Giuseppe Abbritti

Yellow nail syndrome: does protein leakage play a role?

Yellow nail syndrome is characterized by primary lymphoedema, recurrent pleural effusion and yellow discoloration of the nails. Although mechanical lymphatic obstruction is assumed to be the underlying pathology, it cannot explain the common finding of high albumin concentration in the pleural space. This paper describes a case of yellow nail syndrome presenting with the classical triad of lymphoedema, recurrent pleural effusion and yellow discoloration of the nails, associated with persistent hypoalbuminaemia and increased enteric loss of albumin. Based on the findings in this case and those in the literature, it is speculated that increased microvascular permeability may contribute to the pathogenesis of this syndrome.

Serum and salivary magnesium levels in migraine and tension‐type headache. Results in a group of adult patients

It has been suggested that magnesium plays a central role in different etiopathogenetic conditions involved in the onset of migraine. We measured, by atomic absorption spectrophotometry, serum and salivary magnesium levels in drug-free migraine patients with and without aura and in tension-type headache patients. Migraine sufferers with and without aura and tension-type headache had significantly lower levels of serum and salivary magnesium concentrations in the interical periods than a group of healthy young individuals. Serum magnesium levels tended to be further reduced during attacks in all patient groups studied. A statistically significant decrease in salivary magnesium levels was evident only for migraine patients with aura. Serum magnesium levels and to a lesser extent salivary magnesium levels might express indirectly the lowering of brain extracellular magnesium concentration which occurs in migraine patients both in the intererictal periods and ictally.

Red blood cell magnesium levels in migraine patients

In the last few years, it has been suggested that magnesium plays a central role in establishing a threshold for migraine attacks and in intervening with the pathogenetic mechanisms involved in their onset. Accordingly, we determined red blood cell magnesium levels in adult migraine patients with and without aura interictally and in some of them also ictally. In comparison with normal subjects, migraineurs with and without aura had significantly lower red blood cell magnesium levels in the interictal period. Ictal red blood cell magnesium levels did not differ from the interictal values. Low red blood cell magnesium levels could be a peripheral expression of the reduced brain magnesium concentration observed in migraine patients.

Work-related late asthmatic response induced by latex allergy

BACKGROUND The occupational uses of latex gloves may be associated with asthma. Hypersensitivity to latex has been shown to be IgE-mediated. The asthmatic reaction to latex is usually early; however, the natural history of latex asthma is still unknown. OBJECTIVE The purposes of this study were to investigate asthmatic responses induced by natural rubber latex and to assess the long-term respiratory consequences of latex-induced asthma after removal from exposure. METHODS This report describes the clinical and immunologic study of six nurses with work-related respiratory and skin disorders induced by the use of latex gloves. To determine whether the symptoms induced by latex gloves were IgE-mediated, we assessed latex IgE antibody levels by skin prick tests (SPTs) and RASTs with latex extracts. To confirm work-related latex reactions, we assessed respiratory symptoms, skin reactions, and FEV1 after a glove exposure test and an inhalation provocation test with latex gloves. All subjects were followed up for 7 months to 7 years after the first observation. RESULTS All subjects had positive SPT and RAST responses to latex extracts, positive double prick test responses to latex gloves, and negative SPT responses to cornstarch and common allergens. Ten atopic and 10 nonatopic control subjects had negative SPT responses to latex and cornstarch extracts and negative double prick test responses to latex gloves. In three subjects latex allergy was associated with allergy to fruit (banana and chestnut). After the glove exposure test, four of six subjects had contact urticaria, all had rhinoconjunctivitis, and two had a late asthmatic response. The inhalation provocation test was performed on four subjects: all had rhinoconjunctivitis, two had urticaria and late asthmatic response, and one had laryngeal edema. A late asthmatic response was recorded in four subjects. Three subjects continued to have chronic asthma, and four subjects had increased nonspecific bronchial responsiveness 7 months to 7 years after being assigned to duties not involving latex gloves. CONCLUSIONS This study of six nurses shows that latex is a potential cause of occupational asthma, rhinoconjunctivitis, and urticaria-angioedema. Latex seems to include antigens that elicit IgE-mediated hypersensitivity and may cause a late asthmatic reaction. Occupational asthma caused by latex may lead to permanent respiratory disability, even after removal from exposure.

