Giant cell myocarditis (GCM) is a rare but devastating inflammatory cardiac disease characterized by rapid hemodynamic deterioration, malignant arrhythmias, and high rates of death or heart transplantation. Without immunosuppressive treatment, median transplant-free survival is approximately three months. Current evidence identifies GCM as a predominantly T cell-mediated autoimmune disorder driven by a breakdown of immune tolerance, with contributions from macrophage-derived multinucleated giant cells and neutrophil extracellular trap formation. Viral infections and environmental factors have been implicated as potential triggers. GCM typically affects middle-aged adults, with concomitant non-cardiac autoimmune diseases present in approximately 20% of cases. Early diagnosis remains challenging, as clinical presentation and imaging findings are nonspecific and overlap considerably with cardiac sarcoidosis. Endomyocardial biopsy continues to represent the diagnostic gold standard, with a sensitivity of 85%, while cardiac biomarkers including cardiac troponins and NT-proBNP provide important prognostic information. Cardiac magnetic resonance imaging and FDG-PET contribute to the diagnostic workup but cannot reliably differentiate GCM from cardiac sarcoidosis. Management requires prompt initiation of combination immunosuppressive therapy-typically corticosteroids combined with T cell-targeted agents such as cyclosporine and azathioprine or tacrolimus and mycophenolate mofetil, which has substantially improved survival in contemporary registries. Mechanical circulatory support and heart transplantation are frequently required for refractory cases. Given the high arrhythmic burden, systematic evaluation for implantable cardioverter-defibrillator placement is recommended. This review provides a comprehensive overview of the pathogenesis, diagnosis, and current management of GCM and highlights priorities for future research, including noninvasive diagnostic tools and standardized treatment protocols.

ABO-incompatible (ABOi) living donor kidney transplantation (LDKTx) has become an established strategy for overcoming blood group barriers and expanding access to transplantation. However, its implementation remains limited in many developing countries because of the complexity and cost associated with desensitization protocols. We report the first ABO-incompatible LDKTx performed in Morocco. A 23-year-old woman with end-stage kidney disease secondary to congenital uropathy underwent kidney transplantation from her mother despite ABO incompatibility (donor B+, recipient O+). Pre-transplant immunological assessment revealed the absence of anti-HLA antibodies and a negative complement-dependent cytotoxicity crossmatch. Baseline anti-B isoagglutinin titers were 1:64 for IgG and 1:32 for IgM. The desensitization protocol consisted of rituximab administration (500 mg) on day -30, followed by the initiation of tacrolimus, mycophenolate mofetil, and corticosteroids on day-15. Three plasma exchange and one immunoadsorption sessions were subsequently performed before transplantation. No intravenous immunoglobulins were administered. Prior to transplantation, IgM titers became undetectable, while IgG titers decreased to 1:4. There was immediate graft function and no perioperative complications. During one year of follow-up, no episodes of rejection, infectious complications, or graft dysfunction were observed. At one year, i) serum creatinine remained stable at approximately 100 µmol/L, and ii) anti-B isoagglutinin titers remained low (IgG titers of 1:2; undetectable IgM titers). This first Moroccan experience demonstrates that ABO-incompatible LDKTx is both feasible and safe in our setting, using a simplified desensitization protocol without intravenous immunoglobulins. We have recently performed a successful second ABOi case with the same protocol.

Visceral disseminated varicella-zoster virus infection (VD-VZV) is a rare but life-threatening condition, and treatment-response monitoring has not yet been established. We report a case of a 47-year-old woman with systemic lupus erythematosus who developed primary varicella complicated by VD-VZV during prednisolone and mycophenolate mofetil therapy. She presented with a generalized vesicular rash, dyspnea, severe epigastric pain, pneumonia, and acute hepatitis with negative VZV IgM/IgG. Intravenous acyclovir was initiated and escalated, resulting in a clinical improvement. Serum VZV DNA quantified by droplet digital PCR peaked on day 4 (3.1×106 copies/mL) and declined with recovery, suggesting that serial serum VZV DNA monitoring may be useful for assessing the disease activity and treatment response in such patients.

Silage, particularly corn silage, represents one of the major routes of mycotoxin exposure in dairy production systems due to the widespread occurrence of metabolites originating from both field and storage fungi. Although ensiling is intended to preserve forage through anaerobic fermentation, microbiological and biochemical processes occurring before and after harvest and during ensiling, storage, and feed-out, may favor fungal proliferation and mycotoxin accumulation. Consequently, silage should be regarded as a dynamic microbial ecosystem in which regulated and emerging mycotoxins frequently co-occur in complex mixtures. Traditionally, research and regulatory frameworks have focused on a limited group of regulated mycotoxins, including aflatoxins, fumonisins, zearalenone, ochratoxin A, and trichothecenes such as deoxynivalenol and T-2 toxin. However, recent advances in multi-analyte analytical technologies, particularly high-resolution mass spectrometry, have revealed that silage matrices contain a much broader diversity of fungal metabolites than previously recognized, including emerging mycotoxins produced by Fusarium spp. (e.g., enniatins, beauvericin, moniliformin, and fusaric acid) and Penicillium spp. (e.g., mycophenolic acid and roquefortines). This review provides an updated perspective on regulated and emerging mycotoxins in silage-based dairy systems, with emphasis on contamination dynamics along the silage production chain, ecological interactions between fungi and fermentation processes, and current analytical approaches for multi-mycotoxin detection. The review also discusses recent studies questioning the scientific basis of current European Union and US Food and Drug Administration standards for aflatoxin M1 in milk, as well as their broader implications for food security, dairy trade, and milk consumption. Finally, mitigation strategies during ensiling and storage are discussed, highlighting key knowledge gaps and future research priorities for improving feed safety in dairy production systems.

