Vivekananda Institute of Medical Sciences

Atopic dermatitis (AD) is a chronic inflammatory skin disease with significant morbidity. Recognising the need for region-specific guidance, the Skin Allergy Research Society and Society for Eczema Studies have collaborated to develop updated, evidence-based guidelines tailored to the Indian context. These guidelines address AD management across all age groups, special populations while considering local epidemiology, healthcare infrastructure, and treatment accessibility. A structured Delphi consensus process was conducted among 23 dermatology experts over 3 months through virtual and in-person meetings. Literature from MEDLINE, Cochrane, and Google Scholar was systematically reviewed, and the GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) approach was used to assess evidence quality. Clinical recommendations were refined through multiple voting rounds, leading to consensus statements. Recommendations are based on an extensive literature review up to December 2024. This document updates the 2019 Skin Allergy Society guidelines, reinforcing global recommendations while allowing local adaptability. These guidelines provide updated recommendations for topical, systemic, phototherapy, and biologic therapies in AD. Key advancements include the introduction of topical crisaborole and JAK inhibitors for mild to moderate AD, along with a focus on emerging systemic therapies, such as biologics and systemic JAK inhibitors. In the Indian context, the guidelines define the roles of dupilumab and abrocitinib while also addressing the off-label use of tofacitinib and baricitinib in resource-limited settings. Specific recommendations are provided for children, elderly patients, and pregnant women, emphasising safety considerations for systemic and biologic therapies. These guidelines align with global AD management while incorporating India-specific adaptations based on epidemiology, accessibility, and affordability. They serve as a key reference for dermatologists, pediatricians, and general practitioners in India and other resource-limited settings. Though tailored for India, they are also relevant to dermatologists in developing countries, guiding treatment selection based on disease patterns, environmental factors, and medication availability.

This review highlights the causes, types and clinical staging of hepatic encephalopathy (HE). Current concepts on the probable pathogenetic mechanisms and currently practiced therapeutic options are discussed. HE may be covert and overt. Also known as minimal HE. Covert HE, where there are behavioral abnormalities and impairment in activities of daily living with intact sensorium. The pathophysiology of HE remains poorly understood. There is disturbance of the urea cycle due to liver disease leading to increased production of ammonia. The ammonium ion enters the astrocytes along with glutamate (converted to glutamine by ammonia) and myo-inositol, thereby increasing the osmolality of the astrocytic cytoplasm. This osmotic gradient results in accumulation of water inside the astrocytes resulting in cerebral edema and increase in brain volume. Additionally, current research has noted the role of cerebral oxidative/nitrosative stress and the synergistic effects of increased cerebral ammonia and alteration in neurotransmitters, neurometabolites, and cortical excitability due to systemic inflammation. In advanced liver disease with systemic infection or inflammation, neuroinflammatory processes play significant role in the development of HE. Inflammatory cytokines like TNF-α, IL-6, IL-17 in presence of hyperammonemia have been found to induce neurotoxicity of ammonia by passing through the blood brain barrier and causing enlarged/swollen pale astrocytes, resulting in HE. Disrupted enterohepatic circulation in end stage liver disease also causes elevation of bile acids which induces neuroinflammation. Manganese and zinc play as co-factors of enzymatic reaction. These metal deposition causes multiple psychomotor symptoms observed in HE. The gut environment has a major impact on brain function in patients with HE. Toxins such as ammonia and inflammatory cytokines produced by this impaired intestinal flora access the circulation through porto-systemic anastomoses and exacerbate or precipitate HE. Finally, as a result of recurrent cerebral edema from astrocytic dysfunction and neuroinflammation, permanent neurodegeneration occurs with cognitive decline and motor disturbances, especially parkinsonian features and gait disturbances. This is the stage of chronic hepatic encephalopathy. Currently L-ornithine L-aspartate (LOLA) is being used to lower the ammonia level by stimulating the urea cycle. HE comprises a broad spectrum of neurological and/or psychiatric abnormalities caused by hepatic insufficiency and/or portal-systemic shunting in the absence of any other causes of brain dysfunction. HE may be caused or precipitated by several factors like infections, intoxications and drugs. The encephalopathic features may be covert or overt. The pathogenetic mechanisms for HE may be different. In the presence of liver disease, HE primarily results from disturbed urea cycle with hyperammonemia causing astrocytic swelling and cerebral edema. Porto-systemic anastomoses with intact liver function can cause HE by allowing ammonia and other toxins produced by the gut microbial flora and allowing these to bypass detoxification by the liver and exposing the brain to their harmful effects. Principles of therapy are twofold. First protecting the liver and the brain from gut generated ammonia and other toxins by ensuring smooth bowel function and avoiding stagnation with the use of osmotic laxatives like lactulose or lactitol and also reducing the gut microbial load with use of anti-bacterials/bacteriophages like neomycin and rifaximin along with metronidazole. Second, reducing the already generated cerebral edema by use of mannitol and appropriate ventilatory support. Currently L-ornithine L-aspartate (LOLA) is being used to reduce the ammonia load to the liver. LOLA is a stable compound formed from two amino acids. L-ornithine plays a crucial role in stimulating the urea cycle, leading to a reduction in ammonia levels. Both L-ornithine and L-aspartate serve as substrates for the enzyme glutamate transaminase, and their administration results in elevated glutamate concentrations. Ammonia is subsequently utilized in the conversion of glutamate to glutamine through the action of glutamine synthetase. Finally in resistant cases the use of liver transplant needs to be considered. Alternatively extracorporeal liver assist devices may be used like Molecular Adsorbent Recirculating System (MARS) or Single-Pass Albumin Dialysis (SPAD).

