Biomedical subjects
Publications and source records attributed to J Charpin.
Systemic anaphylactic reaction with shock was observed after ingestion of an antipyretic combination product containing quinine. That quinine was responsible for the reaction was proven by immediate skin tests and by oral challenge tests. The demonstration of specific IgE's by a radioallergosorbent test (RAST) provided evidence for an immediate hypersensitivity mechanism.
In an earlier study we confirmed the usefulness of intradermal skin tests and histamine release in diagnosis of patients reactive to muscle relaxants, and we suggested an IgE-mediated reaction rather than an idiosyncratic mechanism. In a later study, we studied the relationship between (Formula: see text) that is one of the muscle relaxants producing the most frequent adverse reactions under anesthesia. Histamine release was measured in five patients with increasing concentrations of suxamethonium in the presence or absence of human serum albumin in Tris buffer. Suxamethonium by itself without any carrier in the buffer could, in vitro, act as a true allergen on target leukocytes in the sensitized patients' group. Acetylcholine (20 and 200 micrograms/ml) did not induce significant histamine release in five patients with positive histamine release in the presence of suxamethonium. Preincubation of leukocytes from 11 patients for 30 min with 20 and 200 micrograms of acetylcholine in Tris albumin CA++ Mg++ buffer decreased the histamine release induced by suxamethonium (10 micrograms/ml); mean maximal histamine release of 46% +/- 4.2 was reduced to 31.4 +/- 5.8 and 7% +/- 4 (p less than 0.001), respectively. However, in eight control subjects similar concentrations of acetylcholine did not change the maximal histamine release induced by anti-IgE (0.2 micrograms/ml). In the same way acetylcholine did not modify histamine release induced by Dermatophagoides pteronyssinus extract (1/10,000 w/v) in six patients allergic to this allergen. This study suggests that suxamethonium acts as a true allergen and that acetylcholine or one of its metabolites may act as a hapten inhibitor in the model of histamine release induced by suxamethonium.(ABSTRACT TRUNCATED AT 250 WORDS)
IgE antibodies cross-reacting with choline and suxamethonium were found in the sera of 15 of 22 patients with life-threatening sensitivity to suxamethonium, one of the most commonly used muscle relaxants. Furthermore, choline that is one of the metabolites of acetylcholine and a monovalent part of the suxamethonium molecule could act as a hapten inhibitor in vitro and in vivo, blocking specifically the basophil histamine release induced by suxamethonium and the positive skin tests to the drug in allergic patients. These results confirm the IgE dependency of allergic reactions to suxamethonium and suggest a possible way of preventing such reactions with choline.
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Acetylsalicylic-acid (ASA) intolerance is well recognized as a possible cause for exacerbating asthma. It has been postulated that if this could be overcome, long-term aspirin administration could improve asthma symptoms and enable reduction of the use of other anti-asthmatic drugs. We succeeded in inducing an ASA tolerance in nine corticosteroid-dependent asthmatics, and this tolerance lasted at least 1 month and at most 1 year. Progressive deterioration in lung function was seen, however, in all patients taking ASA for more than 1 month, unless the corticosteroid intake was increased. These results suggest that ASA long-term treatment is of no help to severe corticosteroid-dependent, ASA-sensitive asthmatics. This conclusion differs from other reports on ASA intolerance in asthma.
The objectives of this study, in which Almitrine bismesylate was administered for one year in chronic bronchitics with obstructive hypoxia, were to assess its clinical and gasometric efficacy and its clinical, laboratory, spirometric and electrocardiac acceptability. The blood gas results show a significant rise in PaO2 (p less than 0.001) rising by 5.5 mmHg after 6 months (T6) and by 6.0 mmHg after 12 months (T12) in comparison with the value at the study's onset. The PaCO2 fell by 3.3 mmHg at T6 and 2.7 mmHg at T12 (p less than 0.001). The dyspnoea of the patient, scored by the doctor on a scale of severity from 0 to 5 was situated on a mean of 3.3 points at the beginning of the study. It was significantly reduced by 0.8 points at T6 and by 0.9 points at T12 (p less than 0.001). The percentage of patients hospitalised during the course of the study fell significantly in comparison with the previous year, from 68% to 49% (p less than 0.001). The improvement in clinical status and in blood gases bore no relation to changes in respiratory function. The clinical acceptability of the product was good; few side effects were observed and the respiratory, digestive and neurological problems were often pre-existing. They only led to cessation of treatment in three cases. The electrocardiogram was unchanged. The laboratory investigations was unchanged, with the exception of a fall in red blood cells in relation to the correction of the hypoxaemia in polycythaemic patients.
