute to the development of T2DM in Romanian population. GSTM1, GSTT1, and GSTP1 gene polymorphisms are not associated with susceptibility of developing diabetic neuropathy in T2DM patients.