Definitive diagnosis of multiple sclerosis (MS) requires exclusion of other central nervous system (CNS) disorders sharing similar clinical, pathological and radiological features. In this review we discuss some relatively uncommon disorders with special emphasis on their differentiation from MS clinically and radiologically. While most conditions have a demyelinating pathology, a few very important mimics may have a non-demyelinating pathology to merit some discussion. Two major areas of diagnostic advances have been made in recent times, the recognition of neuromyelitis optica spectrum disorder (NMOSD), and the myelin oligodendrocyte antibody mediated disorder (MOGAD). These two entities are mediated by completely different antibodies detectable in peripheral blood samples by enzyme-linked immunosorbent assay (ELISA) or cell-based assays and produce clinical disorders could be differentiated from MS by their clinical features, disease course, prognosis, and imaging features. NMOSD is a rare CNS autoimmune disease that predominantly targets the spinal cord, optic nerves and brainstem. In sixty to eighty

Wilson disease (WD), an uncommon autosomal recessive (AR) hereditary disorder characterized by abnormal accumulation of copper primarily in the liver and secondarily in other organs like the brain, is caused by a deficiency in the ATP7B transporter gene. The key to successful therapy is early diagnosis. Mutant genes need to be inherited from both parents for phenotypic expression. The ATP7B gene located on chromosome 13q14.3 comprises 20 introns and 21 exons, encodes a protein of 165 amino acids, and this helps in incorporation of copper into ceruloplasmin, the copper binding protein. So far, more than 800 mutations have been reported, of which 380 have confirmed involvement in the pathogenesis of WD. The most common mutations are H1069Q and R778L in European and Asian populations respectively. Approximately 90

To synthesize evidence on the efficacy of osteoanabolic therapies (teriparatide, abaloparatide, romosozumab) in adults with type 2 diabetes mellitus (T2D), focusing on changes in bone mineral density (BMD) and fractures, and to explore whether responses differ between people with and without diabetes. Following PRISMA guidelines, we searched PubMed/MEDLINE, Embase and Scopus databases till April 30, 2025 (PROSPERO: CRD420251044760). Five studies met criteria (n = 1,469 with T2D; n = 12,052 without diabetes): two post hoc analyses of randomized controlled trials (RCTs) (ACTIVE and ARCH trials) and three observational studies. Using random-effects model, osteoanabolic therapy in T2D increased lumbar spine BMD by a mean difference (MD) of 5.06