This report presents the case of a female patient diagnosed with Takayasu arteritis from childhood, with severe, refractory coronary involvement, leading to two acute coronary syndromes and multiple anginous episodes. Consequently, the patient suffered aorto-bicarotid bypass two times, multiple interventional procedures with stent implantation, balloon angioplasty, and up to ten repeated in-stent restenosis that required reinterventions, despite being on maximal immunosuppressive treatment. In recent years, various studies have been reported that aim to best characterize this particular type of vascular damage and to indicate optimal therapeutic options for treatment. The latter should be based on the activity of the underlying disease; however, no reliable markers are available in TA. The management of TA patients with coronary involvement continues to be a challenge and requires both drug and interventional techniques to avoid life-threatening events.

Although perceived as an adaptative immune disorder, mainly related to Lymphocyte B and T, last years focus on Systemic Lupus Erythematosus (SLE) pathogeny emphasised the important role of innate immunity. This should not take us by surprise since the lupus cell described by Hargraves and colleagues in 1948 was a neutrophil or macrophage with specific aspect after coloration with haematoxylin related to cell detritus engulfment (Hargraves et al., 1948) [1] (Presentation of two bone marrow elements; the tart. Hargraves M, Ricmond H, Morton R. 1948, Proc Staff Meet Mayo Clinic, pp. 23:25–28). Normal immune system maintains homeostasis through innate and adaptative response that are working together to prevent both infection and autoimmunity. Failure of the immune mechanisms to preserve the balance between these two will initiate and propagate autoinflammation and/or autoimmunity. It is well known now that autoinflammation and autoimmunity are the two extremes of different pathologic conditions marked with multiple overlaps in many diseases. Recent findings in SLE demonstrated that innate immune system initiates the abnormal autoimmunity and starts the continuous inflammatory reaction after that, interferon being one of the key cytokines in innate immunity and SLE. Understanding this mechanism might offer a better clue for an efficient treatment in SLE patients. The purpose of this review is to highlight the enormous impact of innate immunity and mostly interferons in SLE.

Giant cell arteritis (GCA) is a large-vessel vasculitis affecting elderly patients and targeting the aorta and its main branches, leading to cranial and extracranial manifestations. The mechanism behind the ischemia is a granulomatous-type inflammation with potentially critical lesions, including visual loss involving the ophthalmic artery. Despite significant progress in unraveling the pathophysiology of this disease, treatment options still rely on glucocorticoids (GCs) to overcome active vascular lesions and disease flares. However, uncertainty still revolves around the optimal dose and tapering rhythm. Few corticosteroid-sparing agents have proven useful in GCA, namely, methotrexate and tocilizumab, benefiting cumulative GC dose and relapse-free intervals. The future looks promising with regard to using other agents like abatacept and Janus-kinase inhibitors or blocking the granulocyte–macrophage colony-stimulating factor receptor.

Hemochromatosis is a genetic disorder characterized by increased iron storage in various organs with progressive multisystemic damage. Despite the reports dating back to 1865, the diagnosis of hemochromatosis poses a challenge to clinicians due to its non-specific symptoms and indolent course causing significant delay in disease recognition. The key organ that is affected by iron overload is the liver, suffering from fibrosis, cirrhosis or hepatocellular carcinoma, complications that can be prevented via early diagnosis and treatment. This review aims to draw attention to the pitfalls in diagnosing hemochromatosis. We present a case with multiorgan complaints, abnormal iron markers and a consistent genetic result. We then examine the relevant literature and discuss hemochromatosis subtypes and liver involvement, including transplant outcome and treatment options. In summary, hemochromatosis remains difficult to diagnose due to its symptom heterogeneity and rarity; thus, further education for practitioners of all disciplines is useful in facilitating its early recognition and management.

Patients with immune-mediated rheumatic disease-related calcinosis comprise a subgroup at risk of encountering a more severe clinical outcome. Early assessment is pivotal for preventing overall disease progression, as calcinosis is commonly overlooked until several years into the disease and is considered as a ‘non-lethal’ manifestation. This single-center retrospective study explored the prevalence, clinical associations, and impact on survival of subcutaneous calcinosis in 86 patients with immune-mediated rheumatic diseases (IMRD). Calcinosis predominantly appeared in individuals with longstanding disease, particularly systemic sclerosis (SSc), constituting 74% of cases. Smaller calcinosis lesions (≤1 cm) were associated with interstitial lung disease, musculoskeletal involvement, and digital ulcerations, while larger lesions (≥4 cm) were associated with malignancy, severe peripheral artery disease, and systemic arterial hypertension. The SSc calcinosis subgroup exhibited a higher mean adjusted European Scleroderma Study Group Activity Index score than those without. However, survival rates did not significantly differ between the two groups. Diltiazem was the most commonly used treatment, and while bisphosphonates reduced complications related to calcinosis, complete resolution was not achieved. The findings underscore current limitations in diagnosing, monitoring, and treating calcinosis, emphasizing the need for further research and improved therapeutic strategies to improve patient care and outcomes.

Systemic lupus erythematosus (SLE) is a multifaceted autoimmune disease with a heterogeneous organ involvement, for which reliable biomarkers are still being studied. The implication of advanced glycation end products (AGEs), resulting from oxidative stress, and their interaction with the receptor for AGEs (RAGE) has been studied in pathologies with chronic proinflammatory status, offering potential relevance in SLE. This systematic review aimed to evaluate the utility of skin autofluorescence (SAF)—a non-invasive proxy for AGE accumulation—as a biomarker for disease severity, activity, and impact in SLE patients. Following PRISMA guidelines, six studies assessing SAF and/or circulating AGEs and soluble RAGE (sRAGE) in SLE were analyzed. Findings consistently showed higher AGE levels in SLE patients compared to healthy controls, with several correlations between SAF/AGEs and disease features such as SLEDAI scores, organ involvement, inflammatory markers, and damage indices. Decreased sRAGE levels were also observed, possibly due to consumption by AGEs. Some studies further reported predictive associations between specific AGEs or their ratios with sRAGE and particular clinical phenotypes. Although heterogeneity among studies limits definitive conclusions, the AGEs–sRAGE axis—and especially SAF—emerges as a promising candidate for future biomarker development in SLE. Further large-scale longitudinal studies are needed to confirm its clinical utility.