Effect of corticosteroid treatment on interleukin-1 and tumour necrosis factor secretion by monocytes from subjects with asthma

Peripheral blood monocytes (PBM) may be activated in asthmatic patients, a condition usually reverted by corticosteroid (CS) treatment. In the present research we have evaluated the spontaneous or lipopolysaccharide (LPS)‐induced production of interleukin 1 (IL‐1) and tumour necrosis factor (TNF) by PBM obtained from 14 asthmatic subjects during an asthmatic attack and after 1 week of CS treatment. The control group included 20 healthy volunteers. PBM obtained during severe asthma showed a pattern of IL‐1 and TNF secretion similar to that of normal subjects. After CS treatment, IL‐1 levels did not change significantly in comparison to baseline values, while LPS‐induced TNF production was apparently related to the degree of airway obstruction after CS treatment. In fact, TNF production by PBM from CS‐responsive subjects was significantly decreased in comparison to the levels determined before CS treatment, while PBM from CS‐resistant subjects produced the same cytokine levels regardless of CS treatment. The present study suggests that the determination of LPS‐induced TNF secretion by PBM could be used to confirm the effectiveness of CS treatment in asthma.

Blood cadmium concentrations in the general population of Umbria, Central Italy

The aims of this study were (a) to assess blood cadmium (B-Cd) concentrations and to establish a tentative reference interval; (b) to identify significant determinants of B-Cd, in a population from Umbria, Central Italy, which was not occupationally exposed to cadmium (Cd). Four hundred and thirty-four healthy blood-donors volunteered to answer a questionnaire and provide a blood sample for B-Cd analysis, which was performed by graphite furnace atomic absorption spectrophotometry. Blood Cd concentrations ranged from non-detectable values, i.e. below 0.1 microgram/l up to 3.4 micrograms/l and were not normally distributed. The median values and the 95th percentiles were 0.7 and 2.0 micrograms/l, respectively. Concentrations of B-Cd were more than double in smokers than in non-smokers, median values being 1.1 micrograms/l and 0.5 microgram/l, respectively. In current smokers, B-Cd values correlated with the number of cigarettes smoked daily (rs = 0.40, P = 0.0001) and with the cumulative exposure to cigarette smoke (rs = 0.35, P = 0.0001). Concentrations of B-Cd correlated with age in the non-smokers, but not in the smokers and were significantly higher in women than in men only in the non-smokers. Both in smokers and non-smokers, B-Cd concentrations were similar in subjects living in urban or in rural areas. In the whole study population the lower and the upper tentative reference limit were < 0.1 and 2.2 micrograms/l, respectively, as computed by a non-parametric rank-based method. The upper limit was approximately double in smokers than in non-smokers (3.1 micrograms/l and 1.6 micrograms/l, respectively). Our results show that B-Cd concentrations in a general population from Umbria are in the range reported for general populations in Northern Italy and other European Countries. Smoking was the strongest determinant of B-Cd concentrations and age had a lesser effect.

Asthma caused by live fish bait.

BACKGROUND Larvae of insects and worms are commonly used as live fish bait (LFB) by anglers. Asthma, rhinoconjunctivitis, and urticaria related to various kinds of LFB have been reported. METHODS We studied 14 subjects with respiratory symptoms associated with exposure to LFB. Skin prick tests and RASTs with Lucilia caesar, Galleria mellonella, and Tenebrio molitor extracts were carried out in all subjects. Monitoring of peak expiratory flow rate and evaluation of bronchial responsiveness to methacholine before and after exposure to LFB were performed in seven subjects. RESULTS Thirteen subjects had asthma, all 14 had rhinoconjunctivitis, and three had contact urticaria. Eleven subjects had respiratory symptoms after fishing with LFB, and the other three subjects had symptoms during their work in a commercial fish bait farm. Positive skin prick test results or significant RAST binding to L. caesar extract were observed in 13 subjects, to G. mellonella extract in four subjects, and to T. molitor extract in three subjects. After exposure to LFB, two subjects had an early asthmatic response, three had a late asthmatic response, and two had no asthmatic response. Late asthmatic response was associated with a long-lasting increase in bronchial responsiveness. CONCLUSIONS This study demonstrates that emanations from LFB are sensitizers, which have the potential to elicit IgE-mediated asthma. Exposure to LFB is common and LFB should be considered as a possible sensitizing agent for asthma.

