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Biomedical subjects

M H Lessof

Publications and source records attributed to M H Lessof.

At least 55 records · Page 3Linked to original sources
PubMed1985

Type I allergy to egg and milk proteins: comparison of skin prick tests with nasal, buccal and gastric provocation tests.

Provocation tests with egg or milk antigens were performed on symptomatic patients or those who were skin prick test positive to these antigens. Skin test positive patients responded immediately in 12/13 to nasal, in 7/15 to buccal and in 5/15 to gastric provocation tests. An immediate gastric response was within 1 h. The threshold dose for a positive result showed that tissue sensitivity from greatest to least was in the order: skin, nasal, buccal and gastric. None of the skin test negative group responded to any of the provocation tests. The results, particularly the nasal provocation, validate the skin prick test as a sensitive measure of type I allergy to defined foods. The relative insensitivity of buccal and gastric mucosae may explain positive skin test responses in asymptomatic subjects.

Dose-Response Relationship, Immunologic↗
PubMed1985

Food intolerance.

Food intolerant symptoms can have various causes, including enzyme deficiencies (of lactase or aldehyde dehydrogenase) and pharmacological effects (e.g., caffeine, salicylates). The irritable bowel syndrome can also be associated with intolerance to specific foods in some cases, but the mechanism is unclear. Immunological causes are less common but may explain the small bowel mucosal changes associated with gluten enteropathy, as well as the childhood enteropathy provoked by cow's milk or, rarely, by other foods. Food allergy of the more immediate and classical type is associated with reactions both within and outside the gastrointestinal tract. Where these include urticaria, asthma and eczema, immunoglobulin E antibodies are often demonstrable by skin or radioallergosorbent tests, but pseudo-allergic reactions can produce a similar clinical picture. Diagnosis of food intolerance depends on withdrawing the food concerned and assessing the response to a blind challenge. Objective ways of detecting subclinical reactions are also useful, including the detection of a mediator response involving prostaglandins, histamine or serotonin.

Aldehyde Dehydrogenase↗
PubMed1984

Effect of aspirin in "aspirin sensitive" patients.

Eighteen patients with a history of urticaria or asthma, or both, induced by aspirin were studied before and after provocation of symptoms with aspirin. The plasma prostaglandin F2 alpha concentration, which was characteristically raised before challenge, fell significantly at the time of adverse reactions. Repeated administration of aspirin up to a dose of 650 mg daily induced tolerance in most of the patients, and several developed bronchodilator responses to aspirin. Although median total IgE concentrations may be raised in patients with aspirin sensitivity, it appears likely that pharmacological rather than immunological mechanisms are chiefly responsible for the phenomena of aspirin sensitivity and desensitisation.

Adolescent↗
PubMed1984

Skin and radioallergosorbent tests in patients with sensitivity to bee and wasp venom.

Intradermal (ID) and prick tests with bee or wasp venom (Pharmalgen) have been performed on 102 subjects with a history of adverse reactions to stings and forty-six control subjects giving no such history. Venom was diluted 100, 10 and 1 microgram/ml for prick testing and 10(-2), 10(-2), 10(-3) and 10(-4) micrograms/ml for ID injections. In forty-six control subjects all were tested with the highest concentration of prick testing solution (100 micrograms/ml), eight (17%) had positive reactions, a similar reaction rate to that reported in control subjects using 10(-1) micrograms/ml ID. In our 102 test subjects skin tests were therefore regarded as positive only if the reaction was elicited by 10 micrograms/ml or less by prick test of 10(-2) micrograms/ml or less ID. In general the results with skin prick tests and ID tests were comparable when the prick solution was 1000 times the concentration of that used for ID testing. ID tests were positive in thirteen with negative skin prick, seven of whom had detectable antibodies when tested by RAST. Conversely four with a positive skin prick test (two of whom were RAST positive) were considered negative on ID testing. As judged either by RAST or skin tests it appeared that sensitivity diminished with the time interval from the last sting (P less than 0.001).

Bee Venoms↗
PubMed1984

Treatment of chronic idiopathic urticaria with terfenadine.

The usefulness of antihistamines is impaired by their sedative side effects. In a double blind crossover study of twenty-four patients with chronic idiopathic urticaria, we have found terfenadine to be a non-sedative and highly effective drug.

Benzhydryl Compounds↗
PubMed1983

Antibodies to purified bee venom proteins and peptides. I. Development of a highly specific RAST for bee venom antigens and its application to bee sting allergy.

IgE antibodies to purified proteins and peptides from honeybee venom have been measured by the RAST. Trace amounts (less than 0.1%) of the major venom protein phospholipase A2 (PLA2) grossly distorted the measurement of IgE antibody to the other venom proteins, acid phosphatase (Acid P) and hyaluronidase (HYAL), and overemphasized their importance. Reduction of antigen coupled to the cellulose paper discs, which were used in the assay, diluted out the contaminating PLA2 without apparent loss in sensitivity. The reduction of disc-bound antigen increased the competition between IgE and IgG antibodies but did not affect measurement of IgE antibodies in sera taken from 35 untreated patients who had a history of general allergic reactions to bee stings. In 54% of sera from bee venom--allergic patients, the greatest IgE antibody response was to PLA2. In all, IgE antibodies to PLA2 were present in 91% of these sera. IgE antibodies to Acid P, HYAL, or melittin were present in 60%, 51%, and 31% of sera, respectively, and accounted for the highest level of binding in 17%, 17%, and 6% of these. Only 6% of sera were positive for whole venom but negative for the isolated antigens. A low level of IgE antibody was found to peptide 401 in 6% of sera. No IgE antibodies were found to apamin. While confirming the central role played by PLA2 in bee sting allergy, these results show that other venom components are also important in some patients.

