PMC:4319657 / 5552-10708 JSONTXT

{"project":"NEUROSES","denotations":[{"id":"T243","span":{"begin":11,"end":16},"obj":"PATO_0000389"},{"id":"T244","span":{"begin":1265,"end":1270},"obj":"PATO_0000389"},{"id":"T245","span":{"begin":20,"end":28},"obj":"PATO_0002091"},{"id":"T246","span":{"begin":127,"end":131},"obj":"PATO_0001026"},{"id":"T247","span":{"begin":217,"end":221},"obj":"PATO_0000600"},{"id":"T248","span":{"begin":281,"end":286},"obj":"CHEBI_23888"},{"id":"T249","span":{"begin":596,"end":600},"obj":"CHEBI_23888"},{"id":"T250","span":{"begin":1402,"end":1406},"obj":"CHEBI_23888"},{"id":"T251","span":{"begin":295,"end":302},"obj":"CHEBI_60056"},{"id":"T252","span":{"begin":295,"end":302},"obj":"CHEBI_27958"},{"id":"T253","span":{"begin":342,"end":357},"obj":"CHEBI_6809"},{"id":"T254","span":{"begin":412,"end":419},"obj":"CHEBI_31836"},{"id":"T255","span":{"begin":466,"end":472},"obj":"CHEBI_27808"},{"id":"T256","span":{"begin":477,"end":486},"obj":"CHEBI_6807"},{"id":"T257","span":{"begin":574,"end":579},"obj":"PATO_0002122"},{"id":"T258","span":{"begin":668,"end":675},"obj":"CHEBI_75324"},{"id":"T259","span":{"begin":668,"end":675},"obj":"CHEBI_78004"},{"id":"T260","span":{"begin":684,"end":688},"obj":"CHEBI_32178"},{"id":"T261","span":{"begin":706,"end":715},"obj":"CHEBI_18246"},{"id":"T262","span":{"begin":723,"end":728},"obj":"PATO_0000694"},{"id":"T263","span":{"begin":747,"end":754},"obj":"PATO_0000006"},{"id":"T264","span":{"begin":814,"end":820},"obj":"PATO_0000122"},{"id":"T265","span":{"begin":825,"end":834},"obj":"PATO_0000044"},{"id":"T266","span":{"begin":1230,"end":1235},"obj":"PATO_0001450"},{"id":"T267","span":{"begin":1495,"end":1500},"obj":"PATO_0001450"},{"id":"T268","span":{"begin":1271,"end":1283},"obj":"PATO_0002419"},{"id":"T269","span":{"begin":1524,"end":1528},"obj":"CHEBI_23888"},{"id":"T270","span":{"begin":1633,"end":1638},"obj":"CHEBI_23888"},{"id":"T271","span":{"begin":1668,"end":1672},"obj":"CHEBI_27889"},{"id":"T272","span":{"begin":1904,"end":1908},"obj":"CHEBI_27889"},{"id":"T273","span":{"begin":1668,"end":1672},"obj":"CHEBI_25016"},{"id":"T274","span":{"begin":1904,"end":1908},"obj":"CHEBI_25016"},{"id":"T275","span":{"begin":1790,"end":1795},"obj":"PATO_0000389"},{"id":"T276","span":{"begin":1877,"end":1882},"obj":"PATO_0001450"},{"id":"T277","span":{"begin":1929,"end":1934},"obj":"PATO_0001450"},{"id":"T278","span":{"begin":2715,"end":2720},"obj":"PATO_0001450"},{"id":"T279","span":{"begin":1986,"end":1992},"obj":"PATO_0001020"},{"id":"T280","span":{"begin":2810,"end":2816},"obj":"PATO_0001020"},{"id":"T281","span":{"begin":2325,"end":2330},"obj":"PATO_0000627"},{"id":"T282","span":{"begin":2334,"end":2341},"obj":"PATO_0001566"},{"id":"T283","span":{"begin":2426,"end":2433},"obj":"PATO_0000392"},{"id":"T284","span":{"begin":2450,"end":2457},"obj":"PATO_0000060"},{"id":"T285","span":{"begin":2583,"end":2588},"obj":"PATO_0000694"},{"id":"T286","span":{"begin":2682,"end":2690},"obj":"PATO_0001851"},{"id":"T287","span":{"begin":2936,"end":2941},"obj":"CHEBI_18059"},{"id":"T288","span":{"begin":3024,"end":3031},"obj":"PATO_0002258"},{"id":"T289","span":{"begin":3055,"end":3060},"obj":"CHEBI_18059"},{"id":"T290","span":{"begin":3072,"end":3077},"obj":"CHEBI_18059"},{"id":"T291","span":{"begin":3166,"end":3171},"obj":"CHEBI_18059"},{"id":"T292","span":{"begin":3313,"end":3318},"obj":"CHEBI_18059"},{"id":"T293","span":{"begin":4081,"end":4086},"obj":"CHEBI_18059"},{"id":"T294","span":{"begin":4195,"end":4200},"obj":"CHEBI_18059"},{"id":"T295","span":{"begin":3133,"end":3139},"obj":"PATO_0001020"},{"id":"T296","span":{"begin":3172,"end":3181},"obj":"CHEBI_25367"},{"id":"T297","span":{"begin":3355,"end":3361},"obj":"PATO_0000608"},{"id":"T298","span":{"begin":3521,"end":3532},"obj":"CHEBI_16113"},{"id":"T299","span":{"begin":3574,"end":3585},"obj":"CHEBI_16113"},{"id":"T300