Silica and Its Antagonistic Effects on Transforming Growth Factor-β in Lung Fibroblast Extracellular Matrix Production

Background Silicosis, a pneumoconiosis marked by interstitial pulmonary fibrosis, is caused by inhalation of free crystalline silica particles. When silica particles are injected into the lower lung, they are translocated across the epithelium into the interstitial space, where macrophage-derived growth factors affect lung fibroblast proliferation and collagen deposition. We hypothesized that silica may act directly on pulmonary fibroblasts modifying extracellular matrix (ECM) synthesis and that the effects of silica may be mediated by transforming growth factor-β (TGFβ) overproduction. Methods To test this hypothesis, we studied a human lung fibroblast cell line (WI-1003) exposed to silica in vitro. We investigated cell morphology by electron microscopic procedure, cell growth, collagen production, and glycosaminoglycans (GAG) composition by radiolabeled precursors. Cytokine and growth factor synthesis were evaluated by specific enzyme-linked immunoadsorbent assay kits and Northern blotting analysis. Results Pulmonary fibroblasts internalized silica particles without detectable cell damage. Silica directly stimulated collagen synthesis and decreased the amount of 3H-glucosamine-labeled GAG. Silica-treated fibroblasts secreted less TGFβ than untreated controls, antagonized the stimulatory effect of TGFβ on ECM synthesis, and reversed TGFβ-induced inhibition of cell proliferation. Northern blotting analysis showed increased interleukin-1α (IL-1α) mRNA after silica treatment. IL-1α had no influence on collagen synthesis but increased the number of WI-1003 fibroblasts. Conclusions These results support our hypothesis that lung fibroblasts are direct silica targets. However, contradicting our hypothesis, silica antagonized TGFβ activities through a TGFβ downregulation and an IL-1α upregulation. The complex pattern of TGFβ and IL-1α regulation in pulmonary fibroblasts is imbalanced by silica exposure and might play a key role in silica-mediated pulmonary fibrosis.

Systemic nicotine exposure in tobacco harvesters

Abstract Several epidemics of nicotine intoxication have been described among tobacco harvesters; however, little is known about nicotine absorption under typical working conditions. To assess systemic nicotine absorption during a regular working shift, the authors performed an observational field study. Included in the study were 10 healthy, nonsmoking, female tobacco harvesters and a control group of 5 healthy, nonsmoking, female hospital workers. Nicotine and cotinine were measured in sequential samples of blood and urine during a regular workshift. Blood nicotine levels rose from a nadir value of 0.79 ± 0.12 ng/ml to a peak value of 3.45 ± 0.84 ng/ml (p < .05 [Tukeys modified t test]) in the exposed group. In the control group, levels were stable at 0.1 ± 0.1 ng/ml (p < .01). Moreover, the mean blood nicotine level measured 3 mo following the end of exposure in 6 of 10 exposed subjects was 0.24 ± 0.12 ng/ml (p < .01). Corresponding higher values of urine nicotine and urine cotinine were observed in the exposed versus control group (comparative P values were < .01 and < .05, respectively). Overall, tobacco harvesters absorbed approximately 0.8 mg of nicotine daily. Given that nicotine can induce adverse health effects, the authors believe that prevention of nicotine absorption in tobacco harvesters should be sought and that workers should be informed about occupational risks.

Long-term pulmonary and systemic toxicity following intravenous mercury injection

Abstract Long-term pulmonary and systemic toxicity following mercury intravenous injection has rarely been assessed. We present the results of a detailed investigation assessing pulmonary and systemic long-term toxic effects in a subject who had pulmonary and systemic mercury microembolism diagnosed more than 11 years previously. Radiographic examination showed the persistence of mercury microemboli in both lungs and elsewhere␣in the body. Lung function tests revealed a decreased diffusing capacity for carbon monoxide and Po2 probably indicative of microscopic inflammation of lung interstitium. Electroneuromyography showed signs of mild axonopathy in both legs. At semen analysis, a high proportion of motionless spermatozoa was present. Urinary excretion of mercury was high. Signs of interstitial lung impairment, peripheral axonopathy and asthenozoospermia in a subject who had mercury microembolism persisting for more than 11 years might be evidence of long-term mercury toxicity.