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INTRODUCTION: Early detection of type 2 diabetes mellitus (T2DM) is imperative to prevent the complications associated with the disease. Current guidelines for diagnosis rely on the assessment of serum glucose (fasting and post-prandial) and glycosylated hemoglobin (HbA1c) levels. Insulin resistance, a phenomenon associated with T2DM, has been observed before the changes in these metrics. The homeostatic model assessment for insulin resistance (HOMA-IR) has been widely used to assess the degree of insulin resistance. The triglyceride-fasting glucose (TyG) index is a newer marker of insulin resistance that merits further study. Aim: The study aimed to assess the validity of the TyG index and HOMA-IR as markers for the development of T2DM in non-obese individuals. Materials and methods: One hundred eight non-obese patients without T2DM were included in this prospective cohort study and followed up for eight years. Anthropometric and biochemical parameters, including fasting glucose levels, HbA1c, fasting serum insulin, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TG), were measured at enrolment and eight years follow-up, and HOMA-IR and TyG index were calculated. Results: Twenty participants out of 108 (18.5%) developed T2DM over eight years. On performing the area under the curve (AUC)-receiver operating characteristic curve analysis, TyG of >8.61 and HOMA-IR of >1.5 had the highest validity (ability) to predict new-onset T2DM in the study population (TyG: AUC: 0.612 (95% CI: 0.514-0.705); HOMA-IR: AUC: 0.529 (95% CI: 0.431-0.626)); however, this was not statistically significant. Conclusion: At an eight-year follow-up, TyG and HOMA-IR were unreliable predictors of the development of T2DM in non-obese individuals.
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Vector-borne microbial diseases are ubiquitous, and their management remains elusive. Such diseases with zoonotic potential result in public health challenges requiring additional control and preventive measures. Despite their cosmopolitan presence, vector-borne infections are neglected due to their endemicity in specified geographical regions. The Kyasanur forest disease (KFD) caused by the Kyasanur forest disease virus (KFDV) is among such diseases transmitted through ticks and localized to India. Despite its prevalence, high transmissibility, and potential to cause fatalities, KFDV has not been given the deserved attention by the governments. Further, KFDV circulates in the rural and wild geographical areas threatening infections to people living in these areas with limited access to medical and healthcare. Therefore, physicians, healthcare workers, and the general population need to understand the KFDV and its ecology, epidemiology, transmission, pathogenesis, laboratory diagnosis, and control and prevention as described comprehensively in this review.
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Currently, there is unavailability of disease-modifying medication for Alzheimer's disease (AD), a debilitating neurological disorder. The pathogenesis of AD appears to be complex and could be influenced by the glymphatic system present in the central nervous system (CNS). Amyloid-beta (Aß) and other metabolic wastes are eliminated from the brain interstitium by the glymphatic system, which encompasses perivascular channels and astroglial cells. Dysfunction of the glymphatic system, which could occur due to decreased aquaporin 4 (AQP4) expression, aging-related alterations in the human brain, and sleep disruptions, may contribute to the pathogenesis of AD and also accelerate the development of AD by causing a buildup of harmful proteins like Aß. Promising approaches have been examined for reducing AD pathology, including non-pharmacological therapies that target glymphatic function, like exercise and sleep regulation. In addition, preclinical research has also demonstrated the therapeutic potential of pharmaceutical approaches targeted at augmenting AQP4-mediated glymphatic flow. To identify the precise processes driving glymphatic dysfunction in AD and to find new treatment targets, more research is required. Innovative diagnostic and treatment approaches for AD could be made possible by techniques such as dynamic contrast-enhanced MRI, which promises to evaluate glymphatic function in neurodegenerative diseases. Treatment options for AD and other neurodegenerative diseases may be improved by comprehending and utilizing the glymphatic system's function in preserving brain homeostasis and targeting the mechanisms involved in glymphatic functioning. This review intends to enhance the understanding of the complex link between AD and the glymphatic system and focuses on the function of AQP4 channels in promoting waste clearance and fluid exchange.