","span":{"begin":3633,"end":3643},"obj":"CHEBI_35195"},{"id":"T301","span":{"begin":3817,"end":3827},"obj":"CHEBI_35195"},{"id":"T302","span":{"begin":3646,"end":3658},"obj":"CHEBI_16247"},{"id":"T303","span":{"begin":3659,"end":3668},"obj":"PATO_0000142"},{"id":"T304","span":{"begin":3875,"end":3884},"obj":"PATO_0000142"},{"id":"T305","span":{"begin":3755,"end":3758},"obj":"PATO_0001737"},{"id":"T306","span":{"begin":3766,"end":3774},"obj":"PATO_0002476"},{"id":"T307","span":{"begin":3840,"end":3849},"obj":"PATO_0000516"},{"id":"T308","span":{"begin":4022,"end":4029},"obj":"PATO_0000498"},{"id":"T309","span":{"begin":4022,"end":4029},"obj":"PATO_0001863"},{"id":"T310","span":{"begin":4034,"end":4047},"obj":"PATO_0002102"},{"id":"T311","span":{"begin":4224,"end":4231},"obj":"CHEBI_46662"},{"id":"T312","span":{"begin":4830,"end":4835},"obj":"CHEBI_41264"},{"id":"T313","span":{"begin":4836,"end":4844},"obj":"CHEBI_25549"},{"id":"T314","span":{"begin":4917,"end":4921},"obj":"CHEBI_25016"},{"id":"T315","span":{"begin":4917,"end":4921},"obj":"CHEBI_27889"},{"id":"T316","span":{"begin":4973,"end":4985},"obj":"PATO_0001628"},{"id":"T317","span":{"begin":5071,"end":5076},"obj":"CHEBI_18059"},{"id":"T318","span":{"begin":1271,"end":1293},"obj":"PM3830"}],"text":"Discussion\nAcute or subacute chemically-induced lung injury is most often caused by accidental inhalation of chemical agent at work, at home or as a consequence of industrial or environmental disaster [2]. There is a wide spectrum of lung disease complications after administering drugs such as cocaine and its derivatives, especially crack; methamphetamine derivatives, including methylphenidate hydrochloride (Ritalin; Novartis, East Hanover, NJ); opiates such as heroin and methadone, among others; and mixtures of these agents. Furthermore, substances that are commonly mixed with an illicit drug, known as “fillers”, may be primarily responsible for the disease. Fillers include talc, cornstarch, and cellulose [3,4].\nEarly in the assessment process it is essential to determine the most probable factor, the length and frequency of exposure, which can be achieved by careful examination of a patient’s medical history or witnesses’ observations.\nToxic lung injury may manifest itself in many different ways and the extent of changes caused by inhaling toxic substances depends on their physicochemical properties and the degree of exposure [5,6].\nChemically-induced lung injury includes bronchitis, bronchiolitis, pulmonary edema, ARDS, organizing pneumonia, acute eosinophilic pneumonia, hypersensitivity pneumonitis and sarcoid-like granulomatous lung disease [7].\nRespiratory complications of drug abuse may involve the upper airways, lungs, and pleura and include pneumonia, pulmonary edema, pulmonary hemorrhage, drug-induced granulomatosis, emphysema, and pneumothorax [3,4,8]. Repeated intravenous injections of various drugs designed for oral intake can lead to severe complications such as pulmonary hypertension or toxic interstitial lung disease [9].\nThe first symptoms in acute exposure are irritation of the upper respiratory tract and bronchitis. Laryngeal edema and bronchospasm may lead to death. Pulmonary edema [5] in the mechanism of alveolar-capillary barrier damage may occur within the first 48 hours [10]. Superinfection is a common complication in the following days. Potential long-term consequences are bronchial hyperreactivity and constrictive bronchiolitis [5]. Organization, characterized by fibroblast proliferation, is a common and nearly universal response to lung injury whether it is focal or diffuse. Despite the vast range of injurious agents, the lung’s response to injury is quite limited, with a similar pattern of reaction seen radiologically and histologically regardless of the underlying cause [11].