Cefotaxim induced a near fatal anaphylactic shock in an infant

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Ibuprofen-induced aseptic meningoencephalitis confirmed by drug challenge.

Drug-induced aseptic meningitis (DIAM) is a diagnostic challenge. The major causative agents are nonsteroidal anti-inflammatory drugs (particularly ibuprofen), antibiotics, intravenous immunoglobulin, and OKT3 monoclonal antibodies. DIAM is more frequently observed in patients with autoimmune diseases. A 36-year-old woman was attended in our department 3 months after being diagnosed with aseptic meningoencephalitis. She had had 2 episodes in 9 months. Neurological symptoms were associated with ibuprofen. A challenge with acetylsalicylic acid was negative, whereas a drug challenge with ibuprofen was positive. Thirty minutes after ingesting 50 mg of ibuprofen, she experienced general malaise and progressively developed chills, fever (39.5 degrees C), headache, and nuchal rigidity. Lumbar puncture showed normal glucose and high protein levels. Neutrophilic pleocytosis was observed at the first admission; lymphocytosis was predominant in the second and third episodes. DIAM is a rare and severe hypersensitivity reaction. Drug challenge enabled us to make an accurate diagnosis.

Occupational asthma due to carrot in a cook.

BACKGROUND: Few previous reports of carrot-induced asthma have been confirmed by objective tests. Hypersensitivity to carrot is frequently associated with allergy to Apiaceae spices and sensitization to birch and mugwort pollens. CLINICAL CASE: A 40-year-old cook woman was seen with sneezing, rhinorrhea, contact urticaria and wheezing within few minutes of handling or cutting raw carrots. She needed to leave out of the kitchen while the other cooks cut raw carrots. METHODS AND RESULTS: Skin tests were positive to carrot, celery, aniseed and fennel. Rubbing test with fresh carrot was positive. Specific IgE to carrot was 4.44 kU/L. Determinations of specific IgE to mugwort, grass and birch pollens were negative. Inhalative provocation test, performed as a handling test, was positive. The IgE-immunoblotting showed two bands in carrot extract: a band with apparent molecular weight of 30 kd and other band of 18 kd. This band of 18 kd was Dau c 1. The band of 30 kd could correspond a phenylcoumaran benzylic ether reductase. Dau c 1 did not appear to be the unique allergen in this case. Additional allergens may induce the sensitization. Primary sensitization due to airborne allergens of foods and the lack of pollen allergy in this patient are notorious events.

Hypersensitivity pneumonitis due to occupational inhalation of fungi-contaminated corn dust.

Hypersensitivity pneumonitis or extrinsic allergic alveolitis can be defined as a lung disease caused by a wide group of antigens that reach the lung by inhalation of organic and/or inorganic dust of various sources. The dust of the stored maize corn has been reported as cause of respiratory symptoms. During the storage process, maize corn dust can be contaminated by moulds and thermophilic actinomycetes, which have not been described until now as the causing antigens of these symptoms. We present a case of occupational hypersensitivity pneumonitis in an agricultural worker who cultured and stored maize corn. Clinical findings, precipitating antibodies, and evolution after having removed him from his work, confirmed the diagnosis. In our case, Aspergillus species contaminating the maize corn dust are probably the antigens that caused the disease.

Carbamazepine induced transient monoclonal gammopathy and immunodeficiency.

Immune abnormalities have been found in many patients receiving anti-epileptic drugs. However, the effects of carbamazepine are still conflicting. We report the case of a 31-year-old woman who began carbamazepine treatment because of idiopathic epilepsy of adulthood. After three years of treatment she developed arthralgias and malaise. Complete immunologic evaluation showed a total absence of immunoglobulin M with decreased levels of immunoglobulin A, positive antinuclear antibodies and monoclonal paraproteinemia type IgG-kappa. The possibility of B cell lymphoma or myeloma was ruled out. Skin testing was negative. Bone marrow examination was normal. After carbamazepine discontinuation, levels of IgA and IgM increased until reaching normal values over 3 years. The monoclonal gammopathy of undetermined significance also disappeared over this period. During this period of immunodeficiency, the patient did not complain of any infectious complications.

Bread eating induced oral angioedema due to alpha-amylase allergy.

Inhalation of dust from different enzymes can be the cause of occupational asthma in exposed workers. Enzymes from different sources are being increasingly used in food. Few cases of food allergy to alpha-amylase induced by eating bread have been reported. Those cases were reported in bakery-related patients and in a pharmaceutical-industry worker. A 25-year-old farmer suffered sneezing, rhinorrhea, oropharyngeal itching, hoarseness, cough, and non-wheezy dyspnea after eating white bread. Skin prick tests (SPT) with common aeroallergens and food allergens revealed only sensitization to Olea europaea pollen. SPT response was positive to Aspergillus oryzae alpha-amylase. Specific IgE against alpha-amylase was positive. A double-blind placebo-controlled challenge with 5 mg of uncooked -amylase induced sneezing, cough, oral angioedema within 10 minutes. The provocation test with 50 g of white bread gave similar findings. This case indicates that alpha-amylase contained in bread may provoke IgE-mediated food allergy. It is worth noting that in this case, the only source of alpha-amylases sensitization was bread.

Anaphylactoid reaction to carboplatin: successful "desensitization".

Carboplatin (CP) hypersensitivity reactions have been reported in nearly 12 % of patients treated with this drug. The pathophysiologic mechanisms of these reactions have not been entirely elucidated. Various hypotheses are under discussion. CP hypersensitivity reactions could be IgE-mediated, caused by low-molecular platinum compounds acting as haptens. Platinum salts are also able to release histamine from basophils and mast cells, and some events seem to be non-immune-mediated direct histamine release. We report a case of CP tolerance induction in a 65-year-old man. During the third course of CP he experienced an anaphylactic reaction. Skin testing was negative. Suspecting the possibility of an anaphylactoid reaction due to histamine release, we developed a protocol to induce tolerance. Pre-medication with corticosteroid and antihistaminic was performed before intravenous CP infusion. The bag with CP was first infused 60 ml/h for 30 minutes; the infusion was well tolerated and infusion was continued at 100 ml/h for the next 60 minutes and thereafter at 120 ml/h until the bag was finished. Following this "desensitization", monthly courses of CP using the same protocol have been well tolerated.