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BACKGROUND:

We aimed to determine the prevalence of contact sensitization in the general population and to investigate associations with important sociodemographic and medical characteristics.

METHODS:

Within a population-based nested, case-control study in Germany, we performed patch tests with 25 standard allergens in 1141 adults (50.4% female, age median 50 years). Additional information was obtained by a dermatologic examination, a standardized interview, and blood analysis.

RESULTS:

At least one positive reaction was exhibited by 40.0% of the subjects, with reactions most frequently observed to fragrance mix (15.9%), nickel (13.1%), thimerosal (4.7%), and balsam of Peru (3.8%). Women were sensitized more often than men (50.2% vs 29.9%, OR 2.36, CI 1.84-3.03), and this was also significant for fragrance mix, nickel, turpentine, cobalt chloride, and thimerosal. Contact sensitization was more frequent in subjects who reported adverse skin reactions (53.8% vs. 32.6%; OR 2.41, CI 1.85-3.14), and this was particularly true for sensitization to nickel (45.5% vs 8.8%, OR 8.64, CI 5.67-13.17) and fragrance mix (29.0% vs 14.0%, OR 2.51, CI 1.60-3.91) and the corresponding intolerance of fashion jewelry and fragrances. Contact sensitization decreased with increasing degree of occupational training (unskilled 45.9%, apprenticeship 40.1%, technical college 40.4%, and school of engineering 12.5%; P=0.023; trend test P=0.042). Significant associations of contact sensitization and presence of allergen-specific IgE antibodies, atopic eczema, or psoriasis were not observed. Frequency estimates for the general adult population based on these findings were 28.0% for overall contact sensitization and 11.4% for fragrance mix, 9.9% for nickel, and 3.2% for thimerosal.

CONCLUSIONS:

It is concluded that contact allergy is influenced by sociodemographic parameters and plays an important role in the general population.

Purpose:

To determine the incidence, risk factors, and morbidity for osteonecrosis (ON) in children with acute lymphoblastic leukemia (ALL) treated with intensive chemotherapy including multiple, prolonged courses of corticosteroid.

PATIENTS AND METHODS:

The occurrence of symptomatic ON was investigated retrospectively in 1, 409 children ages 1 to 20 years old receiving therapy for high-risk ALL on Children’s Cancer Group (CCG) protocol CCG-1882.

RESULTS:

ON was diagnosed in 111 patients (9.3% +/- 0.9%, 3-year life-table incidence). The incidence was higher for older children (> or = 10 years: 14.2% +/- 1.3% v < 10 years: 0.9% +/- 0.4%; P: <.0001), especially females 10 to 15 years old and males 16 to 20 years old (19.2% +/- 2.3% and 20.7% +/- 4.7%, respectively). In patients 10 to 20 years old, the incidence of ON was higher for females versus males (17.4% +/- 2.1% v 11.7% +/- 1.6%, respectively; P: =.03) and for patients randomized to receive two 21-day dexamethasone courses versus one course (23.2% +/- 4.8% v 16.4% +/- 4.3%, respectively; P: =.27). Among ethnic groups, whites had the highest incidence and blacks the lowest, with other groups intermediate (16.7% +/- 1.4% v 3.3% +/- 2.3% v 6.7% +/- 2.2%, respectively; P: =.003). There was no difference in event-free survival in patients with or without ON. ON was diagnosed within 3 years of starting ALL therapy in all but one patient, involved weight-bearing joint(s) in 94% of patients, and was multifocal in 74% of patients. Symptoms of pain and/or immobility were chronic in 84% of patients, with 24% having undergone an orthopedic procedure and an additional 15% considered candidates for surgery in the future.

CONCLUSION:

Children ages 10 to 20 years who receive intensive ALL therapy, including multiple courses of corticosteroid, are at significant risk for developing ON.

The nomination of amide local anesthetics by a private individual is based on their widespread use in dentistry, general medicine, surgery, and in some consumer products (e.g., topical skin preparations). The amide local anesthetics bupivacaine, etidocaine, lidocaine, mepivacaine, and ropivacaine metabolize to 2,6-xylidine and 4-hydroxyxylidine. Prilocaine metabolizes to o-toluidine. Both 2,6-xylidine and o-toluidine have been shown to be carcinogenic in laboratory animals in NTP studies. Two other amide local anesthetics, pyrrocaine and trimecaine, that were considered for inclusion in this report were excluded after it was found that they are not used in the United States. For these reasons, the local anesthetics reviewed in this report are bupivacaine, etidocaine, lidocaine, mepivacaine, prilocaine, and ropivacaine.