\nIn the case of smoke inhalation, early radiological signs in chest X-ray include perihilar bronchial wall thickening and subglottic swelling, frequently – pulmonary edema. Chest radiogram, which is a first-line study, is often enough to evaluate the extent of damage and to monitor the disease [12].\nIn our case, interstitial changes prevailed in the radiological examination. However, lipid bodies in the organizing lesions were found in the microscopic examination, which pointed to the concomitance of lipid pneumonia.\nLipid pneumonia is a rare pulmonary disease. It results from damage to the lung parenchyma by lipid molecules originating from the serum (endogenous form) or entering the lung by aspiration or inhalation (exogenous form) [13–16].\nEndogenous lipid pneumonia most often occurs below a closed bronchus due to a lung tumor [17]. It results from the influx of macrophages accumulating fat coming from alveolar type II epithelial cells. It is also called cholesterol pneumonia due to a significant amount of cholesterol in phagocytes [18,19]. Type II cells produce a surfactant – phospholipid substance regulating the surface tension of the alveoli and thus co-responsible for stabilizing gas in the terminal part of the respiratory system. Pulmonary surfactant is the most sensitive and dynamically changing substance under the influence of various factors damaging pulmonary alveoli [17].\nPathomorphological changes in the exogenous lipoid pneumonia are chronic and proliferative. In the microscopic examination, lipid bodies are encapsulated by connective tissue containing macrophages [18].\nFactors responsible for exogenous lipid pneumonia are varied – mineral oil, petroleum jelly, fish liver oil, oily nose drops, full milk, egg yolk, kerosene, gasoline blend, industrial lubricants, oil, buffalo butter [20].\nIn adult population, they are most commonly diagnosed in fire-eaters [21] but they may result from occupational exposure to mixtures of oil in manufacturing of steel and furniture, in aviation and – non-occupational exposure – in people using lipstick or lip gloss, people using aerosol substances to apply on joints or spraying hair and people who smoke tobacco with oily additives [13]. Aspiration of volatile organic compounds such as amyl and butyl nitrites (commonly known as “poppers”) during attempted inhalation of vapors may lead to the development of lipoid pneumonia [8]. Due to insufficient information on composition and manner of ingestion of novel psychoactive substances, lipid pneumonia should be taken into consideration in people addicted to legal highs."}

{"project":"2_test","denotations":[{"id":"25691919-19953031-131979541","span":{"begin":202,"end":203},"obj":"19953031"},{"id":"25691919-24144776-131979542","span":{"begin":719,"end":720},"obj":"24144776"},{"id":"25691919-9781191-131979543","span":{"begin":1147,"end":1148},"obj":"9781191"},{"id":"25691919-8200187-131979544","span":{"begin":1149,"end":1150},"obj":"8200187"},{"id":"25691919-24853247-131979545","span":{"begin":1369,"end":1370},"obj":"24853247"},{"id":"25691919-24144776-131979546","span":{"begin":1584,"end":1585},"obj":"24144776"},{"id":"25691919-11593152-131979547","span":{"begin":1764,"end":1765},"obj":"11593152"},{"id":"25691919-9781191-131979548","span":{"begin":1936,"end":1937},"obj":"9781191"},{"id":"25691919-9781191-131979549","span":{"begin":2193,"end":2194},"obj":"9781191"},{"id":"25691919-24224590-131979550","span":{"begin":2545,"end":2547},"obj":"24224590"},{"id":"25691919-3338239-131979551","span":{"begin":2845,"end":2847},"obj":"3338239"},{"id":"25691919-15006976-131979552","span":{"begin":3294,"end":3296},"obj":"15006976"},{"id":"25691919-11208509-131979552","span":{"begin":3294,"end":3296},"obj":"11208509"},{"id":"25691919-2093976-131979552","span":{"begin":3294,"end":3296},"obj":"2093976"},{"id":"25691919-18546953-131979552","span":{"begin":3294,"end":3296},"