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Neglected tropical diseases (NTDs) are a group of diseases caused by diverse organisms, affecting millions of people in tropical and subtropical conditions. NTDs are more prevalent among people who live in poverty, without access to clean water, adequate sanitation, and quality health care. Most NTDs are chronic conditions and are potentially disablers than killers, leaving behind a trail of social consequences. Controlling NTDs has become complicated due to limited resources and are frequently ignored by global funding agencies. India experiences a significant burden of global NTDs. The paradox is that NTDs are preventable and treatable at an affordable cost. It then makes no sense as to why we co-exist with such diseases. The World Health Organization (WHO) has donned the leadership role of eliminating, eradicating, and controlling global NTDs. The WHO published a roadmap delineating a plan of action, which was being reviewed periodically. This led to substantive progress in tackling the NTDs. However, many challenges still exist to controlling and preventing NTDs. India has achieved significant progress towards NTD control and elimination by implementing the WHO strategies and action plans. This was evident by an increase in research and funding in this direction. The number of new drugs, vaccines, and investigative tools available and those in the pipeline is testimony to their efforts. Focusing singly on India's NTD problem would substantially reduce the burden of poverty-related neglected diseases and could dramatically advance the global health agenda. This review highlights the problem of NTDs in the Indian and global perspective.
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Allergy and immunological disorders like autoimmune diseases are vastly prevalent worldwide. These conditions account for a substantial amount of personal and social burden. Such illnesses have lengthy, uncertain, and spotted courses with unpredictable exacerbations. A definite tendency for improving the overall quality of life of individuals suffering from such diseases is crucial to tackling these diseases, especially through diet or lifestyle modification. Further, interventions like microbiome-based therapeutics such as prebiotics or probiotics were explored. Changes in the microbial population were evident during the flare-up of autoimmune and allergic conditions. The realization that the human microbiome is a central player in immunological diseases is a hallmark of its potential usefulness in therapy for such illnesses. This review focuses on the intricate symphony in the orchestra of the human microbiome and the immune system. New therapeutic strategies involving probiotics appear to be the future of personalized medicine. Through this review, we explore the narrative of probiotics and reaffirm their use as therapeutic and preventive agents in immunological disorders.
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Leprosy is a chronic infectious disease caused by Mycobacterium leprae, which primarily affects the skin and peripheral nerves. The variants that can be identified include tuberculoid (TT), borderline tuberculoid (BT), mid-borderline (BB), borderline lepromatous (BL), and lepromatous forms (LL). Type one lepra reactions are delayed hypersensitivity reactions that are often observed in borderline variants due to an unstable immunological response. They can exacerbate skin lesions and neuritis, leading to a higher risk of disabilities and deformities. Early detection and management would play a major role in limiting morbidity. Here, we present a case of a 46-year-old male diagnosed with borderline tuberculoid leprosy on multidrug therapy who developed features suggestive of type one lepra reaction. Early recognition of this entity helps in mitigating the risk of permanent nerve damage, disability, deformity, and morbidity.
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This case report presents a unique case of a 15-year-old male with post-streptococcal glomerulonephritis (PSGN) who developed posterior reversible encephalopathy syndrome (PRES). The patient presented with symptoms of fever, headache, emesis, visual disturbances, and involuntary movements of all four limbs. On examination, the patient had elevated blood pressure, decreased visual acuity of the left eye, leukocytosis, and uremia. MRI findings showed symmetrical enhancement of superficial and deep watershed areas, predominantly in the occipital and temporal regions. Treatment with antibiotics and anti-hypertensives resulted in the complete resolution of hyperintense lesions seen in brain MRI after three weeks, and the patient remained symptom-free for one month. This case highlights the rare association between PSGN and PRES and emphasizes the importance of monitoring and managing hypertension in patients with PSGN. Understanding the association between these two conditions may lead to earlier diagnosis and treatment of PRES, ultimately improving patient outcomes.