A study of the genealogy of a 53 year old lady (A.M...) suffering from diffuse interstitial pulmonary fibrosis (FID) has revealed several cases of FID in her forbears and relations. Two brothers of A.M... died of histologically proven FID; FID was also discovered in one of their daughters. A sister died young of some unclassified respiratory problem. Two cousins died likewise at a young age of acute FID proven histologically. The level of spontaneous pneumothorax was particularly elevated in this family which represented a clinical peculiarity when compared to sporadic FID. The most probable mode of transmission of familial FID is autosomal dominant with variable penetrance. The HLA group seen in A.M... showed the A2 and B12 alleles. The B12 allele was also present in the niece of A.M...
In recent years associations have been reported between male infertility and chronic pulmonary infections. These disorders include immotile-cilia syndrome, cystic fibrosis and Young's syndrome. For each disorder, case reports or small groups of patients have been described. However, it remains to be determined if these congenital disorders play a significant role in primary bronchiectasis (P.B). To do this, we compared the fertility rate of 35 patients (24 males, 11 females) with clinical and radiological evidence of P.B. and of 71 patients (54 males, 17 females) with secondary bronchiectasis (S.B) due to a defined chest disease (mainly tuberculosis and chronic bronchitis with emphysema). We abstracted the clinical records of this group of 106 patients, hospitalized between 1966 and 1983 for: age at the time of hospitalization, sex, diagnosis (P.B. vs. S.B.), association with sinusitis and situs inversus, socio-economic status, ethnic group, marital status and fertility (graded as 0 or 1+). The crude association between P.B. and infertility is strong (p greater than 0.10). However age may represent a confounding factor as patients with P.B. are younger (p less than 0.01) than patients with S.B., and more often single (p less than 0.01). Initially we restricted the analysis to married patients of both groups, and still got a significant association. Then we compared mean age in childless married people of both groups and observed a non-significant difference. Moreover, when we compared fertility in older patients, for example in people over 30 years old, the association still persists (p less than 0.03). In conclusion, the congenital disorders associating bronchiectasia and infertility must be looked for in the check up of P.B., all the more so as some can be cured of their infertility.
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Eleven patients with severe bronchopulmonary infection due to Pseudomonas were treated with azlocillin in doses of 250 mg/kg/day. Severe preexisting respiratory diseases, such as bronchopulmonary carcinoma, bronchiectasis or respiratory insufficiency were present in all cases. All patients had been unsuccessfully treated with various antibiotics before they received azlocillin. The pathogenicity of the isolates was assessed by germ counts in sputum. Comparative in vitro sensitivities to carbenicillin and azlocillin were determined by the disc method and by measurement of the minimum inhibitory concentrations in liquid medium. All strains of Pseudomonas aeruginosa isolated were sensitive to azlocillin with minimum inhibitory concentrations of 0.5 to 64 micrograms/ml. When tested against carbenicillin, 4 of the strains were resistant and 1 had intermediate sensitivity. The carbenicillin/azlocillin minimum inhibitory concentrations ratio was usually equal to 4. Clinical results were satisfactory in 7 cases; inadequate response or failure was observed in 4 cases and attributed to the replacement of Pseudomonas by another pathogen (Proteus morganii or Klebsiella pneumoniae). This study suggests that azlocillin is of value in the treatment of bronchopulmonary infections caused by Ps. aeruginosa.