obj":"18546953"},{"id":"25691919-9769783-131979553","span":{"begin":3392,"end":3394},"obj":"9769783"},{"id":"25691919-20028911-131979554","span":{"begin":3601,"end":3603},"obj":"20028911"},{"id":"25691919-18138024-131979555","span":{"begin":3604,"end":3606},"obj":"18138024"},{"id":"25691919-9769783-131979556","span":{"begin":3952,"end":3954},"obj":"9769783"},{"id":"25691919-20028911-131979557","span":{"begin":4156,"end":4158},"obj":"20028911"},{"id":"25691919-16756150-131979558","span":{"begin":4378,"end":4380},"obj":"16756150"},{"id":"25691919-23269939-131979559","span":{"begin":4453,"end":4455},"obj":"23269939"},{"id":"25691919-15006976-131979560","span":{"begin":4767,"end":4769},"obj":"15006976"}],"text":"Discussion\nAcute or subacute chemically-induced lung injury is most often caused by accidental inhalation of chemical agent at work, at home or as a consequence of industrial or environmental disaster [2]. There is a wide spectrum of lung disease complications after administering drugs such as cocaine and its derivatives, especially crack; methamphetamine derivatives, including methylphenidate hydrochloride (Ritalin; Novartis, East Hanover, NJ); opiates such as heroin and methadone, among others; and mixtures of these agents. Furthermore, substances that are commonly mixed with an illicit drug, known as “fillers”, may be primarily responsible for the disease. Fillers include talc, cornstarch, and cellulose [3,4].\nEarly in the assessment process it is essential to determine the most probable factor, the length and frequency of exposure, which can be achieved by careful examination of a patient’s medical history or witnesses’ observations.\nToxic lung injury may manifest itself in many different ways and the extent of changes caused by inhaling toxic substances depends on their physicochemical properties and the degree of exposure [5,6].\nChemically-induced lung injury includes bronchitis, bronchiolitis, pulmonary edema, ARDS, organizing pneumonia, acute eosinophilic pneumonia, hypersensitivity pneumonitis and sarcoid-like granulomatous lung disease [7].\nRespiratory complications of drug abuse may involve the upper airways, lungs, and pleura and include pneumonia, pulmonary edema, pulmonary hemorrhage, drug-induced granulomatosis, emphysema, and pneumothorax [3,4,8]. Repeated intravenous injections of various drugs designed for oral intake can lead to severe complications such as pulmonary hypertension or toxic interstitial lung disease [9].\nThe first symptoms in acute exposure are irritation of the upper respiratory tract and bronchitis. Laryngeal edema and bronchospasm may lead to death. Pulmonary edema [5] in the mechanism of alveolar-capillary barrier damage may occur within the first 48 hours [10]. Superinfection is a common complication in the following days. Potential long-term consequences are bronchial hyperreactivity and constrictive bronchiolitis [5]. Organization, characterized by fibroblast proliferation, is a common and nearly universal response to lung injury whether it is focal or diffuse. Despite the vast range of injurious agents, the lung’s response to injury is quite limited, with a similar pattern of reaction seen radiologically and histologically regardless of the underlying cause [11].\nIn the case of smoke inhalation, early radiological signs in chest X-ray include perihilar bronchial wall thickening and subglottic swelling, frequently – pulmonary edema. Chest radiogram, which is a first-line study, is often enough to evaluate the extent of damage and to monitor the disease [12].\nIn our case, interstitial changes prevailed in the radiological examination. However, lipid bodies in the organizing lesions were found in the microscopic examination, which pointed to the concomitance of lipid pneumonia.