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Tubercular meningitis is a rare yet devastating type of extrapulmonary tuberculosis (TB) posing great diagnostic challenges due to the nonspecific clinical presentation of the patients. Here, we present a rare diagnosis of hypertrophic pachymeningitis due to Mycobacterium tuberculosis. A 36-year-old male presented with a history of headaches and giddiness for one month. Neurological examination revealed hypo-reflexive triceps and ankle reflexes. Routine blood tests and autoimmune workup were normal. Brain MRI with contrast revealed diffuse dural thickening, focal leptomeningeal enhancement in the right temporal sulci, and enhancement in both the frontal and parietal convexity and the falx cerebri and along the tentorium cerebelli. Cerebrospinal fluid (CSF) analysis revealed elevated proteins, suggestive of aseptic meningitis. Meningeal biopsy revealed a chronic ill-formed granulomatous inflammatory lesion with occasional acid-fast bacilli, consistent with tubercular pachymeningitis. The patient was administered intravenous (IV) methylprednisolone for five days, following which the symptoms subsided. He was advised tablet prednisolone on discharge, and immunomodulation with rituximab was recommended as outpatient treatment. Hypertrophic pachymeningitis is a rare diagnosis characterized by the inflammation and fibrosis of the dura matter due to a diverse etiology. Tubercular etiology must be considered when the routine laboratory tests are negative, and the diagnosis should be confirmed by meningeal biopsy. The treatment of the underlying cause and corticosteroids remain the mainstay management of hypertrophic pachymeningitis. Hence, mycobacterial tuberculosis should be considered as a possible differential diagnosis while evaluating hypertrophic pachymeningitis, especially when the routine laboratory tests and immunological workup are negative.
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Gitelman syndrome (GS) is a rare renal tubulopathy, classically characterized by renal salt wasting and metabolic alkalosis. It is usually an incidental diagnosis, being asymptomatic or with mild symptoms. GS manifesting with acute flaccid paralysis is extremely uncommon. We report a case of GS that mimicked Guillain-Barré syndrome (GBS), manifesting with acute hypokalemic paralysis. A middle-aged male with no known comorbidities presented to our center with paresthesias of all four limbs for one month and progressive, asymmetric limb weakness over the past eight days. Neurological examination revealed hypotonia, global areflexia, and power ranging from 3/5 to 4/5 in all four limbs, leading to our initial clinical diagnosis of GBS. Our patient's laboratory panel revealed hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalcemia, characteristic of GS. Additionally, he had significantly elevated creatine phosphokinase, suggestive of rhabdomyolysis. Further urine studies revealed renal potassium wasting, confirming the diagnosis of GS. Whole exome genome sequencing for common causative genes and workup for autoimmune disease were both negative. With gradual electrolyte correction, the patient rapidly improved symptomatically. Our case highlights an uncommon initial presentation of GS and emphasizes the need for more literature on its manifestations from the Indian subcontinent.
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Mitochondrial DNA (mtDNA) is a small, circular, double-stranded DNA inherited from the mother during fertilization. Evolutionary evidence supported by the endosymbiotic theory identifies mitochondria as an organelle that could have descended from prokaryotes. This may be the reason for the independent function and inheritance pattern shown by mtDNA. The unstable nature of mtDNA due to the lack of protective histones, and effective repair systems make it more vulnerable to mutations. The mtDNA and its mutations could be maternally inherited thereby predisposing the offspring to various cancers like breast and ovarian cancers among others. Although mitochondria are considered heteroplasmic wherein variations among the multiple mtDNA genomes are noticed, mothers can have mitochondrial populations that are homoplasmic for a given mitochondrial mutation. Homoplasmic mitochondrial mutations may be transmitted to all maternal offspring. However, due to the complex interplay between the mitochondrial and nuclear genomes, it is often difficult to predict disease outcomes, even with homoplasmic mitochondrial populations. Heteroplasmic mtDNA mutations can be maternally inherited, but the proportion of mutated alleles differs markedly between offspring within one generation. This led to the genetic bottleneck hypothesis, explaining the rapid changes in allele frequency witnessed during the transmission of mtDNA from one generation to the next. Although a physical reduction in mtDNA has been demonstrated in several species, a comprehensive understanding of the molecular mechanisms is yet to be demonstrated. Despite initially thought to be limited to the germline, there is evidence that blockages exist in different cell types during development, perhaps explaining why different tissues in the same organism contain different levels of mutated mtDNA. In this review, we comprehensively discuss the potential mechanisms through which mtDNA undergoes mutations and the maternal mode of transmission that contributes to the development of tumors, especially breast and ovarian cancers.
