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Biomedical subjects

D Vervloet

Publications and source records attributed to D Vervloet.

At least 217 records · Page 12Linked to original sources

Aspirin intolerance and asthmal induction of a tolerance and long-term monitoring.

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.

Adult↗

[Diffuse familial interstitial pulmonary fibrosis. Study of a family].

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...

Bronchi↗

Seasonal increase of carbachol airway responsiveness in patients allergic to grass pollen. Reversal by corticosteroids.

By measuring airway resistance (Raw) as an index of response, dose-response curves to aerosolized carbachol were constructed in 10 patients suffering from grass pollen allergy. The subjects were first tested before the pollen season (March). During the pollen season (May and June), another control test was performed; the patients were then treated (double blind and at random) with placebo or methylprednisolone (16 mg/day given orally) for 7 days and then retested. After a 10-day interval devoid of treatment, the 2 treatments were crossed over and a fourth carbachol test was performed. Baseline function values were comparable for all 4 tests. In all but one subject (who was a smoker), carbachol increased Raw by more than 150% over baseline for each of the 4 tests. In these 9 patients, carbachol responsiveness significantly increased during the pollen season and returned to its preseason level after corticosteroid treatment. The data suggest that airway inflammation was responsible for the seasonal increase in airway reactivity.

Adolescent↗

Induction of late cutaneous reaction by kallikrein injection: comparison with allergic-like late response to compound 48/80.

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.

Biopsy↗

Anaphylactic reactions to modified fluid gelatins.

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.

Adult↗

Adverse reactions to suxamethonium and other muscle relaxants under general anesthesia.

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.

Adult↗

In vitro evaluation of blocking antibodies by RAST interference during pollen desensitization: role of the IgG fraction.

RAST interference was used to study the changes in blocking antibodies during hyposensitization. At the onset of desensitization blocking antibodies levels were correlated to IgE antibody titers. They progressively rose during the treatment. IgG isolated by adsorption onto protein A Sepharose were only a part of blocking antibodies. The isolated antibodies gave 80% of RAST interference values. Results showed that RAST interference may be used routinely to determine changes of immunological parameters of immunotherapy.

Adult↗