Cardiac Amyloidosis Mimicking Non-ST-Segment Myocardial Infarction: A Case Report.

Cardiac amyloidosis is a rare but increasingly recognized condition characterized by the deposition of amyloid fibrils in cardiac tissue, leading to structural and functional heart impairment. This infiltrative cardiomyopathy often mimics more common cardiac conditions, posing significant diagnostic challenges. Particularly deceptive is its presentation as non-ST-segment elevation myocardial infarction (NSTEMI), where the clinical overlap necessitates considering amyloidosis in differential diagnoses. A 75-year-old male presented with muscle weakness, respiratory infection symptoms, and elevated cardiac enzymes. His history included a recent hospitalization for NSTEMI, with normal coronary angiography. Initial evaluations showed elevated troponin and CRP levels. A comprehensive cardiac assessment revealed a dilated ascending aorta, moderate systolic dysfunction (left ventricular ejection fraction (LV-EF), 47%), and asymmetrical interventricular septal thickening, suggesting hypertrophic cardiomyopathy or amyloidosis. The patient improved and was referred for further specialized care. Cardiac amyloidosis can mimic acute coronary syndrome (ACS), presenting with chest pain and elevated cardiac biomarkers. Differentiation is critical as amyloidosis involves myocardial infiltration by amyloid proteins, leading to restrictive cardiomyopathy. Advanced imaging techniques like cardiac MRI and nuclear scintigraphy are essential for accurate diagnosis and appropriate management, impacting therapeutic strategies and patient outcomes.

Diabetic nephropathy in type 1 diabetes.

Diabetic nephropathy (DN) also named diabetic kidney disease (DN) is one of the leading causes of mortality in people with diabetes. The aim of this review is to update the medical literature, the theories behind its early natural history, the pathways of its pathogenesis, its diagnosis and treatment. Poor glycemic control, hyperlipidemia, smoking, oxidative stress, accumulation of advanced glycated end products, environmental, genetic and epigenetic factors play an important role in the pathophysiological development of DN. Microalbuminuria has been traditionally used as the primary early diagnostic marker of microvascular complication unraveling the risk for progress to severe cardiorenal outcomes, but its prognostic role has been recently debated. The disease often leads to end-stage renal disease and it is often associated with major cardiovascular outcomes. Its early diagnosis is crucial for the patients in order to have a chance for proper treatment.

Increased Frequency of Peripheral B and T Cells Expressing Granulocyte Monocyte Colony-Stimulating Factor in Rheumatoid Arthritis Patients.

OBJECTIVES: Granulocyte monocyte colony-stimulating factor (GM-CSF) is currently considered a crucial inflammatory mediator and a novel therapeutic target in rheumatoid arthritis (RA), despite the fact that its precise cellular sources remain uncertain. We studied the expression of GM-CSF in peripheral lymphocytes from RA patients and its change with antirheumatic therapies. METHODS: Intracellular GM-CSF expression was assessed by flow cytometry in stimulated peripheral B (CD19+) and T (CD3+) cells from RA patients (n = 40), disease (n = 31 including osteoarthritis n = 15, psoriatic arthritis n = 10, and systemic rheumatic diseases n = 6) and healthy (n = 16) controls. The phenotype of GM-CSF+ B cells was assessed as well as longitudinal changes in GM-CSF+ lymphocytes during methotrexate (MTX, n = 10) or anti-tumor necrosis factor (anti-TNF, n = 10) therapy. RESULTS: Among untreated RA patients with active disease (Disease Activity Score 28-C-reactive protein = 5.6 ± 0.89) an expanded population of peripheral GM-CSF+ B (4.1 ± 2.2%) and T (3.4 ± 1.6%) cells was detected compared with both disease (1.7 ± 0.9%, p < 0.0001 and 1.7 ± 1.3%, p < 0.0001, respectively) and healthy (0.3 ± 0.2%, p < 0.0001 and 0.6 ± 0.6%, p < 0.0001) controls. RA GM-CSF+ B cells displayed more commonly a plasmablast or transitional phenotype (37.12 ± 18.34% vs. 14.26 ± 9.46%, p = 0.001 and 30.49 ± 15.04% vs. 2.45 ± 1.84%, p < 0.0001, respectively) and less a memory phenotype (21.46 ± 20.71% vs. 66.99 ± 16.63%, p < 0.0001) compared to GM-CSF- cells. GM-CSF expression in RA patients did not correlate to disease duration, activity or serological status. Anti-TNF treatment led to a statistically significant decrease in GM-CSF+ B and T cells while MTX had no significant effect. DISCUSSION: This is the first study showing an expanded population of GM-CSF+ B and T lymphocytes in patients with active RA which declined after anti-TNF therapy.