Statins, the lipid-lowering drugs, and non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH), a lipid-related pathology, share a complex relationship, one known to be hepatotoxic and other being hepatic injury. NASH is an unresolved mystery in terms of treatment. Could statins prove to be a promising solution due to their pleiotropic properties in addition to the cholesterol-lowering effect? This study aims to find statin effectiveness in NAFLD/NASH treatment and prevention of associated adverse outcomes. An extensive data search was done to identify the studies assessing statin effect on NAFLD/NASH and then analyzed to establish the relationship. Several studies demonstrated a reduction in NAFLD/NASH-associated inflammation and fibrosis with statin treatment. These anti-inflammatory and anti-fibrotic effects were through their pleiotropic properties, which were in addition to their cholesterol-lowering effect. In various animal studies, statins were found to improve hepatic lipotoxicity, oxidative stress, inflammatory responses, and fibrosis associated with NASH through multiple pathways. Statins exert these protective effects by recovering the gene expression level of peroxisomal proliferator-activated receptor alpha (PPARα) and therefore restore the mitochondrial and peroxisomal fatty acid oxidation (FAO). Statin treatment also increased the levels of paraoxonase 1 (PON1), an antioxidant and antiatherogenic enzyme that is reduced in NAFLD as well as encounter the hepatic lipotoxicity by resolving cholesterol crystals and Kupffer cells (KCs) with crown-like structures (CLSs). They exhibited antitumor properties by inhibiting proinflammatory cytokines and vascular proliferative factors. Moreover, they restored a healthy liver sinusoidal endothelial cell (LSEC) and hepatic stellate cells (HSC) along with inhibiting the activation of HSC via modulating inducible nitric oxide synthase (iNOS) and expressions of endothelial nitric oxide synthase (eNOS). Besides, they were protective against cardiovascular disease (CVD)-related morbidity and mortality, hepatocellular carcinoma (HCC), and metabolic syndrome (MS) associated with NAFLD/NASH. NASH and its precursor, NAFLD, could be treated and prevented with statins owing to their pleiotropic properties. This study helps to prove this by looking back at different literature and has successfully enlightened the point. Once proved through large clinical trials on humans, it could revolutionize the NASH therapy.

Takotsubo syndrome (TTS), also called broken heart syndrome, is an acute and transient cardiac wall motion abnormality of the left ventricle. The patient prototype is a post-menopausal woman with myocardial infarction-like symptoms (angina pectoris, breathlessness, palpitations, etc.) who has experienced sudden emotional or physical stress. Although prognosis is generally considered relatively benign, both complications and recurrence rates are not insignificant. Pathophysiological mechanisms underlying TTS are not entirely understood, but the sympathetic system over-activity has a leading role. Moreover, since emotional stress frequently triggers TTS and since precedent diagnosis of psychiatric disorders sometimes coexists, the psychological response to stress could be another potential therapeutic target. Indeed, this article aims to explore the association between underlying depression and anxiety disorders and TTS, as well as to find ideal therapeutic options useful to treat and prevent TTS. Thus in our review, we considered case reports, case-control studies, and review articles from PubMed. Papers dealing with Takotsubo syndrome and anxiety disorder or depression were selected. We included papers published since 2010 and whose abstract was in English. We concluded that anxiety disorders, but not depression, are associated with a higher occurrence of TTS. There is a link between anxiety, TTS, and inflammation leading to increased sympathetic activity. Nevertheless, patients with pre-admission psychiatric disorders have a higher risk of recurrent TTS. Importantly, the use of selective serotonin reuptake inhibitors (SSRIs) could be a potential therapeutic aid in preventing TTS's recurrence in selected patients.

With idiopathic Parkinson's disease being a common entity, parkinsonism in acquired hepatocerebral degeneration (AHD) in the context of Manganese (Mn) has gained importance in recent years. An insight into the pathomechanisms behind this disease has been put forth. How can Mn as a divalent metal exert its effect in leading to chronic neurodegenerative disorder? Secondary to decreased excretion in liver cirrhosis, Mn significantly alters the striatal dopaminergic system. Management of this debilitating disease also focuses on different aspects where Mn has been involved in the pathogenesis. We have put forth the details behind Mn effects in Parkinson’s, which will be a guide for better understanding and management of this disease. A literature search was performed using PubMed as a sole database, and all the articles were peer-reviewed. The author tried to follow the PRISMA guidelines. Inclusion criteria were set for 10 years, with most studies with in the last seven years. All types of study designs were included relevant to the topic, clearly delineating the pathomechanisms of Mn in the disease and also its management. After extensive research, through the PubMed database, we found that Parkinson's disease is one of the neurological complications in advanced liver cirrhosis. Mn is an essential element behind its pathogenesis; it works at different cellular levels to promote neurotoxicity. From its influx to its effects on dopamine transporters (DAT), where it disrupts dopamine homeostasis also altering postsynaptic dopamine (D2) receptors, it disrupts mitochondria and the endoplasmic reticulum (ER) promotes oxidative stress and neuroinflammation. Misfolding of alpha-synuclein (α-Syn) is promoted on chronic exposure to Mn where α-Syn from being neuroprotective becomes neurotoxic. It also alters glutaminergic and gabaergic neurotransmission. In a nutshell, the diversity of its effect on nigrostriatal denervation is challenging. The importance of neuroimaging and various approaches to management is also discussed. AHD, an uncommon entity in advanced liver cirrhosis, needs more awareness so that it can be diagnosed earlier and better therapeutic options can be sought. Our study highlighted Mn mechanisms behind this clinical entity, putting forth grounds for a better understanding of this disease. Advanced research targeting Mn for managing this disease will be revolutionary.

Vitamin D is well known for its effects on the homeostasis of calcium and phosphorus. Lately, considerable research has brought the extra-skeletal role of vitamin D under the spotlight, including its anti-cancer activity. Colorectal cancer (CRC) is the most extensively studied neoplasia that has been observed to be affected by vitamin D; the list includes breast, prostate, and ovarian cancer. This review aims to shine a light on the influence of vitamin D over CRC and to further understand its ability to be used as a potential economical treatment for CRC patients. For this review, PubMed was used as the main database for the literature search. Studies on the role of vitamin D on CRC within 10 years and all of the study types were included. Post the extensive research over PubMed, it was noted that vitamin D, through its effect on multiple pathways, especially Wnt/β-catenin, apoptosis, and inflammation, hinders the progression of CRC carcinogenesis. High levels of this steroid hormone can delay the progression and may provide a cost-effective way of treating CRC patients. Further research and additional human trials are still due to bring about more knowledge on this topic. In conclusion, high serum levels of vitamin D are associated with a lower risk of incidence and progression of CRC.

Post-traumatic seizures (PTS) have become an emerging challenge for neurologists worldwide with the rise of brain injuries. Trauma can lead to various outcomes, ranging from naive spasms to debilitating post-traumatic epilepsy (PTE). In this article, we will explore the pathogenesis of convulsions following a concussion. We will look at multiple studies to explain the various structural, metabolic, and inflammatory changes leading to seizures. Additionally, we will explore the association between severity and location of injury and PTE. PTE's pathophysiology is not entirely implicit, and we are still in the dark as to which anti-epileptic drugs will be useful in circumventing these attacks. The purpose of this narrative review is to explain the post-traumatic brain changes in detail so that such attacks can be either thwarted or treated more resourcefully in the future.