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This article discusses the interplay between the gut-brain axis and stroke, a multifaceted neurological disorder that affects millions of people worldwide. The gut-brain axis is a bidirectional communication network linking the central nervous system (CNS) to the gastrointestinal tract (GIT), including the enteric nervous system (ENS), vagus nerve, and gut microbiota. Dysbiosis in the gut microbiota, alterations in the ENS and vagus nerve, and gut motility changes have been linked to increased inflammation and oxidative stress, which are contributing factors in the development and progression of stroke. Research on animals has shown that modifying the gut microbiota can impact the results of a stroke. Germ-free mice displayed improved neurological function and decreased infarct volumes, indicating a positive effect. Furthermore, studies in stroke patients have shown alterations in the gut microbiota composition, indicating that targeting dysbiosis could be a potential therapeutic strategy for stroke. The review suggests that targeting the gut-brain axis may represent a potential therapeutic approach to reduce the morbidity and mortality associated with stroke.
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Influenza A virus (IAV), particularly the H3N2 variant, is known to cause respiratory manifestations, but it can also lead to neurological complications ranging from mild symptoms like headache and dizziness to severe conditions such as encephalitis and acute necrotizing encephalopathy (ANE). In this article, the correlation between the H3N2 variant of the IAV and neurological manifestations is discussed. Additionally, prompt recognition and treatment of influenza-associated neurological manifestations are highlighted to prevent infection-related long-term complications. This review briefly discusses various neurological complications linked to IAV infections, such as encephalitis, febrile convulsions, and acute disseminated encephalomyelitis, and the potential mechanisms involved in the development of neurological complications.
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Focal segmental glomerulosclerosis (FSGS) is a common cause of nephrotic syndrome (NS) and one of the leading causes of end-stage kidney disease. Endocrinological abnormalities due to the urinary loss of hormone-binding proteins, such as transient hypothyroidism, are well documented in FSGS. Secondary FSGS can arise due to viral infections, drugs, and pre-existing glomerular diseases. Few reports have highlighted the occurrence of FSGS in the background of hypothyroidism. We present a case of a young male with primary hypothyroidism who developed the tip variant of FSGS. A combination of oral corticosteroids and angiotensin-converting enzyme (ACE) inhibitors was successful in causing remission of the FSGS with no relapse.
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Antiphospholipid syndrome (APS) is a rare autoimmune disorder characterized by thromboembolic events, fetal loss during pregnancy, and evidence of antiphospholipid (aPL) antibodies such as beta-2-glycoprotein I (B2-GPI) and anticardiolipin (aCL). The diagnosis and treatment of this condition in the pediatric population have limited literature evidence due to the rarity of the condition in this age group. Guidelines have been adopted from the adult counterpart of the affected population, thereby giving rise to diagnostic and therapeutic challenges. In this report, we describe a rare case of a 15-year-old male who presented with lepromatous leprosy and developed deep vein thrombosis in his right leg. The laboratory evidence of positive aPL antibodies guided our diagnosis of APS and treatment with oral anticoagulants. This report highlights the importance of screening and timely diagnosis of APS in the pediatric population presenting with venous thrombosis in the backdrop of infection.
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Hemosuccus pancreaticus (HP) is a rare cause of upper gastrointestinal bleeding caused by bleeding from the ampulla of Vater into the duodenum. HP most commonly results from a rupture of pseudoaneurysms secondary to chronic pancreatitis. The low incidence of HP and the wide spectrum of its clinical presentation poses diagnostic challenges. We present a case of a 39-year-old male with acute-on-chronic pancreatitis resulting in HP and obstructive jaundice due to pancreatic pseudocyst with secondary hematoma. This case highlights the rare occurrence of hypovolemic shock due to massive hemorrhage in HP and the successful management with prompt cardiovascular support and angiographic coil embolization of a bleeding pancreatic pseudoaneurysm.
