RESUMO
Background: Studies reporting collective and comprehensive data on plaque regression of different lipid-lowering therapies (LLTs) are limited. Objectives: We evaluated plaque regression of LLTs based on multiple markers and performed subgroup analyses based on LLT type and post-treatment LDL-C levels. Methods: A literature search was performed to identify studies assessing plaque regression from LLTs. The following LLTs groups were included: High-intensity statin (HIS), HIS+ eicosapentaenoic acid (EPA), HIS + ezetimibe, Low-intensity statin (LIS), LIS + EPA, LIS + Ezetimibe, and PCSK9 inhibitors. Our primary outcomes were change in percent atheroma volume (PAV). Secondary outcomes included mean differences in total atheroma volume (TAV), lumen, plaque, and vessel volumes, fibrous cap thickness (FCT), and lipid arc (LA). Subgroup analyses were performed on LLT type and post-treatment LDL-C levels. Meta-regression was performed to control for covariates. Results: We identified 51 studies with 9,113 adults (22 % females). LLTs reduced PAV levels (-1.10 % [-1.63, -0.56], p < 0.01), with significant reduction observed with HIS, LIS + ezetimibe, LIS + EPA, and PCSK9 inhibitors. LLTs reduced TAV levels (-5.84 mm3 [-8.64 to -3.04] p < 0.01), mainly driven by HIS (-7.60 mm3 [-11.89, -3.31] p < 0.01). LLTs reduced plaque volume and LA and increased FCT. Conclusion: The plaque regression associated with LLTs is observed to be mainly driven by HIS, reducing both TAV and PAV. This suggest that HIS is the most effective LLT for plaque regression. Unstructured abstract: We evaluated plaque regression of LLTs from 51 studies. We found that while reduction of PAV (-1.10 % [-1.63, -0.56], p < 0.01) were present across different LLT types, reduction of TAV (-5.84 mm3 [-8.64 to -3.04] p < 0.01) was mainly driven by HIS (-7.60 mm3 [-11.89, -3.31] p < 0.01). These results suggest that HIS is the most effective LLT for plaque regression.
RESUMO
The chromosomal band 17q12 is characterized by a high density of genes and is bordered by segmental duplications, the structural arrangement of which increases the susceptibility of the region to deletions and duplications. Duplication of 17q12 is a rare genetic condition associated with variable characteristics from clinically asymptomatic to intellectual disabilities, seizures, and behavioral problems. The variability in phenotype is primarily due to variable expressivity and incomplete penetrance. Diagnosis is mostly established by chromosomal microarray. Treatment involves a multidisciplinary approach. We present a case of a 43-year-old female who initially presented with hyperphagia and was eventually diagnosed with bulimia nervosa, anxiety, mood disorder, and personality disorder. Additional research is required to better understand the impact of 17q12 duplication syndrome on the development of bulimia nervosa since its pathogenesis has not been adequately described in the current literature.
RESUMO
Nicolau syndrome is a rare condition characterized by severe pain at the site of injection, leading to ulceration and necrosis of the local tissues. Its presentation is usually acute. Nicolau syndrome is commonly seen in patients after intramuscular, intra-articular, or subcutaneous injections of non-steroidal anti-inflammatory drugs, antiepileptics, antipsychotics, antibiotics, antihistamines, and corticosteroids. Immediate diagnosis and management of this syndrome are of great importance. We herein report a rare presentation of Nicolau syndrome in a 36-year-old married male who suffered from paranoid schizophrenia for the past 3 years. The patient presented with dull pain, mild swelling, and necrotic ulceration over the injection site after receiving intramuscular fluphenazine. The patient underwent wound debridement and was given prophylactic antibiotics. Despite a wide range of therapeutic options for the management of Nicolau syndrome described in the literature, there exist limited guidelines for its management.
