Recurrent respiratory papillomatosis (RRP) is a benign disease of the upper aero-digestive tract caused by human papillomavirus (HPV) infection, which affects children and young adults. The aim of this review is to describe the main etiological, epidemiological, clinical, diagnostic, and treatment aspects of RRP. Most infections in children occur at birth, during passage through the birth canals of contaminated mothers. In adults, HPV is transmitted sexually. Papillomas usually appear as exophytic nodules, primarily in the larynx, but occasionally involving the nasopharynx, tracheobronchial tree, and pulmonary parenchyma. The disease course is unpredictable, ranging from spontaneous remission to aggressive persistent or recurrent disease. Although it occurs rarely, RRP has the potential for malignant transformation to squamous cell carcinoma. Clinically, RRP usually presents with nonspecific symptoms of airway involvement, including chronic cough, hoarseness, wheezing, voice change, stridor, and chronic dyspnea. Helical computed tomography (CT) is highly accurate for the identification and characterization of focal or diffuse airway narrowing caused by nodular vegetant lesions. The typical CT pattern of lung papillomatosis consists of numerous multilobulated nodular lesions of various sizes, frequently cavitated, scattered throughout the lungs. Bronchoscopy is the most reliable method for the diagnosis of RRP; it enables direct visualization of lesions in the central airways and collection of biopsy samples for histopathological diagnosis, and is also useful for therapeutic planning. The definitive diagnosis of RRP is based on histopathological analysis. Currently, no definitive curative treatment for RRP is available; despite the availability of adjunctive treatments, surgery remains the mainstay of treatment.

Lipoid pneumonia results from the pulmonary accumulation of endogenous or exogenous lipids. Host tissue reactions to the inhaled substances differ according to their chemical characteristics. Symptoms can vary significantly among individuals, ranging from asymptomatic to severe, life-threatening disease. Acute, sometimes fatal, cases can occur, but the disease is usually indolent. Possible complications include superinfection by nontuberculous mycobacteria, pulmonary fibrosis, respiratory insufficiency, cor pulmonale, and hypercalcemia. The radiological findings are nonspecific, and the disease presents with variable patterns and distribution. For this reason, lipoid pneumonia may mimic many other diseases. The diagnosis of exogenous lipoid pneumonia is based on a history of exposure to oil, characteristic radiological findings, and the presence of lipid-laden macrophages on sputum or BAL analysis. High-resolution computed tomography (HRCT) is the best imaging modality for the diagnosis of lipoid pneumonia. The most characteristic CT finding in LP is the presence of negative attenuation values within areas of consolidation. There are currently no studies in the literature that define the best therapeutic option. However, there is a consensus that the key measure is identifying and discontinuing exposure to the offending agent. Treatment in patients without clinical symptoms remains controversial, but in patients with diffuse pulmonary damage, aggressive therapies have been reported. They include whole lung lavage, systemic corticosteroids, and thoracoscopy with surgical debridement.

Metastatic pulmonary calcification (MPC) is a subdiagnosed metabolic lung disease that is commonly associated with end-stage renal disease. This interstitial process is characterized by the deposition of calcium salts predominantly in the alveolar epithelial basement membranes. MPC is seen at autopsy in 60-75% of patients with renal failure. It is often asymptomatic, but can potentially progress to respiratory failure. Chest radiographs are frequently normal or demonstrate confluent or patchy airspace opacities. Three patterns visible on high-resolution computed tomography have been described: multiple diffuse calcified nodules, diffuse or patchy areas of ground-glass opacity or consolidation, and confluent high-attenuation parenchymal consolidation. The relative stability of these pulmonary infiltrates, in contrast to infectious processes, and their resistance to treatment, in the clinical context of hypercalcemia, are of diagnostic value. Scintigraphy with bone-seeking radionuclides may demonstrate increased radioactive isotope uptake. The resolution of pulmonary calcification in chronic renal failure may occur after parathyroidectomy, renal transplantation, or dialysis. Thus, the early diagnosis of MPC is beneficial. The aim of this review is to describe the main clinical, pathological, and imaging aspects of MPC.