ACCESS is a prospective, multicenter phase II trial evaluating peripheral blood stem cell (PBSC) transplantation using 4-7/8 HLA-mismatched unrelated donors (MMUD) with post-transplant cyclophosphamide (PTCy), tacrolimus, and mycophenolate. Adults undergoing first HCT with myeloablative (MAC) or reduced-intensity/nonmyeloablative (RIC/NMA) conditioning were enrolled, with donors aged 18-35 years and matched at 4/8-7/8 HLA loci by high-resolution typing. This expanded analysis includes all enrolled adult PBSC recipients, including the protocol-specified RIC/NMA cohort expansion, to improve precision of outcome estimates and provide descriptive analyses by HLA match level. Among 268 adults, 183 received 7/8 and 85 received <7/8 MMUD grafts; 82.4% of the <7/8 cohort received 6/8 grafts. Median follow-up among survivors was 11.9 months. At 1-year, overall survival was 78.6% (95% CI, 71.9-83.9) in the 7/8 cohort and 85.6% (95% CI, 76.0-91.5) in the <7/8 cohort. One-year relapse, non-relapse mortality, and GVHD-free relapse-free survival were 17.1%, 13.7%, and 51.1% versus 22.8%, 8.4%, and 54.6%, respectively. The cumulative incidence of grade II-IV and grade III-IV acute GVHD by day 100 was 36.6% and 7.7% in the 7/8 cohort versus 28.3% and 5.9% in the <7/8 cohort. Moderate-to-severe chronic GVHD at 1 year was 11.3% versus 7.7%, respectively. Among adult ACCESS recipients treated on a uniform young-donor PBSC/PTCy platform, short-term outcomes with predominantly 6/8 MMUD transplantation were encouraging. Because donor match level was not prospectively assigned and between-group comparisons were exploratory, these findings are descriptive and should not be interpreted as establishing equivalence with 7/8 MMUD transplantation. (Registered as NCT04904588 at CT.gov).

Purpureocillium lilacinum (P. lilacinum) is a rare opportunistic mold that predominantly affects immunocompromised hosts and exhibits intrinsic resistance to several conventional antifungal agents. Pulmonary infection is uncommon, and only a limited number of cases have been reported in patients with autoimmune connective tissue diseases receiving immunosuppressive therapy. We report a 37-year-old male hospital social worker with anti-Jo-1-positive myositis-associated interstitial lung disease receiving corticosteroids and mycophenolate mofetil who presented with hemoptysis and dyspnea. Computed tomography of the thorax demonstrated bilateral ground-glass opacities, multilobar consolidation, tree-in-bud nodularity, and mediastinal lymphadenopathy. Bronchoalveolar lavage fungal culture yielded P. lilacinum, with species identification confirmed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Because second-generation triazoles were unavailable at the time of diagnosis, treatment was initiated with oral itraconazole (200 mg twice daily) together with temporary cessation of immunosuppressive therapy. The patient experienced rapid clinical improvement, with resolution of the acute pulmonary infiltrates on follow-up computed tomography after three months and a negative follow-up sputum fungal culture after six months of therapy. Immunosuppressive treatment was subsequently reintroduced without recurrence of infection or progression of interstitial lung disease during follow-up. This case highlights the diagnostic challenge of probable pulmonary P. lilacinum infection in immunosuppressed patients with myositis-associated interstitial lung disease. It demonstrates a favorable clinical course during prolonged oral itraconazole therapy when preferred antifungal agents were unavailable. However, treatment outcomes should be interpreted with caution, as this is a single case, and concomitant antibacterial therapy, along with temporary modification of immunosuppressive therapy, may also have contributed to recovery.

Dermatomyositis is an immune-mediated inflammatory myopathy characterized by progressive proximal muscle weakness with sparing of distal muscles, accompanied by cutaneous manifestations. Laryngeal involvement in patients with dermatomyositis is extremely rare, with only seven cases described in the literature. We report the case of a 21-year-old man with dermatomyositis who presented with dysphonia, breathiness, and asthenia with a voice handicap index-10 score of 24/40. Laryngeal examination showed whitish mucosal patches on the upper surface of both vocal folds with bowing of the vocal folds. Video-stroboscopy revealed incomplete closure of the vocal folds during phonation, a decrease in vocal fold vibration amplitude, and diminished mucosal waves. One month after therapy with mycophenolate mofetil, the patient's voice quality improved and his VHI-10 score decreased to 16/40.