Gelatine matrix with human thrombin decreases blood loss in adolescents undergoing posterior spinal fusion for idiopathic scoliosis: a multicentre, randomised clinical trial.

AIMS: In a multicentre, randomised study of adolescents undergoing posterior spinal fusion for idiopathic scoliosis, we investigated the effect of adding gelatine matrix with human thrombin to the standard surgical methods of controlling blood loss. PATIENTS AND METHODS: Patients in the intervention group (n = 30) were randomised to receive a minimum of two and a maximum of four units of gelatine matrix with thrombin in addition to conventional surgical methods of achieving haemostasis. Only conventional surgical methods were used in the control group (n = 30). We measured the intra-operative and total blood loss (intra-operative blood loss plus post-operative drain output). RESULTS: Each additional hour of operating time increased the intra-operative blood loss by 356.9 ml (p < 0.001) and the total blood loss by 430.5 ml (p < 0.001). Multiple linear regression analysis showed that the intervention significantly decreased the intra-operative (-171 ml, p = 0.025) and total blood loss (-177 ml, p = 0.027). The decrease in haemoglobin concentration from the day before the operation to the second post-operative day was significantly smaller in the intervention group (-6 g/l, p = 0.013) than in the control group. CONCLUSION: The addition of gelatine matrix with human thrombin to conventional methods of achieving haemostasis reduces both the intra-operative blood loss and the decrease in haemoglobin concentration post-operatively in adolescents undergoing posterior spinal fusion for idiopathic scoliosis. TAKE HOME MESSAGE: A randomised clinical trial showed that gelatine matrix with human thrombin decreases intra-operative blood loss by 30% when added to traditional surgical haemostatic methods in adolescents undergoing posterior spinal fusion for idiopathic scoliosis.

Effect of dimethylamine on the gas phase sulfuric acid concentration measured by Chemical Ionization Mass Spectrometry.

Sulfuric acid is widely recognized as a very important substance driving atmospheric aerosol nucleation. Based on quantum chemical calculations it has been suggested that the quantitative detection of gas phase sulfuric acid (H2SO4) by use of Chemical Ionization Mass Spectrometry (CIMS) could be biased in the presence of gas phase amines such as dimethylamine (DMA). An experiment (CLOUD7 campaign) was set up at the CLOUD (Cosmics Leaving OUtdoor Droplets) chamber to investigate the quantitative detection of H2SO4 in the presence of dimethylamine by CIMS at atmospherically relevant concentrations. For the first time in the CLOUD experiment, the monomer sulfuric acid concentration was measured by a CIMS and by two CI-APi-TOF (Chemical Ionization-Atmospheric Pressure interface-Time Of Flight) mass spectrometers. In addition, neutral sulfuric acid clusters were measured with the CI-APi-TOFs. The CLOUD7 measurements show that in the presence of dimethylamine (<5 to 70 pptv) the sulfuric acid monomer measured by the CIMS represents only a fraction of the total H2SO4, contained in the monomer and the clusters that is available for particle growth. Although it was found that the addition of dimethylamine dramatically changes the H2SO4 cluster distribution compared to binary (H2SO4-H2O) conditions, the CIMS detection efficiency does not seem to depend substantially on whether an individual H2SO4 monomer is clustered with a DMA molecule. The experimental observations are supported by numerical simulations based on A Self-contained Atmospheric chemistry coDe coupled with a molecular process model (Sulfuric Acid Water NUCleation) operated in the kinetic limit.

Occupational allergic airbone contact dermatitis and delayed bronchial asthma from epoxy resin revealed by bronchial provocation test.

Diglycidyl ether of bisphenol A (DGEBA) epoxy resins belong to the most common causes of occupational allergic contact dermatitis. DGEBA has on rare occasions caused occupational asthma. Here we present a patient who first developed occupational allergic contact dermatitis (ACD) caused by a single accidental exposure to DGEBA. Then, on continued occupational exposure to DGEBA, the patient developed occupational asthma from DGEBA, in addition to ACD. A bronchial provocation test with DGEBA caused a 36% drop in the peak expiratory flow, reflecting a delayed type of occupational asthma. This bronchial provocation test caused a strong dermatitis of the exposed skin of the face, in accordance with airborne ACD from DGEBA.

Humidifier-associated extrinsic allergic alveolitis.

Three cases of allergic alveolitis due to indoor humdification systems are described. Thermoactinomyces vulgaris precipitins were detected in the serum of a 37-year-old female patient who had typical febrile attacks during exposure to cool-mist from a home humidifier. When the cause was detected and eliminated, the symptoms and signs disappeared and the woman's gas transfer factor improved from 56% to normal within six months. In a printing office a 60-year-old woman had had febrile attacks with cough for more than a year. The patient herself associated the respiratory disease with a cool-mist humidifier sometimes used at work. The water reservoir was heavily contaminated with amoebas (Amoeba proteus), which might have been the causative organisms in this case. Aspergillus fumigatus precipitins were found in the serum of a 53-year-old female printer with the clinical picture of occupational allergic alveolitis. The same organism was detected in the ambient air of the printing office.