BACKGROUND:

In the medical community, little is known regarding bone marrow necrosis (BMN) as a clinicopathologic entity, although to the authors’ knowledge it was described for the first time more than 50 years ago. To identify the rate of prevalence, the symptoms and signs, the underlying disease associations, and the usefulness of diagnostic procedures, an extensive literature search was made.

METHODS:

Only cases identified as extensive necrosis and diagnosed during life were selected. Two hundred forty cases met these criteria.

RESULTS:

Bone pain (75%) and fever (68.5%) were the most important symptoms, whereas anemia (91%) and thrombocytopenia (78%), associated with a leukoerythroblastic picture (51%), were the most frequent hematologic abnormalities. Nearly 50% of patients showed elevated lactate dehydrogenase and alkaline phosphatase levels. In 90% of the patients an underlying malignancy was identified.

CONCLUSIONS:

Bone marrow necrosis is caused by hypoxemia after failure of the microcirculation. Given the high rate of malignancy as an underlying disease association, an extensive search for neoplastic disease is justified whenever BMN is diagnosed. Pancytopenia and embolic processes are major complications that should be managed with supportive measures until effective treatment of the underlying disease has been administered. When necrosis resolves, repopulation of the bone marrow cavity with normal hematopoiesis is observed.

Dysbaric osteonecrosis is associated with exposure to large ambient pressure changes, and comprises necrotic lesions in the fatty marrow-containing shafts of the long bones, and the ball and socket joints (hips and shoulders). The fundamental causes are still in question and the illness remains a significant health hazard. Radiological and pathological features of both dysbaric and non-dysbaric osteonecrosis are indistinguishable and both are characterized by intramedullary venous stasis, ischemia and necrosis of bone. It has been generally accepted that gas bubbles (probably by initiating intramedullary venous stasis) are the prime cause of dysbaric osteonecrosis, as well as being responsible for Type 1 Decompression Sickness or ‘the bends’. Importantly, however, not all series have found a correlation between dysbaric osteonecrosis and ‘the bends’. Thus even though it is likely that gas bubbles remain the prime cause of dysbaric osteonecrosis, workers have proposed that in some cases there is another etiological factor which may exaggerate the pathologic effects of gas bubbles, making the bone more susceptible to necrosis. It is proposed that rapid compression by impeding venous drainage from bone initiates intramedullary venous stasis. In the presence of intramedullary gas bubbles, this may progress to thrombosis, ischemia and bone necrosis. The review offers an explanation for total sparing of the knee joint in dysbaric osteonecrosis, and sole involvement of the hip and shoulder (in terms of sub-articular lesions and subsequent joint collapse). In addition to continued observance of proper decompression procedures, a slower rate of compression may further reduce the incidence of dysbaric osteonecrosis. Bone death or osteonecrosis is a concept which Hippocrates put forward in antiquity (1), but it was not until 1794 that James Russell of Edinburgh wrote the first modern-day descriptions. In these cases infection was the predominant etiology (1,2). In 1888 Konig described necrosis of the adult femoral head without infection (3) (aseptic necrosis of bone) and in the same year Twynam reported a case of osteonecrosis in a caisson worker (4) in which there was still a significant infective component. In 1911 Bornstein and Plate, followed later and independently by Bassoe in 1913, presented radiological confirmation of aseptic necrosis of bone in compressed air workers (5). The first report of aseptic necrosis in an underwater diver subsequently appeared in 1936 (6). The condition of aseptic necrosis of bone in association with exposure to raised ambient pressure (previously referred to as caisson disease, pressure-induced osteoarthropathy (7), ‘bone rot’ (8) and other synonyms (6)) is now generally known as dysbaric osteonecrosis (6). Despite detailed examination of this problem by many authorities, dysbaric osteonecrosis still remains a significant occupational hazard with serious medico-legal consequences (5-13). This suggests that preventative measures are being based upon an incomplete understanding of the pathophysiology of the disease, and that other etiological factors are perhaps being overlooked.