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Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease, with the skin being the second most affected organ after the joints. We present a unique case of a 44-year-old female who presented with an acute flare of SLE and the concurrent onset of keratoderma on both lower limbs. She presented with high-grade fever, arthralgia, and generalized edema of four months duration. A general physical examination revealed pallor and scaly hyperpigmented plaques on both lower limbs, which was confirmed to be keratoderma on histopathological examination. Blood investigations revealed pancytopenia, elevated erythrocyte sedimentation rate (ESR) and C- reactive protein (CRP), and positive titers for anti-nuclear antibody (ANA) and anti-Po ribosomal P proteins (RPP) antibodies. Immunosuppressive medications and topical keratolytics were used to treat her successfully. Post medical management, she showed significant improvement in her symptoms. On follow-up, the patient had a complete resolution of the symptoms and remained well. This case demonstrates keratoderma as a rare incidental finding in a patient with SLE flare. Understanding SLE's various cutaneous manifestations are critical for holistically diagnosing and treating the disease.
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Diabetes mellitus (DM) is a chronic metabolic disease characterized by inappropriately elevated blood glucose levels. If not treated at the early stage, it can lead to complications like diabetic retinopathy (DR) and diabetic nephropathy (DN) which are often associated with severe morbidity and mortality. This study was designed to identify the prevalence of retinopathy and nephropathy in diabetic patients and also to determine the correlation between DR and DN. In this cross-sectional study, a total of 84 diabetic patients (Male: Female- 53:31) were included. The mean age at presentation was 54.06 ± 9.85 years. Among them, 28% of patients had a duration of diabetes of < 5 years. Nearly 42% and 30% of patients had diabetes between 5-10 years, and more than 10 years respectively. At the time of presentation to us, a total of 42.8% of patients had a combination of nephropathy and retinopathy, 40.4% of patients had only retinopathy, and 16.6% of patients with only nephropathy. Among patients with nephropathy and microalbuminuria, only 5.9% had DR ranging from mild to a moderate degree and none had severe DR. In patients with macroalbuminuria, 26.2% had moderate to severe DR. Microvascular complications are more prevalent in diabetics with disease progression. Microalbuminuria is a marker for retinopathy and these patients require ophthalmic evaluation at the earliest. Early recognition and management of these, can reduce the occurrence of complications as well as disease progression, thus reducing the related mortality.
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Introduction Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis and is the second leading infectious cause of death worldwide. The higher prevalence of pulmonary TB in patients with type 2 diabetes mellitus (T2DM) is a well-known fact. The inverse relationship is also being increasingly recognized. Very few studies are available on the correlation of glycemic parameters with grades of sputum acid-fast bacilli (AFB) positivity and disease severity. Hence, this study is undertaken to determine the prevalence of impaired glucose tolerance (IGT), new-onset T2DM, and to correlate glycemic parameters with sputum positivity grades in pulmonary TB patients. Methods The is a cross-sectional study that included 93 patients with confirmed pulmonary TB, who presented to the General Medicine and Pulmonary Medicine departments of a tertiary care teaching hospital in southern India. All the patients included in the study underwent oral glucose tolerance (OGTT; 75 g) and glycated hemoglobin (HbA1c) tests. The results were analyzed and interpreted using statistical applications (SPSS software version 21, IBM Corp., Armonk, NY). Results Among the 93 patients included in the study, 73 (78.4%) were males and the mean age was 42.5+1.5 years. The OGTT revealed abnormal results in 44 (47.3%) patients. Thirteen (14%) patients showed IGT and 31 (33.3%) had newly been detected with T2DM. The mean HbA1C of the study participants was noted to be 6.413%. Conclusion The prevalence of IGT and T2DM among pulmonary TB patients was noted to be 14% and 33.3%, respectively. The grade of sputum positivity and the severity of the disease did not correlate with the serum of HbA1c levels.