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INTRODUCTION: Diabetic foot ulcers (DFUs) are a common complication of diabetes that affects patients' quality and prognosis of life. The study aims to assess the correlation between fibrinogen and glycated hemoglobin (HbA1c) in DFUs at the first and sixth months and to compare fibrinogen levels with Wagner classification in DFU patients. METHODS: This observational study was conducted at SRM Medical College Hospital and Research Centre from January 2021 to July 2022. Fifty diabetes patients with DFUs were selected, and informed consent was obtained before the study started. Blood samples were collected from all the participants for HbA1C, serum fibrinogen, hemoglobin, and white blood cells. In this study, data were entered into MS Excel (Microsoft Corporation, Redmond, WA) and analyzed using SPSS version 24 (IBM Corp., Armonk, NY). ANOVA and Pearson's correlation were used to examine the relationships between serum fibrinogen levels and clinical parameters. RESULTS: Among 50 patients, the females were 16 (32%), and the males were 34 (68%). Most patients (34%) were in the 56-60 age group. Twenty patients had diabetes for 10 years, and 24 were diabetic for 11-15 years. The ankle-brachial index (ABI score) was mild in 14 patients (28%), moderate in 28 patients (56%), and normal in eight patients (16%). There is a significant difference in comparison between the Wagner classification and ABI. A significant difference was observed in fibrinogen at the first and sixth months between HbA1c first, third, and sixth months. Significant differences were also observed in fibrinogen and ABI in the first and sixth months. CONCLUSION: Key findings include significant differences between fibrinogen and HbA1c levels (p < 0.0001) and a strong association between fibrinogen levels and ABI scores (p < 0.0001), underscoring fibrinogen's potential as an early marker for glycemic control and peripheral arterial disease in DFU patients. We concluded that simple fibrinogen estimation helps predict glycemic control in diabetic patients with DFUs.
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INTRODUCTION: Diabetes mellitus type 2 (T2DM) is a metabolic disorder, and its prevalence is rising worldwide. The objective of the study was to investigate the association between mean platelet volume (MPV) and red cell distribution width (RDW) and the glycemic control marker HbA1c. So MPV and RDW could be used as prognostic indicators of deterioration of gluco-regulation in diabetes mellitus type 2 and the associated microvascular complications. METHODOLOGY: A cross-sectional study was conducted on 216 type 2 diabetic patients, who were divided into two groups based on HbA1c values (<7% and >7%). Red blood cell distribution width, mean platelet volume, plasma glucose estimation, fasting lipid profile, spot urine albumin creatinine ratio (ACR), direct ophthalmoscopic examination, and nerve conduction study were tested in all the patients. RESULTS: Of the 216 individuals diagnosed with type 2 diabetes mellitus, 210 exhibited inadequate glycemic control, establishing a statistically significant correlation with triglyceride levels, mean platelet volume, and blood sugar levels. The study revealed a significant association between MPV and RDW and HbA1c levels. Additionally, microvascular complications such as retinopathy, proteinuria, and neuropathy exhibited strong correlations in this patient cohort, emphasizing the interconnectedness of glycemic control and various health indicators in individuals with T2DM. CONCLUSION: This study provides significant results that mean platelet volume and red cell distribution can be used as markers in the diagnosis of microvascular complications in type 2 diabetes mellitus.
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Introduction Acute myocardial infarction (AMI) is frequently preceded by arrhythmias, which continue to be a prominent cause of abrupt fatality in AMI. Abnormal magnesium levels have been linked to the emergence of arrhythmia because it enhances myocardial metabolism and cardiac output and prevents calcium buildup and myocardial cell death by lowering arrhythmias. The objectives of this study were to evaluate serum magnesium levels and QTc interval as prognostic indicators in AMI patients during the initial 48 hours of hospital stay and to correlate these parameters with the Global Registry of Acute Coronary Events (GRACE) scoring. We studied AMI patients by dividing them into two groups: those with abnormal and those with normal serum magnesium levels. Methods After obtaining ethical approvals, patients were subjected to detailed history, which included sociodemographic details, drug history, clinical examination, and investigations such as creatine kinase myocardial band (CK-MB), CK-total, troponin-T, ECG (QTc interval), two-dimensional echocardiogram (2D-ECHO), serum creatinine and magnesium levels, heart rate, and blood pressure. We also calculated the GRACE score for all patients. Results We found that patients in the age group of 51-60 years were more prone to developing arrhythmias, and while AMI was more prevalent in males, the occurrence of arrhythmias was slightly higher in females with AMI. Anterior wall motion abnormality (AWMA) was the most predominant abnormality, and 12.3% of AWMA patients had arrhythmias. QTc interval was significantly longer in patients who developed arrhythmias. Interestingly, among patients with QTc prolongation, 35% patients had abnormal magnesium levels, while 65% had normal magnesium levels. In our study, of the 25 patients with hypermagnesemia, nine (36%) developed arrhythmias, while of the 75 patients with hypomagnesemia, 15 (20%) patients developed arrhythmias. Interestingly, we found that there was a positive correlation between GRACE score and serum magnesium as well as QTc interval prolongation. Lastly, among the six deaths reported, three (50%) patients had arrhythmias. Conclusion Overall, we conclude that serum magnesium levels play a pivotal role as a prognostic tool for arrhythmias and are a useful investigation during the initial 48 hours of admission in AMI patients.
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Antiphospholipid syndrome (APS) is an autoimmune disease that primarily affects young adults. It is characterized by the development of antiphospholipid antibodies (APL) and a wide range of macro- and microvascular symptoms. The primary causes of morbidity and mortality in APS are cardiovascular events. Subclinical atherosclerosis and cardiovascular events are associated with high-risk APL profiles, particularly with the presence of lupus anticoagulant and triple APL positivity (all three APL subtypes), co-existence with systemic lupus erythematosus (SLE), and traditional risk factors like smoking, hypertension, obesity, and hyperlipemia. We present a case series involving three female stroke patients with APS. This series highlights the importance of immunological profiles in all stroke patients.
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Chronic kidney disease (CKD) is a progressive and long-term condition marked by a gradual decline in kidney function. CKD is prevalent among those with conditions such as diabetes mellitus, hypertension, and glomerulonephritis. Affecting over 10% of the global population, CKD stands as a significant cause of morbidity and mortality. Despite substantial advances in understanding CKD pathophysiology and management, there is still a need to explore novel mechanisms and potential therapeutic targets. Urotensin II (UII), a potent vasoactive peptide, has garnered attention for its possible role in the development and progression of CKD. The UII system consists of endogenous ligands UII and UII-related peptide (URP) and their receptor, UT. URP pathophysiology is understudied, but alterations in tissue expression levels of UII and UT and blood or urinary UII concentrations have been linked to cardiovascular and kidney dysfunctions, including systemic hypertension, chronic heart failure, glomerulonephritis, and diabetes. UII gene polymorphisms are associated with increased risk of diabetes. Pharmacological inhibition or genetic ablation of UT mitigated kidney and cardiovascular disease in rodents, making the UII system a potential target for slowing CKD progression. However, a deeper understanding of the UII system's cellular mechanisms in renal and extrarenal organs is essential for comprehending its role in CKD pathophysiology. This review explores the evolving connections between the UII system and CKD, addressing potential mechanisms, therapeutic implications, controversies, and unexplored concepts.