A case of occupational asthma caused by inhalation of vancomycin powder

Choi, Gil-Soon; Sung, Jung-Joon; Lee, J.‐W.; Ye, Y.‐M.; Park, Hae‐Sim

doi:10.1111/j.1398-9995.2009.02067.x

Cited by 14 publications

(9 citation statements)

References 5 publications

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“…Between 2000 and 2010, twelve (12) new drugs were found to induce OA [17–28] (Table 1), including six (6) antibiotic components: 7-aminocephalosporanic acid (7-ACSA), 7-amino-3-thiomethyl-3-cephalosporanic acid (7-TACA), cefteram, vancomycin, colistin, and thiamphenicol. Three (15%) of these cases occurred in health care workers and 15 (75%) in pharmaceutical employees.…”

Section: Resultsmentioning

confidence: 99%

“…In the case exposed to vancomycin powder [17], specific SPT and IgE were negative, but positive intradermal reaction and histamine release test suggested a direct histamine releasing effect of vancomycin instead of an IgE-mediated mechanism.…”

Section: Resultsmentioning

confidence: 99%

“…In this paper, the presence of specific IgE antibodies was documented for eight (8) (20%) of the newly described agents, including thiamphenicol, cefteram, 7-ACSA, cedroarana, angelim pedra, sapele, antiaris, and chlorendic anhydride. Other postulated mechanisms involved are a direct histamine releasing effect for vancomycin-induced OA [17] or an IgG-mediated reaction for falcate-induced OA [31]. …”

Section: Discussionmentioning

confidence: 99%

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Occupational Asthma: New Low-Molecular-Weight Causal Agents, 2000–2010

et al. 2012

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Background. More than 400 agents have been documented as causing occupational asthma (OA). The list of low-molecular-weight (LMW) agents that have been identified as potential causes of OA is constantly expanding, emphasizing the need to continually update our knowledge by reviewing the literature. Objective. The objective of this paper was to identify all new LMW agents causing occupational asthma reported during the period 2000–2010. Methods. A Medline search was performed using the keywords occupational asthma, new allergens, new causes, and low-molecular-weight agents. Results. We found 39 publications describing 41 new LMW causal agents, which belonged to the following categories: drugs (n = 12), wood dust (n = 11), chemicals (n = 8), metals (n = 4), biocides (n = 3), and miscellaneous (n = 3). The diagnosis of OA was confirmed through SIC for 35 of 41 agents, peak expiratory flow monitoring for three (3) agents, and the clinical history alone for three (3) agents. Immunological tests provided evidence supporting an IgE-mediated mechanism for eight (8) (20%) of the newly described agents. Conclusion. This paper highlights the importance of being alert to the occurrence of new LMW sensitizers, which can elicit OA. The immunological mechanism is explained by a type I hypersensitivity reaction in 20% of all newly described LMW agents.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Occupational Asthma: New Low-Molecular-Weight Causal Agents, 2000–2010

et al. 2012

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“…Three cases of OA from thiamphenicol—a methyl-sulfonyl analogue of chloramphenicol—were reported by Ye et al [27]. Vancomycin has been described as a cause of OA in a single patient [28], the diagnosis confirmed by serial peak flow measurements. The most recently reported case was of OA due to the polymyxin antibiotic colomycin in an antibiotic transport and storage worker, who demonstrated an early asthmatic reaction following specific inhalation challenge [29]; no evidence of specific IgE was found despite extensive in vitro immunological testing.…”

Section: Resultsmentioning

confidence: 99%

Occupational Asthma in Antibiotic Manufacturing Workers: Case Reports and Systematic Review

Angulo¹,

Szram

Welch

et al. 2011

Journal of Allergy

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Background. The risks of occupational asthma (OA) from antibiotics are uncertain. We report 4 new cases and a systematic review of the literature. Methods. Cases were identified through a specialist clinic, each underwent specific provocation testing (SPT). We subsequently reviewed the published literature. Results. The patients were employed in the manufacture of antibiotics; penicillins were implicated in three cases, in the fourth erythromycin, not previously reported to cause OA. In two, there was evidence of specific IgE sensitisation. At SPT each developed a late asthmatic reaction and increased bronchial hyperresponsiveness. 36 case reports have been previously published, 26 (citing penicillins or cephalosporins). Seven cross-sectional workplace-based surveys found prevalences of 5–8%. Conclusions. OA in antibiotic manufacturers may be more common than is generally recognised. Its pathogenesis remains unclear; immunological tests are of uncertain value and potential cases require confirmation with SPT. Further study of its frequency, mechanisms, and diagnosis is required.

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“…Examples of recently reported new agents or new exposures to high or low molecular weight causes for OA cases include predatory mites used for biological control in tomato and sweet pepper greenhouses, 9 Chrysonilia sitophila contaminating coffee grounds from vending machines, 10 octopus particles in a canning factory, 11 malt in manufacturing and unloading, 12 vancomycin powder inhalation, 13 surfactant composed of amines, 14 turpentine in an art painter, 15 gel flux containing dodecanedioic acid used in electronic soldering, 16 and colistin in a pharmaceutical worker. 17 There are resources for lists of recognized sensitizers and exposures (eg, asmanet.com, and the appendix to the textbook Asthma in the Workplace), 8,18,19 but none can be fully complete as new causes arise each year.…”

Section: Causes Of Sensitizer-induced Oamentioning

confidence: 99%

Occupational Asthma (Work-caused), and Work-exacerbated Asthma

Tarlo¹

2011

Clinical Pulmonary Medicine

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Asthma that is caused by work (occupational asthma) continues to be much less frequently recognized on a clinical basis than would be expected from epidemiologic studies. The diagnosis will often not be suspected without questions from the healthcare provider regarding work exposures and especially asking about temporal relationships of work with asthma symptoms. Early detailed investigations while the patient is still working at the job in question allow the best chance of a clear diagnosis and best advice to the patient regarding further work exposures. Work-exacerbated asthma can range from short occasional worsening of asthma to a daily or near-daily worsening at work. When symptoms are frequent and when there is no history of asthma preceding the work exposures, the diagnosis may be difficult to distinguish from occupational asthma without detailed investigations. The socioeconomic impact of work-exacerbated asthma may be similar in severity as for occupational asthma when symptoms have been frequent at work, and if they are not controlled by optimizing general asthma management and by simple preventive measures at work. As for many occupational lung diseases, preventive measures are often feasible. The pulmonologist and asthma educators may have a role in primary prevention by providing information to young asthmatics considering their future careers as to potential effects of work exposures on asthma, the importance of asthma control, and of methods to limit exposure to asthma triggers when possible.

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A case of occupational asthma caused by inhalation of vancomycin powder

Cited by 14 publications

References 5 publications

Occupational Asthma: New Low-Molecular-Weight Causal Agents, 2000–2010

Occupational Asthma: New Low-Molecular-Weight Causal Agents, 2000–2010

Occupational Asthma in Antibiotic Manufacturing Workers: Case Reports and Systematic Review

Occupational Asthma (Work-caused), and Work-exacerbated Asthma

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