Post-tuberculosis lung disease (PTLD) is a major cause of chronic respiratory impairment globally, yet it remains a critically neglected complication in high-burden, low-resource settings. This narrative review synthesizes evidence on PTLD, with a specific focus on Ethiopia, to analyze the health system gaps and propose actionable solutions. We conducted a narrative review of published and grey literature on the clinical burden, socioeconomic impact, and health system challenges of PTLD, with a particular emphasis on Ethiopia. Evidence was selected for relevance to PTLD phenotypes, diagnosis, management, and health system integration. PTLD, encompassing conditions like bronchiectasis, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis, affects a substantial proportion of tuberculosis (TB) survivors, leading to chronic respiratory symptoms, lung function disability, and socioeconomic impact. In Ethiopia, despite its inclusion as a priority lung disease in the national strategic plan, critical gaps persist. These include a profound lack of clinical and patient awareness, severely limited diagnostic capacity (spirometry, imaging), absent treatment and rehabilitation pathways, a scarcity of local epidemiological and implementation research, and unaddressed policy system barriers that impact infectious and chronic disease care. Ethiopia's policy recognition of PTLD is a pivotal first step. An urgent, coordinated effort is required to translate this into functional, equitable care. Success depends on concurrent action by researchers to generate local evidence, public health institutes to integrate surveillance and develop guidelines, clinicians to pioneer service delivery models, and policymakers to mandate and fund integration. Bridging the PTLD care gap is essential to safeguard the long-term health of TB survivors and strengthen the health system's capacity to manage chronic disease.

Granulomatosis with polyangiitis (GPA) is a rare ANCA-associated small-vessel vasculitis that predominantly affects the respiratory tract and kidneys, while cutaneous manifestations occur less frequently. Opportunistic fungal infections complicating GPA are uncommon, particularly involving rare filamentous basidiomycetes. We describe a 32-year-old male with a prolonged history of crusting rhinitis, tinnitus, and progressive nodular and ulcerative skin lesions on the trunk and extremities, accompanied by fever and lower limb edema. Laboratory evaluation revealed elevated inflammatory markers and positive c-ANCA (anti-PR3). Histopathology demonstrated granulomatous inflammation consistent with GPA. The clinical course was complicated by a secondary cutaneous infection caused by Hormographiella aspergillata, isolated from a skin lesion. Initial antifungal therapy with itraconazole was ineffective; subsequent treatment with voriconazole resulted in resolution of the fungal infection. The patient was then successfully treated with systemic immunosuppressive therapy, achieving long-term remission. To our knowledge, this is the first reported case of GPA complicated by a cutaneous infection with H. aspergillata. This case highlights the diagnostic challenges of GPA with atypical skin manifestations and underscores the importance of microbiological evaluation of skin lesions prior to initiating aggressive immunosuppressive therapy. KEYWORDS: granulomatosis with polyangiitis; ANCA-associated vasculitis; Hormographiella aspergillata; opportunistic fungal infection Granulomatosis with polyangiitis (GPA), formerly Wegener's granulomatosis, is a necrotizing granulomatous vasculitis affecting small to medium-sized blood vessels and belonging to the group of ANCA-associated vasculitides (AAV) (1). The disease is characterized by granulomatous inflammation, necrotizing vasculitis, and the presence of antineutrophil cytoplasmic antibodies, most commonly proteinase-3 ANCA (PR3-ANCA) (2). GPA may involve virtually any organ system, with predominant involvement of the upper and lower respiratory tract and kidneys (3). Cutaneous manifestations are reported in approximately 30-50% of patients and are usually associated with systemic disease activity (4). Opportunistic infections may complicate the course of GPA, particularly in the context of delayed diagnosis or immunosuppressive therapy. Infections caused by rare filamentous fungi such as Hormographiella (H) aspergillata are exceptionally rare and have predominantly been reported in immunocompromised patients with hematological malignancies (5, 6). A 32-year-old male was admitted with multiple painful ulcerations and nodules on the trunk and extremities, accompanied by high fever and marked bilateral lower limb edema. Four months before admission, nodular lesions on the left auricle and right nipple regressed spontaneously after purulent discharge. Six weeks prior to referral, painless nodules on the back and right upper arm were surgically incised and treated with antibiotics, followed by clinical deterioration with fever, progressive ulcerations, and painful swelling of the feet and ankles (figures 1a and !b). The patient had a two-year history of nasal obstruction, crusting rhinitis, and intermittent right-sided tinnitus. Rhinoscopy revealed mucosal thickening and septal perforation with crusts and synechiae. Dermatological examination showed deep ulcerations with yellow-brown crusts on the back, right upper arm, and left cheek (figures 1a and 1b). Laboratory evaluation demonstrated elevated inflammatory markers (ESR 76 mm/h, CRP 47.4 mg/L), hypoalbuminemia, and positive c-ANCA (anti-PR3). Initial microbiological cultures were sterile. Histopathology revealed granulomatous panniculitis with abscess formation. Fungal culture isolated H. aspergillata. Itraconazole therapy was ineffective; subsequent voriconazole treatment led to complete resolution of the cutaneous infection. Due to persistent systemic inflammation and c-ANCA positivity, the patient was treated with high-dose glucocorticoids and cyclophosphamide, which gradually led to completely remission of skin lesions (figure 2). Renal involvement developed during treatment, manifested as proteinuria. Long-term immunosuppressive therapy resulted in sustained remission with mild residual renal impairment. GPA is a rare multisystem autoimmune disease with heterogeneous clinical presentation, often leading to delayed diagnosis. Cutaneous involvement may be the initial manifestation and includes purpura, nodules, necrosis, and ulcerations, reflecting underlying vasculitis and granulomatous processes (2). In our patient, prominent skin lesions preceded the diagnosis by several months and contributed to diagnostic uncertainty. Opportunistic infections are a recognized complication in GPA, particularly following immunosuppression; however, fungal infections caused by filamentous basidiomycetes are exceedingly rare (5, 6). Hormographiella aspergillata, the anamorphic form of Coprinopsis cinerea, is an environmental fungus that has been implicated almost exclusively in invasive infections in patients with hematological malignancies, with reported mortality rates up to 70% (5, 6). To our knowledge, no previous case of GPA complicated by cutaneous infection with H. aspergillata has been reported. The present case underscores the importance of thorough microbiological evaluation of atypical or non-healing skin lesions in patients with suspected systemic vasculitis, particularly before initiation of intensive immunosuppressive therapy. Failure to recognize opportunistic infections may lead to significant morbidity and mortality. This case emphasizes the crucial role of dermatologists in the early recognition of systemic vasculitis presenting with skin manifestations. Comprehensive clinical, histological, and microbiological assessment is essential to establish the correct diagnosis and to identify rare infectious complications. Multidisciplinary management and careful monitoring are necessary to achieve long-term remission and to minimize treatment-related complications.

