Le allergopatie professionali: passato e presente.

Summary. Il percorso conoscitivo della Medicina del Lavoro nel campo delle Allergopatie professionali pu\uf2 essere cos\uec schematizzato: 1) individuazione di nuovi agenti etiologici per patologie professionali gi\ue0 note (ad es. l'asma bronchiale); 2) individuazione di meccanismi patogenetici su base immunitaria come momenti essenziali di numerose patologie professionali; 3) approfondimento delle conoscenze dei meccanismi fisiopatologici delle malattie professionali su base allergica nota; 4) messa a punto di nuove metodiche diiagnostiche che consentono di evidenziare la sensibilizzazione a sostanze presenti nell'ambiente di lavoro. Le Allergopatie professionali, in cui l'agente causale \ue8 noto e l'esposizione misurabile forniscono un modello di studio e di ricerca per le analoghe patologie legate ad agenti non occupazionali

Le malattie cutanee.

Riassunto. Viene discussa la fisiologia della risposta cutanea a Noxae esogene e i meccanismi di difesa della cute. Le dermopatie professionali sono state classificate come Dermatiiti Allergiche da contatto, Dermatiti da contatto irriitante, Dermatiti tossiche , Dermatiti da infezione o infestazione da agenti biologici e Neoplasie cutanee. Per ciascuna categoria viene discusso il quadro clinico, l'etiopatogenesi, i protocolli diagnostici e diagnostico-differenziali. Infine vengono trattati gli aspetti preventivi, con particolare riguardo ai Dispositivi Individuali di Prevenzione e alle misure legate alla protezione della cute con adeguati detergenti e idratanti

Le malattie degli organi di senso: l'apparato uditivo.

L'esposizione professionale a rumore con intensit\ue0 superiore agli 80 dB provoca una progressiva perdita dell'udito nei lavoratori esposti. L'innalzamento della soglia uditiva inizia alla frequenza audiometrica di 4000 Hz, per estendersi successivamente alle frequenze vicine, 3000 e 8000 Hz. Proseguendo l'esposizione, vengono coinvolte le frequenze della voce parlata e l'ipoacusia diviene sordit\ue0 manifesta. Si tratta di sordit\ue0 percettiva, bilaterale e simmetrica. Non si osservano peggioramenti dopo la cessazione dell'esposizione. Anche l'esposizione a determinatesostanze tossiche, per lo pi\uf9 farmaci pu\uf2 essere causa di ipoacusia. Vengono discussi gli aspetti diagnostici e le strategie preventive

Natural latex allergy. Patient management: from clinic to prevention. A review Allergia a latice naturale. Gestione del paziente: dalla clinica alla prevenzione. Rassegna critica

Abstract The widespread use of latex devices has been followed, in the last 25 years, by an increase in IgE mediated sensitization. The clinical manifestations of latex allergy affect the skin (urticaria and angioneurotic oedema), the lower and the upper respiratory tracts (rhinoconjunctivitis, asthma and glottis oedema), and the cardiovascular system (anaphylaxis). There is also an anaphylactic risk during surgery and invasive diagnostic procedures. Vegetable food cross-reacts with latex so that more than half of the patients show specific IgE against some food. Further than traditional groups at risk, as health care workers, other work categories have to be protected, because of the inappropriate use of latex gloves (food or drug industry workers, mechanics, panel beaters and so on). Recently the latex most important allergenic fractions have been characterized and recombinant allergens are now available. The recombinant allergens allow a better standardization of the extracts for diagnostic use, the production of safer extracts for immunotherapy as well as a more accurate evaluation of food cross-reactions. The recombinant allergens will allow a more accurate dosage of latex concentrations in air and in objects and, in future, to establish threshold limit values. The main aims of prevention are the replacement of latex with alternative elastomers, the reduction of work and extra work exposure and an efficient health survey in working environment. The use of latex gloves and devices among general population has to be discouraged. Specific immunotherapy has to be considered a second choice and restricted to highly qualified workers in order to realize a rehabilitation to their previous jobs. The actually obtained protection must be verified

Five cases of "fluoride asthma" [Osservazione di cinque casi di asma da fluoro]

Abstract Five cases of bronchial asthma in aluminium potroom workers with no previous occupational exposure to respiratory irritants, no history of asthma or other respiratory - heart disease are described. The first attack of asthma occurred on average 1.5 years (7 to 36 months) after the subjects had started work in the potrooms and the symptoms appeared both at the time of exposure as well as after a work shift. In 4 cases, symptoms disappeared completely within a week of being transferred from the potroom; only one worker still suffered from occasional wheezing after a year. Two subjects had positive skin tests for common allergens. Six to 24 months after cessation of exposure, all workers had normal lung volumes but they showed high sensitivity to a bronchial provocation test with inhaled carbachol. On the basis of the patients' histories and clinical and respiratory function findings, it is concluded that a causal relationship exists betweet potroom work and the onset of asthma

Phenological and aerobiological monitoring of allergenic flora in Padua (Italy). Preliminary data.