\nLipid pneumonia is a rare pulmonary disease. It results from damage to the lung parenchyma by lipid molecules originating from the serum (endogenous form) or entering the lung by aspiration or inhalation (exogenous form) [13–16].\nEndogenous lipid pneumonia most often occurs below a closed bronchus due to a lung tumor [17]. It results from the influx of macrophages accumulating fat coming from alveolar type II epithelial cells. It is also called cholesterol pneumonia due to a significant amount of cholesterol in phagocytes [18,19]. Type II cells produce a surfactant – phospholipid substance regulating the surface tension of the alveoli and thus co-responsible for stabilizing gas in the terminal part of the respiratory system. Pulmonary surfactant is the most sensitive and dynamically changing substance under the influence of various factors damaging pulmonary alveoli [17].\nPathomorphological changes in the exogenous lipoid pneumonia are chronic and proliferative. In the microscopic examination, lipid bodies are encapsulated by connective tissue containing macrophages [18].\nFactors responsible for exogenous lipid pneumonia are varied – mineral oil, petroleum jelly, fish liver oil, oily nose drops, full milk, egg yolk, kerosene, gasoline blend, industrial lubricants, oil, buffalo butter [20].\nIn adult population, they are most commonly diagnosed in fire-eaters [21] but they may result from occupational exposure to mixtures of oil in manufacturing of steel and furniture, in aviation and – non-occupational exposure – in people using lipstick or lip gloss, people using aerosol substances to apply on joints or spraying hair and people who smoke tobacco with oily additives [13]. Aspiration of volatile organic compounds such as amyl and butyl nitrites (commonly known as “poppers”) during attempted inhalation of vapors may lead to the development of lipoid pneumonia [8]. Due to insufficient information on composition and manner of ingestion of novel psychoactive substances, lipid pneumonia should be taken into consideration in people addicted to legal highs."}

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M3543"},{"id":"T202","span":{"begin":4386,"end":4391},"obj":"Patient"},{"id":"T203","span":{"begin":4404,"end":4408},"obj":"Patient"},{"id":"T204","span":{"begin":4613,"end":4619},"obj":"Patient"},{"id":"T205","span":{"begin":4649,"end":4655},"obj":"Patient"},{"id":"T206","span":{"begin":4721,"end":4727},"obj":"Patient"},{"id":"T207","span":{"begin":4728,"end":4731},"obj":"Patient"},{"id":"T208","span":{"begin":5125,"end":5131},"obj":"Patient"},{"id":"T209","span":{"begin":4461,"end":4465},"obj":"Patient"}],"text":"Discussion\nAcute or subacute chemically-induced lung injury is most often caused by accidental inhalation of chemical agent at work, at home or as a consequence of industrial or environmental disaster [2]. There is a wide spectrum of lung disease complications after administering drugs such as cocaine and its derivatives, especially crack; methamphetamine derivatives, including methylphenidate hydrochloride (Ritalin; Novartis, East Hanover, NJ); opiates such as heroin and methadone, among others; and mixtures of these agents. Furthermore, substances that are commonly mixed with an illicit drug, known as “fillers”, may be primarily responsible for the disease. Fillers include talc, cornstarch, and cellulose [3,4].\nEarly in the assessment process it is essential to determine the most probable factor, the length and frequency of exposure, which can be achieved by careful examination of a patient’s medical history or witnesses’ observations.\nToxic lung injury may manifest itself in many different ways and the extent of changes caused by inhaling toxic substances depends on their physicochemical properties and the degree of exposure [5,6].\nChemically-induced lung injury includes bronchitis, bronchiolitis, pulmonary edema, ARDS, organizing pneumonia, acute eosinophilic pneumonia, hypersensitivity pneumonitis and sarcoid-like granulomatous lung disease [7].