Fast-growing ulcerations in the oral cavity are clinically challenging lesions with potentially different pathogenesis. Traumatic ulcerative granuloma with stromal eosinophilia represents a benign oral mucosa lesion with unclear pathogenesis, most commonly occurring on the tongue. The etiology of this uncommon disease remains to be elucidated, although several triggering factors are thought to be implicated in pathogenesis including trauma, viral or toxic agents. We report a case of a 42-year-old female patient with traumatic ulcerative granuloma with stromal eosinophilia involving the lateral aspect of the tongue, clinically assessed with the auxilium of dermatoscopy. Since clinical and dermatoscopic evaluation could not give a precise diagnosis, additional serological methods and a biopsy of the lesion were performed with pathohistological evaluation. This case report highlights the need for awareness amongst dermatologists for traumatic ulcerative granuloma with stromal eosinophilia of the tongue as a great clinical and dermatoscopical simulator.

Apalutamide is a widely used second-generation androgen receptor inhibitor for the treatment of metastatic castration-sensitive and nonmetastatic castration-resistant prostate cancer. Although generally well tolerated, rare cases of interstitial lung disease and drug-induced pneumonitis have been reported. Early recognition is critical because of the potential for significant morbidity and mortality. We present a case of suspected apalutamide-induced pneumonitis in a 69-year-old man with metastatic prostate cancer who developed progressive shortness of breath, severe hypoxia, and bilateral ground-glass opacities on imaging. Extensive evaluation excluded infectious, cardiac, and autoimmune etiologies. The patient demonstrated marked clinical and radiographic improvement following the discontinuation of apalutamide and corticosteroid therapy. This case highlights the importance of maintaining a high index of suspicion for drug-induced pulmonary toxicity in patients receiving apalutamide. Prompt diagnosis and early initiation of corticosteroids may significantly improve outcomes.