Immediate and delayed allergy from epoxy resins based on diglycidyl ether of bisphenol A.

This case report presents two patients with immediate and delayed allergy to epoxy resins based on diglycidyl ether of bisphenol A (DGEBA). In patch testing, the epoxy resin (DGEBA-based) of the standard series gave allergic reactions. Both patients had a prick test reaction of histamine size or larger to the human serum albumin (HSA) conjugate of DGEBA-based epoxy resins. One had been occupationally exposed to methyl tetrahydrophthalic anhydride (MTHPA) and had a histamine-size prick test reaction to the HSA conjugate of MTHPA; the other did not react to the conjugate. Determinations of specific immunoglobulin E were carried out with HSA-DGEBA conjugates, two DGEBA-based epoxy resins, and phthalic anhydrides. The first patient had positive tests to DGEBA, the DGEBA-based epoxy resins, and two phthalic anhydrides, and the second to DGEBA and the DGEBA-based epoxy resins, but not to the phthalic anhydrides.

Cellulase allergy and challenge tests with cellulase using immunologic assessment.

OBJECTIVES: This study attempted to develop and evaluate a challenge test for diagnosing allergic asthma and rhinitis due to cellulase. METHODS: Challenge tests in a chamber were performed on 11 persons sensitized to cellulase. Four different enzyme-lactose mixtures, starting from a 0.03% mixture, were used. The enzyme dust was generated from a dry enzyme preparation mixed with lactose powder, using pressurized air. The cellulase concentration in the air was measured with an immunochemical method. RESULTS: Nasal, pharyngeal, or bronchial symptoms could be elicited at cellulase air concentrations of 1 to 1300 microg/m3. A dose-response relationship was observed for symptoms in repeated challenge tests with increasing concentrations of cellulase. For 2 persons skin symptoms could also be reproduced. CONCLUSION: The challenge method proved to be a practical means with which to simulate conditions at the worksite and elicit the specific respiratory symptoms of the patients.

Agents causing occupational asthma in Finland in 1986-2002: cow epithelium bypassed by moulds from moisture-damaged buildings.

BACKGROUND: Occupational asthma is an avoidable form of asthma. In Finland, the diagnosis of occupational asthma entitles substantial compensation to the employee. The diagnostics are based on symptoms, exposure assessment, allergologic investigations, follow-up of peak expiratory flow (PEF) at work and at home and, in many cases, specific challenge tests. OBJECTIVE: To study the causative agents of occupational asthma in Finland. METHODS: The causative agents and the numbers of new occupational asthma cases notified to the Finnish Register of Occupational Diseases (FROD) during 1986-2002 are reported. RESULTS: The number of occupational asthma cases increased from 1986 until 1995, after which a downward trend, stabilizing during the last few years, has been observed. The majority of the cases (59%) in the beginning of the period (1986-1990) were associated with agriculture, but the percentage has fallen thereafter (42% of the cases in 1998-2002) along with the fall in the total number of cases. Since 1995, indoor moulds from water-damaged buildings have caused an increasing number of cases and have become the most important causative agents (0.5% cases, in 1986-1990 and 18% of the cases in 1998-2002). Chemicals have caused 10-30% of the cases, a decreasing number since 1990. The most important chemicals causing occupational asthma have been diisocyanates and welding fumes, followed by hairdressing chemicals and formaldehyde. CONCLUSIONS: The number of occupational asthma cases in Finland reached its height in the mid-1990s. The decrease in the number of total cases is because of the decrease in agriculture-associated cases, reflecting the number of employees in agriculture-associated occupations, which has greatly decreased since Finland joined the EU in 1995. An epidemic of mould-induced asthma, affecting mostly white-collar employees working in moisture-damaged buildings, has taken place since 1995.

Occupational asthma due to manual metal-arc welding of special stainless steels.

Occupational asthma (OA) can be induced by fumes of manual metal-arc welding on stainless steel. In recent years, the use of special stainless steels (SSS) with high chromium content has increased. This study presents two cases of OA caused by manual metal-arc welding on SSS. In both cases, the diagnosis of OA was based on respiratory symptoms, occupational exposure and positive findings in the specific challenge tests. In the first case, a 46-yr-old welder had experienced severe dyspnoea while welding SSS (SMO steel), but not in other situations. Challenge tests with both mild steel and stainless steel using a common electrode were negative. Welding SSS with a special electrode caused a delayed 37% drop in forced expiratory volume in one second (FEV1). In the second case, a 34-yr-old male had started to experience dyspnoea during the past few years, while welding especially SSS (Duplex steel). The workplace peak expiratory flow monitoring was suggestive of OA. Challenge tests with both mild steel and stainless steel using a common electrode did not cause bronchial obstruction. Welding SSS with a special electrode caused a delayed 31% drop in FEV1. In conclusion, exposure to manual metal-arc welding fumes of special stainless steel should be considered as a new cause of occupational asthma.

Occupational asthma in Finland.