\nRespiratory complications of drug abuse may involve the upper airways, lungs, and pleura and include pneumonia, pulmonary edema, pulmonary hemorrhage, drug-induced granulomatosis, emphysema, and pneumothorax [3,4,8]. Repeated intravenous injections of various drugs designed for oral intake can lead to severe complications such as pulmonary hypertension or toxic interstitial lung disease [9].\nThe first symptoms in acute exposure are irritation of the upper respiratory tract and bronchitis. Laryngeal edema and bronchospasm may lead to death. Pulmonary edema [5] in the mechanism of alveolar-capillary barrier damage may occur within the first 48 hours [10]. Superinfection is a common complication in the following days. Potential long-term consequences are bronchial hyperreactivity and constrictive bronchiolitis [5]. Organization, characterized by fibroblast proliferation, is a common and nearly universal response to lung injury whether it is focal or diffuse. Despite the vast range of injurious agents, the lung’s response to injury is quite limited, with a similar pattern of reaction seen radiologically and histologically regardless of the underlying cause [11].\nIn the case of smoke inhalation, early radiological signs in chest X-ray include perihilar bronchial wall thickening and subglottic swelling, frequently – pulmonary edema. Chest radiogram, which is a first-line study, is often enough to evaluate the extent of damage and to monitor the disease [12].\nIn our case, interstitial changes prevailed in the radiological examination. However, lipid bodies in the organizing lesions were found in the microscopic examination, which pointed to the concomitance of lipid pneumonia.\nLipid pneumonia is a rare pulmonary disease. It results from damage to the lung parenchyma by lipid molecules originating from the serum (endogenous form) or entering the lung by aspiration or inhalation (exogenous form) [13–16].\nEndogenous lipid pneumonia most often occurs below a closed bronchus due to a lung tumor [17]. It results from the influx of macrophages accumulating fat coming from alveolar type II epithelial cells. It is also called cholesterol pneumonia due to a significant amount of cholesterol in phagocytes [18,19]. Type II cells produce a surfactant – phospholipid substance regulating the surface tension of the alveoli and thus co-responsible for stabilizing gas in the terminal part of the respiratory system. Pulmonary surfactant is the most sensitive and dynamically changing substance under the influence of various factors damaging pulmonary alveoli [17].\nPathomorphological changes in the exogenous lipoid pneumonia are chronic and proliferative. In the microscopic examination, lipid bodies are encapsulated by connective tissue containing macrophages [18].\nFactors responsible for exogenous lipid pneumonia are varied – mineral oil, petroleum jelly, fish liver oil, oily nose drops, full milk, egg yolk, kerosene, gasoline blend, industrial lubricants, oil, buffalo butter [20].\nIn adult population, they are most commonly diagnosed in fire-eaters [21] but they may result from occupational exposure to mixtures of oil in manufacturing of steel and furniture, in aviation and – non-occupational exposure – in people using lipstick or lip gloss, people using aerosol substances to apply on joints or spraying hair and people who smoke tobacco with oily additives [13]. Aspiration of volatile organic compounds such as amyl and butyl nitrites (commonly known as “poppers”) during attempted inhalation of vapors may lead to the development of lipoid pneumonia [8]. Due to insufficient information on composition and manner of ingestion of novel psychoactive substances, lipid pneumonia should be taken into consideration in people addicted to legal highs."}