Catarina Santos Reis

Giant cell arteritis (GCA) is a chronic large-vessel vasculitis that may present with systemic, neurological or ophthalmological manifestations. Lingual and scalp ischaemia are rare but can have severe potential complications that pose a diagnostic challenge and require immediate treatment to prevent irreversible outcomes. We report the case of an 87-year-old woman who initially presented with holocranial headaches and tongue pain with partially detachable whitish plaques. She was diagnosed with GCA based on clinical features, elevated inflammatory markers and ultrasonographic findings of thickened temporal arteries. High-dose corticosteroid therapy was promptly initiated, leading to marked improvement of the reported symptoms. Nevertheless, on day 14 of hospitalisation, she developed septic shock from an abdominal source and subsequently died. This case reports an atypical presentation of GCA – lingual and scalp ischaemia – emphasising the need to maintain a high index of suspicion even before these non-classical manifestations. A holistic clinical approach is essential to identify the various possible manifestations of this complex disease. Although tongue and/or scalp necrosis are rare complications, treatment remains aligned with current GCA guidelines. Most patients respond to corticosteroid therapy, or tocilizumab in cases of steroid-refractory lingual necrosis; non-responders are typically associated with a poorer prognosis.

Epstein-Barr virus (EBV) typically causes a self-limiting disease characterized by fever, pharyngitis, and lymphadenopathy. Clinically overt renal and cardiac involvement is rare, and its presentation ranges from subclinical manifestations to severe organ dysfunction. In cases where renal biopsies have been performed, the most common pathology identified is interstitial nephritis. We report a case of a 24-year-old male with a history of recurrent tonsillitis - the most recent episode occurring one month prior - who presented to the Emergency Department with a three-day symptom of asthenia, diffuse abdominal pain, and vomiting. His blood tests showed acute kidney injury (AKI) and elevated natriuretic peptide levels, with negative troponin levels. Viral markers were consistent with primary EBV infection. Renal biopsy revealed moderate acute tubular necrosis, with no glomerular injury. Renal function showed signs of improvement within the initial three days following the initiation of fluid therapy. Given the high index of clinical suspicion, a cardiac MRI was performed, revealing myocarditis. This case underscores the potential for EBV to present with AKI and myocarditis, contributing valuable insights into the diverse clinical manifestations of EBV infection.

Background: The impact of systolic blood pressure (SBP) variation on chronic heart failure (HF) is largely unknown. We assessed the impact of SBP variation in patients with chronic HF. Methods: This is a retrospective analysis of adult ambulatory patients with HF with left ventricular systolic dysfunction (LVSD). SBP variation = SBP at the index visit – SBP at the 1-year visit. Patients dying in the first year or with missing data concerning SBP were excluded. Patients with SBP increase ≥10 mmHg during the first year were compared with the remaining. Determinants of SBP increase were assessed by binary logistic regression analysis. The patients were followed up from the 1-year visit up to 5 years. The primary end point was all-cause mortality. A Cox regression analysis was used to determine the association of SBP variation with mortality. Results: We studied 787 patients (68% male), with a mean age of 70 years. SBP increased by ≥10 mmHg in 277 patients (35.2%) and remained stable or decreased in 510. Patients in whom SBP increased more often presented severe LVSD and nonischemic HF; they had lower baseline SBP and were more medicated with loop diuretics. Independent predictors of SBP increase were lower basal SBP and loop diuretic use. Patients with a SBP increase ≥10 mmHg had a crude hazard ratio (HR) of all-cause mortality of 0.74 (0.59–0.94), and the multivariate-adjusted HR was 0.61 (0.46–0.79). Conclusions: Patients with chronic HF with SBP increase ≥10 mmHg over the first year have a 39% reduction in the all-cause mortality risk irrespective of basal SBP, severity of ventricular dysfunction, and evidence-based drug use. Patients with SBP stability or decrease have a similarly poor prognosis.