Abstract A phenological study on allergenic plants was carried out in Padua during 1995 in order to identify spontaneous and cultivated allergenic species in an urban area and their distribution, and to evaluate the relationship between anthesis length and airborne pollen concentrations. In some cases, there was no temporal overlap between phenological and aerobiological data, in particular for Corvlaceae, Betulaceae, Chenopodiaceae, Amaranthaceae, Polygonaceae and Fagaceae. 9 1998 Published by Elsevier Science Ireland Ltd. All rights reserved

All cats are gray in the dark or: not all NSAIDs give adverse reactions. A case report.

Background: Intolerance to acetylsalicilic acid (ASA) and nonsteroidal antiinflammatory drugs (NSAIDs) is a crucial problem in medical practice. The prevalence of NSAIDs intolerance is estimated as 0.6\u20132.5 in the general population, rising to over 10\u201320% in asthmatic patients. In general practice, NSAIDs are always supposed to cross-react with each other. Because the use of ASA as platelet antiaggregant is mandatory in many cardiological diagnostic and therapeutic procedures, ASA intolerance is a common and a severe problem in Coronary Intensive Care Unit (CICU). Here we describe the case of a Diclofenac intolerant patient who tolerates ASA treatment without any reaction. Case Report: A 57 years old male patient, affected with mild hypertension and osteoarthritis suffered a severe anaphylaxis after the application of a Diclofenac suppository. A few minutes after the drug application he had symptoms of glottis oedema and rapidly fell unconscious. The rescue team found him pulseless. He underwent to resuscitation procedures with success. Then, he was admitted into the CICU and the tests performed there showed: nonspecific, diffused alterations of the repolarization (DII, DIII; V3-V6) at the electrocardiogram; a mild increment of troponine I (maximum 3.17 mg/L); no pathological findings at the echocardiography. The ventricular coronarography showed a 95% stenosis of a collateral vessel of the right coronary artery that underwent to a successful placement of a drug-eluting stent. Chest X-Ray, ultrasound scans of the abdomen and of the chest, and brain Computer Tomography were normal. When he was in CICU he was started on therapy with ASA 100 mg daily under medical control. He tolerated ASA without any complication during all the eleven days of hospitalization. The allergy consultant suggested to avoid stopping the therapy with ASA and to avoid taking Diclofenac, Aceclofenac and any other NSAIDs, apart from paracetamole in the future. This case demonstrates that patients with severe Diclofenac hypersensitivity could tolerate other NSAIDs, in particular ASA, mandatory in some medical procedures. Other authors (1) described tolerance of indomethacin, piroxicam, methamizole but not ASA in 12 Diclofenac hypersensitive patients. Conclusion: In conclusion, patients referring previous reactions to NSAIDs should not be a priori excluded from treatment requiring ASA

Reduced cancer mortality in dairy farmers: is endotoxin exposure the key factor?

Abstract: From two areas in the Province of Padova, we selected 2,283 male farmers who worked either in cattle raising or in crop/orchard cultivation. There were 422 cohort deaths from 1970 to 1992. Using the regional population as a reference, the standardized mortality ratio (SMR) was calculated with 95% confidence intervals (CI) based on the Poisson distribution. Cancer mortality was significantly reduced among the 1,561 dairy farmers (SMR = 0.65; CI = 0.53-0.81); there was a significant decrease in lung cancer (SMR = 0.49; CI = 0.31-0.74), whereas a significant increase from brain tumors was found (SMR = 2.83; CI = 1.04-6.17). Neither overall cancer mortality nor the lung cancer SMR deviated significantly from unity for the 722 crop/orchard farmers. Among dairy farmers, moreover, lung cancer SMRs showed a significant downward trend across the quartiles of increasing length of work, 0.96 bl the first quartile, and 0.48, 0.40, and 0.25 in the second, third, and fourth quartiles, respectively. Moreover, lung cancer risk decreased with increasing farm land area, with SMRs in the quartiles of 0.89, 0.37, 0.41, and 0.19. This decrease cannot be attributed to either a selection (healthy worker effect) or a confounding (lower percentage of smokers) bias. Nor was it dire to an artifact introduced by differences in age distribution among the quartiles. Dairy farmers are known to be exposed to higher airborne endotoxin concentrations; reasonably, this cumulative exposure increases further with years of work and area of farm. Endotoxins may have protected the dairy farmers against lung cancer through the tumor necrosis factor produced by alveolar macrophages