Acid Phosphatase↗
PubMed1983

Antibodies to purified bee venom proteins and peptides. II. A detailed study of changes in IgE and IgG antibodies to individual bee venom antigens.

Antibodies to individual bee venom antigens were studied in detail in nine bee sting-allergic patients who received venom immunotherapy without side effects, in two patients who failed to reach maintenance, and in two whose sensitivity returned. The study was confined to patients who had IgE antibodies to at least one of four purified bee venom antigens at the start of treatment. IgE and IgG antibodies to phospholipase A2 (PLA2), hyaluronidase (HYAL), and acid phosphatase (ACID P) and IgE antibodies to melittin (MEL) were measured, and changes in the antibody levels were followed during bee venom immunotherapy. Two contrasting patterns of antibody response were seen in the nine successfully treated patients. In five patients there was a rise in serum IgG antibodies to the same antigens as the IgE antibodies. In two patients' serum IgE antibody to HYAL or ACID P fell without a marked IgG antibody response to these antigens, although high levels of IgG antibody to PLA2 were present in both. Although the first pattern is consistent with a "blocking" role for IgG antibody, clearly the second is not. Not all patients can be conveniently divided into these two categories, and two patients did not show any significant change in either IgG or IgE antibody but were nevertheless able to tolerate the maintenance dose of 100 micrograms of venom. Two patients who failed to reach the maintenance dose of 100 micrograms because of their allergic reactions to the injections of venom were distinguished by (1) very high serum IgE antibody and (2) a low ratio of IgG/IgE antibody. Passive immunization with IgG antibody from a hyperimmune beekeeper was, however, protective in these patients, although it did not raise their overall serum IgG antibody level very much. We are unable to explain either the failure of conventional therapy or the beneficial effect of passive immunization in these two patients. Two bee sting--allergic beekeepers lost their sensitivity to stings, but later, when their sera contained IgE antibody to another bee venom antigen, they reacted to stings and inhalation of beehive dander. These data suggest that either falling IgE antibody or IgG- "blocking" antibody could be responsible for providing clinical protection to bee venom--allergic subjects. Renewed clinical sensitivity was observed when the IgE response was modulated, with patients making IgE antibody first to one antigen and then to another.

Acid Phosphatase↗
PubMed1983

Specific desensitization in 'aspirin-sensitive' urticaria; plasma prostaglandin levels and clinical manifestations.

Six out of eight patients with a history of aspirin-provoked urticaria/angioedema responded with adverse reactions, including urticaria and bronchospasm, to provoking doses of oral aspirin from 30-515 mg. The other two patients did not react to 1.2 g of aspirin on three occasions. Five of the six patients who had reacted became desensitized after their initial aspirin reaction, tolerating 650 mg on the second day. They then took 650 mg day-1 of aspirin for three weeks, during which time the ingestion of foods which had previously caused a variety of moderate or severe reactions caused no symptoms. The resting plasma PGF2 alpha in ten 'aspirin-sensitive' urticaria patients (24.89 +/- 2.79 pg m-1) was significantly higher than the levels in ten normal subjects (6.75 +/- 1.1 pg ml-1) (P less than 0.01). In the patient group the lowest levels of PGF2 alpha were found in the two patients who subsequently did not experience a positive reaction after aspirin provocation. The PGF2 alpha/PGE2 ratio in 'aspirin-sensitive' urticaria patients (1.83 +/- 0.026) was significantly higher than that in normal subjects (0.63 +/- 0.14) (P less than 0.01).

Adolescent↗
PubMed1983

Food intolerance and allergy--a review.

Specific food intolerance needs to be distinguished from obsessional states in which those who are affected have an aversion to numerous foods. Even in cases where specific food intolerance can be demonstrated, the diagnosis of food allergy depends on additional evidence that the patient's reaction is based on an abnormal immunological response. In food allergy, skin and laboratory tests may detect the presence of an IgE-mediated reaction, particularly in patients with asthma or eczema and especially where the foods involved are highly allergenic--such as egg, fish, nuts and milk. However, many patients with proven food intolerance have negative tests, suggesting that other immunological or non-immunological mechanisms are responsible. Laboratory tests for non-IgE reactions are unreliable. Where it is difficult to show a connection between individual foods and an allergic response--as in patients with urticaria provoked by food additives--one of the reasons for diagnostic difficulty is that the offending substances may be present in a wide range of common foods. If the diagnosis is to be firmly established in such cases, it is necessary to show that symptoms remit on an elimination diet and recur after a placebo-controlled challenge.

Animals↗
PubMed1983

Prostaglandins in the pathogenesis of food intolerance.

Prostaglandins appear to have cytoprotective effects in the upper bowel and are released in increased amounts in patients with abnormal peristalsis and diarrhea. Drugs which interfere with prostaglandin (PG) synthesis often prevent the symptoms of food intolerance and have been reported as improving food-related symptoms in the irritable bowel syndrome.

Adult↗