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The airborne fungal flora was studied in different departments of a hospital by using a slit sampler (Casella, London) where the measured volume of air is impacted to the surface of culture medium contained in Petri dishes. Colonies were counted after 3 days incubation at 25 degrees C and 37 degrees C. Many species of hyphomycetes were identified. The main fungi isolated were Cladosporium sp (especially C. cladosporioides), Penicillium sp., Alternaria alternata, Aspergillus sp. (A. flavus, A. niger, A. fumigatus). The results show that the variability of the spore number is related to the ventilation. The number of spores found indoors seemed proportional to those present outdoors in naturally ventilated rooms. The results are quite different in the air-conditioned wards. Also, there might be a correlation between the counts and the activity and occupation of wards.
Although IgE antibody is able to provoke a late cutaneous allergic response (LCAR), the mechanism of its development is not clear. It seems to involve vasoactive and clotting mediators released from mast cells and basophils. Substances biologically similar to plasma kallikrein (KK), a Hageman factor activator, have been shown to be released by basophils in the course of an IgE-dependent reaction. Because compound 48/80 induces LCAR-like responses in the skin, we compared the ability of tissue KK and compound 48/80 to induce late cutaneous reactions (LCRs). All 40 test subjects showed an immediate wheal and flare reaction (WF) after both KK and 48/80. The WF was followed by an LCR characterized by diffuse edema, pain, and erythema in 36 of 40 subjects with 48/80 and 26 of 40 with KK. The LCRs evoked by the two agents did not differ in their appearance or in their time of development. These reactions increased until the 5 hr mark, began to decrease at the 10 hr mark, and were gone after 24 hr. Histologic study showed edema and a mixed cell infiltration with fibrin deposition. Challenge of the original injection site and a new site after 1 or 2 wk showed a local refractory state lasting 2 wk. Prednisone almost totally suppressed the LCRs induced by both KK and 48/80.
Use of modified fluid gelatins as a plasma expander is of interest in human clinical medicine due to osmotic pressure similarities with plasma proteins. However, adverse reactions such as urticaria, edema, and/or anaphylactic shock occur and can lead to diagnostic problems. In addition, mechanisms of these reactions are poorly understood. We report three cases of anaphylactic shock studied by skin tests and, for the first time, in vitro leukocyte histamine release (LHR). Intradermal skin tests were significantly positive for concentrations of 1:1000 to 1:10 of the commercial preparation used before the reaction in each patient. Thirty control subjects were negative even for the undiluted preparation. Positive LHR was obtained from patients' leukocytes washed and then incubated in Tris-albumin Ca++ Mg++ buffer with serial dilutions of fluid gelatins; controls were negative. Addition of D2O (50%) caused significant increase of LHR in patients but had no effect on controls. In conclusion, skin tests and LHR might be valuable in diagnosis of patients reactive to gelatins. Furthermore, these findings suggest release of mediators from mast cells or basophils, but discrimination between immunologic and idiosyncratic pharmacologic mechanism was not obtained.
The mechanisms of anaphylactic reactions to muscle relaxants under general anesthesia are not completely understood. Extending an earlier study, we report 41 cases of anaphylactic shock investigated by intradermal skin tests with muscle relaxants (suxamethonium, pancuronium, gallamine, nortoxiferine), in vitro leukocyte histamine release, and Prausnitz-Küstner tests. Intradermal tests were significantly positive at concentrations ranging from 10 to 10(5) times less than those in controls. Reproducibility tested for suxamethonium at a 1-year interval in five patients was good. Histamine release induced by muscle relaxants in Tris-albumin-Ca++-Mg++ buffer showed positive results in 8/25 instances and was inhibited by antigen excess in seven cases. Addition of 50% deuterium oxide (D2O) caused significant increase of histamine release in positive cases and induced release in all five negative cases studied. Muscle relaxant-induced histamine release was inhibited by in vitro anti-IgE leukocyte desensitization. The mean maximal histamine release dropped from 58.2% +/- 9.7 to 5.8% +/- 2 (p less than 0.01). Similarly, leukocyte desensitization also inhibited histamine release induced by anti-IgE but not by formyl-L-methionyl-L-leucyl-L-phenylalanine or poly-L-arginine. Prausnitz-Küstner tests were positive in five out of 21 cases studied and became negative after heat inactivation. These results confirm the usefulness of intradermal skin tests in diagnosis of patients' reaction to muscle relaxants and suggest an IgE-mediated rather than an idiosyncratic mechanism.