In Finland occupational asthma caused by protein allergens and reactive chemicals present in the air of work environments is increasing. This communication describes provocative challenge tests and methods for measuring exposure under simulated work conditions. The importance of lung function measurements during non-exposure and placebo periods is stressed. Especially late reactions are difficult to assess because of the great circadian variation in the lung function parameters of asthmatics. For a positive challenge test, a decrease in peak flow values of at least 15% and a clear deviation from normal circadian variation and placebo periods is required. The allergens of vegetable or animal origin primarily affect patients with an atopic constitution. Chemical allergens seem to attack all exposed workers in the same way. The report lists the occupations with risk for asthma and refers to the population at risk; bakers seem to be the group with the most risk. The importance of early diagnosis, removal of the worker from exposure and improvement of the hygienic aspects of the work environment are stressed.

Formaldehyde asthma--rare or overlooked?

A total of 230 persons who had been exposed to formaldehyde and suffered from asthma-like respiratory symptoms were examined between January 1, 1977, and May 31, 1983. All the subjects had a bronchial provocation test with formaldehyde. On the basis of the medical and occupational history of the patients, the specific bronchial provocation test, and other test results, 12 cases were considered to be caused by specific sensitization to formaldehyde. All subjects had been exposed occupationally. An exposure period of between 1 mo and 19 yr preceded the onset of symptoms. Three persons displayed no bronchial hyperreactivity as assessed with a histamine or metacholine provocation test. Eleven of the 12 reactions were triggered by about 2.5 mg/m3 and one reaction by about 1.2 mg/m3 of formaldehyde. The late reaction in 1 patient was completely blocked by the inhalation of 100 micrograms of beclomethasone di-isoproprionate before the challenge with formaldehyde. Seventy-one of the 218 subjects who did not react when they were challenged with formaldehyde demonstrated bronchial hyperreactivity. We conclude that formaldehyde asthma, although apparently a rare disease, is under reported. Removal from exposure has a favorable effect on the symptoms. Low domestic exposures, however, may maintain the symptoms in individuals already sensitized.

Dentist's occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.

BACKGROUND: Allergic contact dermatitis (ACD) caused by (meth)acrylates (MA) is common in dental personnel. MAs have also caused asthma and rhinoconjunctivitis, but asthma, rhinoconjunctivitis and ACD caused by MAs in the same patient appears to be very rare. METHODS: Occupational asthma and rhinoconjunctivitis were diagnosed in a dentist according to patient history, PEF monitoring, and a work-simulated bronchial provocation test. ACD was diagnosed by skin-patch testing with MAs with the occlusive Finn Chamber-technique. RESULTS: The patient's skin-prick test reactions to common environmental allergens and MAs were negative. The total IgE was not elevated. Occupational asthma was diagnosed by a specific inhalation challenge test in which the patient handled liquid dental MAs for 30 min causing a delayed 23% reduction in FEV1. The provocation test also resulted in rhinoconjunctivitis. On patch testing, positive reactions were provoked by several MAs including 2-hydroxyethyl methacrylate (2-HEMA) to which the patient was occupationally exposed. The patient has not been able to continue her work with dental MAs. CONCLUSIONS: A case of occupational asthma, rhinoconjunctivitis and ACD caused by dental acrylate compounds is presented. Patients with respiratory hypersensitivity from MAs have to stop working with MAs, whereas patients with ACD from MAs need to avoid direct contact with MAs, but can often continue in their present job if they use no-touch techniques.

Occupational asthma due to stainless steel welding fumes.

Seven patients with respiratory symptoms after welding were examined. Five had occupational asthma caused by fumes from manual metal are stainless steel welding. The detailed clinical results of two patients with repeated challenge tests are reported. One patient was nonatopic and had earlier had contact dermatitis due to chromium. He experienced a non-immediate type of asthmatic reaction after welding stainless steel. The other patient was atopic and showed an immediate-type reaction. Both reactions were repeated in the second provocation test after about 2 years. In addition both disodium cromoglycate and beclomethasone pretreatments inhibited the reaction of the two patients, but a placebo medication did not. A remarkable amount of chromium and nickel are detected in the fumes released during stainless steel welding but not in the fumes from mild steel welding, with which all provocation tests were negative. The chromium or the nickel in welding fumes might be the aetiological factor of the reaction.

Experiences of specific IgE in asthma due to diisocyanates.

The specific IgE antibodies were studied with the Phadebas RAST technique in 35 patients with asthma due to diisocyanates. Two had been sensitized to toluene diisocyanate (TDI), 17 to methylene diisocyanate (MDI) and 16 to hexamethylene diisocyanate (HDI). In each case the diagnosis was confirmed with a bronchial provocation test (BPT). The asthmatic reaction was immediate in 17 cases, of which three had also a late reaction (dual). Eighteen patients reacted only with a late reaction. Seven (20%) had specific IgE to diisocyanates. All RAST-positive patients had an immediate asthmatic reaction. None of the late reactors and referents had positive RASTs. RAST inhibition tests with 94-100% inhibition confirmed the specificity of the method. There was cross-reactivity between different diisocyanates, however. The patients with positive RAST to diisocyanates had a higher level of total IgE than the RAST negative group and the referents.