Anti-glomerular basement membrane antibody (anti-GBM) disease is a rare yet aggressive autoimmune disorder that affects the kidneys and lungs. Patients with renal involvement often progressed to death or end-stage renal disease. Treatment with plasmapheresis, along with cyclophosphamide and corticosteroids, has been suggested to improve renal and patient survival; however, it showed little benefit in patients who presented with severe disease. We herein report a critically ill case with anuria, creatinine value of 752 μmol/L, anti-GBM antibody titer of 92.54 RU/mL, and 96.7% fibro-cellular crescent formation at renal biopsy. The patient was diagnosed with anti-GBM disease and treated with plasmapheresis and immunosuppressive therapy. Plasmapheresis was not ceased until the total clearance of pathogenic autoantibodies. The patient's renal function was successfully rescued and maintained normal during the 5-year follow-up. Our experience implicated that early and persistent plasmapheresis could rescue the kidney function of anti-GBM patients who have extremely poor prognosis.

Interstitial lung disease (ILD) underlies morbidity and mortality in connective tissue diseases (CTDs) such as systemic sclerosis. ILD encompasses a range of inflammatory and fibrotic pneumopathies, some of which manifest progressive characteristics. Up to 40% of ILDs are progressive, marked by radiologic progression, lung function decline, and increased symptoms. Immunosuppression is standard therapy for ILD, whereas antifibrotics like nintedanib are used in progressive fibrotic cases. Many patients deteriorate despite treatment, underscoring the need for biomarkers and targeted interventions. Type I interferon (IFN-I) signaling is implicated in CTD-ILD: interferon stimulated gene expression correlates with accelerated pulmonary decline and sustained IFN-I can precipitate ILD. In addition, IFN-I blocking agents like anifrolumab are under clinical investigation for CTD-ILD. This review examines IFN-I's role and therapeutic targeting in ILD.

Severe pulmonary involvement in primary Sjögren's syndrome presents a therapeutic challenge, particularly when conventional immunosuppression is insufficient. We report on the case of a 50-year-old woman with interstitial lung disease and profound gas exchange impairment (DLCO 17%). Despite initial treatment with azathioprine, clinical response was inadequate. Early escalation to tocilizumab was followed by marked clinical and radiological improvement. This case highlights the potential importance of timely biologic intervention in severe disease and suggests that advanced functional impairment may still be reversible. Limitations include a single-case design and concomitant therapy.

Dermatomyositis-spectrum inflammatory myopathy may present without characteristic cutaneous findings, and overlap phenotypes can delay recognition when early neuromuscular examination is not yet diagnostic. We describe the case of a patient with rheumatology-diagnosed dermatomyositis without rash and PM/Scl-positive overlap myositis with systemic sclerosis features whose course was marked by interstitial lung disease, progressive weakness, and objectively confirmed pharyngeal dysphagia. A 64-year-old female with interstitial lung disease presented with several weeks of polyarthralgia, severe fatigue, and marked muscle enzyme elevation. Initial examination showed no rash, sclerodactyly, or proximal weakness. Laboratory evaluation demonstrated a creatine kinase level of 12,810 U/L, elevated transaminases, a high-titer antinuclear antibody, positive PM/Scl-100 and PM/Scl-75 antibodies, and a weakly positive Mi-2 antibody. She was diagnosed with dermatomyositis without rash and PM/Scl-positive overlap myositis with systemic sclerosis features and treated with prednisone, mycophenolate mofetil, hydroxychloroquine, and antimicrobial prophylaxis. Intravenous immunoglobulin (IVIG) was recommended but was not initially approved. Her course progressed to severe weakness and dysphagia, ultimately preventing oral medication administration. During hospitalization, a videofluoroscopic swallow evaluation demonstrated aspiration with thin liquids and pharyngeal phase dysphagia. She received IVIG, with subsequent improvement in swallowing and functional status. This report highlights the importance of an overlap-informed approach to inflammatory myopathy when classic cutaneous features are absent. Progressive dysphagia should be treated as a marker of severe disease because it increases the risk of aspiration, contributes to malnutrition, and may prevent the administration of oral immunosuppressive therapy.