[Chondritis of the ears in a patient with primary antiphospholipid syndrome].
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Biomedical subjects
Publications and source records attributed to S Ollier.
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BACKGROUND: Allergen challenge of subjects with asthma produces an early asthmatic response, late asthmatic response, and increases bronchial responsiveness. Histamine partly mediates the early asthmatic response, and may play a role in late-phase responses. Azelastine has antiallergic properties and has been proposed as a treatment for asthma. We therefore investigated the contribution of histamine to late-phase responses with the use of the potent H1-receptor antagonist azelastine. METHODS: Ten subjects with atopic asthma were studied in a double-blind, randomized, placebo-controlled trial. Azelastine was administered over 4 days before allergen challenge. Changes in airway caliber were followed with measurements of forced expiratory volume in 1 second, and changes in bronchial responsiveness were followed by methacholine and prostaglandin D2 bronchial provocation tests. RESULTS: Azelastine significantly inhibited the development of the early asthmatic response. Azelastine had no effect on the late asthmatic response or on the development of allergen-induced increases in bronchial responsiveness. The power of the study was sufficient to have had a high probability of detecting any important differences between placebo and azelastine during the late phase. CONCLUSIONS: Azelastine had no significant effect on the late-phase response model of asthma. This study does not support the hypothesis that histamine is an important mediator of the late asthmatic response or allergen-induced increases in bronchial responsiveness.
Licorice abuse is a wellknown cause of high blood pressure, myopathy, and cardiac rhythm trouble. It should be considered as a cause of diffuse acute edema, as shown in the three following case-reports.
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In our Internal Medicine department, we conducted a retrospective study of prognostic factors in patients with malignant hypercalcaemia. The records of 51 patients who had both hypercalcaemia and a histologically proven cancer were analyzed; 42 had a solid tumour and 9 had a myeloma. In 61% of the patients cancer had been revealed by hypercalcaemia. The main warning signs were alteration of the general condition (68.6%), pain in the bones (54.9%) and polyuria with dehydration (58.8%). Osteolysis was observed in 75% of the cases. The overall median survival was 86 days. Patients with myeloma had a significantly longer survival than patients with other tumours (312 versus 60 days; p < 0.05). Patients who had received a causal treatment had a longer survival (176 versus 36 days, p < 0.001). In patients with solid tumours we found a negative correlation between survival and initial calcaemia, and a positive correlation between phosphoraemia, albuminaemia and survival. Multivariate analysis showed that the initial calcaemia level and the possibility of causal treatment were the two cardinal prognostic factors. Although the overall survival rate is mediocre, we believe that hospitalization of patients with malignant hypercalcaemia is justified for their better survival comfort and for the possibility of discovering a neoplasia that could benefit from an effective causal treatment, which is the principal factor of improved prognosis.
Among 8 of the 20 records of primary hyperparathyroidism examined in search of neurological and/or psychiatric manifestations, the authors extracted 5 clinical cases reported here. These 5 cases were selected because these manifestations had been well evaluated before and after curative surgery of the disease. Among the manifestations reported, there was one corpus striatum syndrome, one cervical myelopathy and three cases of "chronic" psychiatric disorders of several years duration completely cured after parathyroidectomy. The authors underline that such psychiatric disorders should be taken into account in the discussion of treatment.
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The effect of single dose topical nasal therapy with azelastine hydrochloride (azelastine) on the response of nasal airways resistance (NAR) to provocation testing was studied in 36 patients with seasonal allergic rhinitis. Nasal provocation testing (NPT) with histamine or grass pollen was performed after a single dose of azelastine, 0.28 mg to each nostril, or placebo. NAR was assessed by rhinomanometry for 10 hr following NPT. Compared to placebo the NAR response to histamine was inhibited at both 1 and 2 hr following azelastine administration, significant at 1 hr (P less than 0.02) and 2 hr (P less than 0.0001). No such effect was observed in relation to allergen-induced changes in NAR. Azelastine also inhibited numbers of sneezes for up to 10 hr following both histamine NPT (P less than 0.02) and allergen NPT (P less than 0.05), when compared to placebo. Forty-seven per cent of participants experienced bitter or unpleasant taste sensations after azelastine administration but no other unwanted effects were clearly related to azelastine therapy.
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The aim of this study was to reduce the side effects of corticosteroid therapy responsible for high morbidity in giant cell arteritis. Nine patients were admitted consecutively for temporal arteritis (7 cases) or polymyalgia rheumatica (2 cases) without ocular involvement (mean age: 69.3 years; positive temporal biopsy: 6 cases). The following protocol was used: methylprednisolone, 500 mg/d, i.v., for 3 consecutive days, then low doses (an average of 22.5 mg/d) of prednisone or an equivalent drug. The mean length of follow-up was 15.1 months (range: 6-22 months). The mean lapse of time until the erythrocyte sedimentation rate returned to normal was 10.6 days (range: 3-30 days). The mean dose of prednisone or an equivalent drug at 6 months was 13 mg/d (range: 5-22.5 mg/d). One patient was cured after 17 months of treatment. Another suffered a biological relapse after 13 months of treatment. All the other patients were asymptomatic with no biological signs of an inflammatory syndrome. The complications included: electrocardiogram modifications without necrosis during pulse therapy in 1 woman; unstable angina developed 2 months after the onset of treatment in 1 man; recurrent urinary infections in 1 predisposed male patient. No bone or metabolic side effects have been noted to date. We think that 3 days of intensive intravenous corticotherapy followed by low doses of corticoïds per os constitute an effective and well-tolerated regimen. Additional studies including comparison with conventional treatments should be carried out to confirm these results and, even better, to evaluate the long-term benefits of this protocol in terms of side effects.
In a randomized, double-blind placebo-controlled study we investigated the effect of single oral doses of 8 mg azelastine and 2 mg ketotifen on the immediate response to platelet-activating factor (PAF) inhalation and to increasing doses of PAF injected intradermally. Bronchial provocation with 100 micrograms of PAF resulted in marked bronchoconstrictor responses, but neither azelastine nor ketotifen had any significant effect on these responses. Intradermal injection of PAF (100, 200 and 400 ng) resulted in a dose-related weal and flare response. Azelastine and ketotifen both caused significant reductions in this response (P less than 0.002-P less than 0.01). There was no significant difference between the effect of the two drugs.
We report a case of thrombo-embolic disease in which we were able to detect the presence of serum antiphospholipid auto-antibodies. The existence of antiphospholipid auto-antibodies has already been described in cases of recurrent thrombo-embolism. The thrombogenic role is only partially explained, but would for the greater part be linked to an action on the fibrolytic activity of the vascular parietal wall. Amongst these antibodies one can find amongst others VDRL, antiprothrombinase and anticardiolipin. The association of other stigmata of auto immunity is not rare, especially disseminated lupus erythematosus (LED). When phospholipids are found in an isolated fashion in cases of recurrent thrombo-embolism they produce the syndrome of antiphospholipids. The long term prognosis of this syndrome has not yet been established but the risk of a secondary systemic disease developing justifies a clinical follow up and regular blood checks.
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