Diffuse alveolar hemorrhage (DAH) represents a syndrome that can complicate many clinical conditions and may be life-threatening, requiring prompt treatment. It is recognized by the signs of acute- or subacute-onset cough, hemoptysis, diffuse radiographic pulmonary infiltrates, anemia, and hypoxemic respiratory distress. DAH is characterized by the accumulation of intra-alveolar red blood cells originating most frequently from the alveolar capillaries. It must be distinguished from localized pulmonary hemorrhage, which is most commonly due to chronic bronchitis, bronchiectasis, tumor, or localized infection. Hemoptysis, the major sign of DAH, may develop suddenly or over a period of days to weeks; this sign may also be initially absent, in which case diagnostic suspicion is established after sequential bronchoalveolar lavage reveals worsening red blood cell counts. The causes of DAH can be divided into infectious and noninfectious, the latter of which may affect immunocompetent or immunodeficient patients. Pulmonary infections are rarely reported in association with DAH, but they should be considered in the diagnostic workup because of the obvious therapeutic implications. In immunocompromised patients, the main infectious diseases that cause DAH are cytomegalovirus, adenovirus, invasive aspergillosis, Mycoplasma, Legionella, and Strongyloides. In immunocompetent patients, the infectious diseases that most frequently cause DAH are influenza A (H1N1), dengue, leptospirosis, malaria, and Staphylococcus aureus infection. Based on a search of the PubMed and Scopus databases, we review the infectious diseases that may cause DAH in immunocompetent patients.

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Leptospirosis, a spirochetal zoonosis, is frequently unrecognized due to its manifestation as an undifferentiated fever. It is an emerging infectious disease that has changed from an occupational disease of veterinarians, farmers, butchers, and other animal handlers to a cause of epidemics in poor and decayed urban communities in developing countries. Humans are infected when mucous membranes or abraded skin come into direct contact with the urine of infected animals, especially rats and dogs. Mortality from severe leptospirosis is high, even when optimal treatment is provided. The diagnosis of leptospirosis is based on clinical findings, history of direct or indirect exposure to infected animals in endemic areas, and positive serological tests. It should be considered in the differential diagnosis of patients with febrile illnesses associated with pneumonitis and respiratory failure, especially when hemoptysis is present. Severe pulmonary involvement in leptospirosis consists primarily of hemorrhagic pneumonitis. In advanced cases, adult respiratory distress syndrome and massive pulmonary hemorrhage may occur. Chest radiographs show bilateral alveolar infiltrates and/or resemble viral pneumonia, bronchopneumonia, tuberculosis, adult respiratory distress syndrome, and other causes of pulmonary hemorrhage such as Goodpasture syndrome. High-resolution computed tomography scans may show nodular infiltrates, areas of consolidation, ground-glass attenuation, and crazy-paving patterns. Bronchoalveolar lavage and autopsy studies have suggested that ground-glass opacities and air-space consolidations are secondary to pulmonary hemorrhage. Although not specific, the presence of these computed tomography findings in a febrile patient with an appropriate history should suggest a diagnosis of leptospirosis.

Talc is a mineral widely used in the ceramic, paper, plastics, rubber, paint, and cosmetic industries. Four distinct forms of pulmonary disease caused by talc have been defined. Three of them (talcosilicosis, talcoasbestosis, and pure talcosis) are associated with aspiration and differ in the composition of the inhaled substance. The fourth form, a result of intravenous administration of talc, is seen in drug users who inject medications intended for oral use. The disease most commonly affects men, with a mean age in the fourth decade of life. Presentation of patients with talc granulomatosis can range from asymptomatic to fulminant disease. Symptomatic patients typically present with nonspecific complaints, including progressive exertional dyspnea, and cough. Late complications include chronic respiratory failure, emphysema, pulmonary arterial hypertension, and cor pulmonale. History of occupational exposure or of drug addiction is the major clue to the diagnosis. The high-resolution computed tomography (HRCT) finding of small centrilobular nodules associated with heterogeneous conglomerate masses containing high-density amorphous areas, with or without panlobular emphysema in the lower lobes, is highly suggestive of pulmonary talcosis. The characteristic histopathologic feature in talc pneumoconiosis is the striking appearance of birefringent, needle-shaped particles of talc seen within the giant cells and in the areas of pulmonary fibrosis with the use of polarized light. In conclusion, computed tomography can play an important role in the diagnosis of pulmonary talcosis, since suggestive patterns may be observed. The presence of these patterns in drug abusers or in patients with an occupational history of exposure to talc is highly suggestive of pulmonary talcosis.

Pulmonary alveolar microlithiasis (PAM) is a rare genetic lung disease characterized by calcifications within the alveoli. Mutations in the SLC34A2 gene, which encodes a type IIb sodium-phosphate cotransporter, are responsible for this disease, leading to intra-alveolar accumulation of phosphate that favors the formation of microliths. The hallmark of this disorder is clinical-radiological dissociation, with typical imaging findings that correlate well with specific pathological findings. The long-term prognosis is poor and no treatment has been discovered to date. The aim of this review is to describe the main pathological, clinical, and imaging aspects of PAM, ranging from its genetic basis to treatment.