Allergy and Immunology: An Annotated Bibliography of Recent Literature
Journal: Annals of Internal Medicine (1982)

The Literature of Medicine1 November 1982Allergy and Immunology: An Annotated Bibliography of Recent LiteratureReferences to Journal Articles and Other PapersALLERGY AND IMMUNOLOGY COMMITTEEALLERGY AND IMMUNOLOGY COMMITTEESearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-5-791 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis bibliography includes references to 123 recently published journal papers and similar sources that represent important developments in the concept and practice of internal medicine. It has been compiled by the Allergy and Immunology Committee* as part of the Medical Knowledge Self-Assessment Program VI Syllabus.In preparing this bibliography, the committee reviewed MEDLINE†bibliographic printouts of journal articles published since the beginning of 1978 and also drew on sources in libraries of hospitals and other clinical institutions in the United States and Canada; thus, only papers in English are listed, and most are from American journals....Basic Concepts of the Immune Response Immunologic Mechanisms of Tissue Injury Approach to the Patient with Allergic Disease Common Allergic Disorders RHINITIS BRONCHIAL ASTHMA ANAPHYLAXIS CUTANEOUS ALLERGIC DISORDERS: URTICARIA AND ANGIOEDEMA DRUG HYPERSENSITIVITY Hypersensitivity Lung Disease Defects in Host Defense Systemic Diseases with Prominent Immunologic Features Immunomodulation Tumor Immunology1. COLTENALPERROSEN HCF. Genetics and biosynthesis of complement proteins. N Engl J Med. 1981;304:653-6. Summarizes the disorders related to a deficiency of individual complement components or of inhibitors of complement systems. The relation of structural loci for certain complement proteins to the major histocompatibility complex and biosynthesis are reviewed. CrossrefMedlineGoogle Scholar2. DIAMONDYELTONSCHARFF BDM. Monoclonal antibodies: a new technology for producing serologic reagents. N Engl J Med. 1981;304:1344-9. Describes the method for producing hybrids of normal antibody-producing cells and neoplastic plasma cells, and the properties and uses of the resulting homogeneous antibodies, their applications, and limitations of the technique. CrossrefMedlineGoogle Scholar3. FEARONAUSTEN DK. The alternative pathway of complement—a system for host resistance to microbial infection. N Engl J Med. 1980;303:259-63. Reviews the activating and effector sequences of both classic and alternative complement pathways, and the control proteins that regulate the latter. Describes the distinction between activating and nonactivating microbial and mammalian cells, and aberrant regulation by C3 nephritic factor. CrossrefMedlineGoogle Scholar4. GLENNER G. Amyloid deposits and amyloidosis: the β-fibrilloses. N Engl J Med. 1980;302:1283-92, 1333-43. Many proteins can assume the beta-pleated sheet configuration characteristic of the major fibril constituent of amyloid, including intact light chains or their VL segment, amyloid fibril protein AAL associated with secondary amyloidosis, hormone precursors, and prealbumin. Classifies the beta-fibrilloses, and reviews diagnosis and treatment of amyloidosis. CrossrefMedlineGoogle Scholar5. HERZENBERGHERZENBERG LL. Analysis and separation using the fluorescence activated cell sorter (FACS) (Chapter 22). In: WEIR DM, ed. Handbook of Experimental Immunology. 3rd ed. Oxford: Blackwell Scientific Publications; 1978:1-21. Describes how the fluorescence activated cell sorter works, how data are displayed and analysed, and how lymphocytes stained with fluorescinated antibodies can be separated and characterized. Google Scholar6. NATHANMURRAYCOHN CHZ. The macrophage as an effector cell. N Engl J Med. 1980;303:622-6. Reviews the role of the macrophage in interactions involving cellular and humoral components of the inflammatory and immunologic networks, its secretory role, and the current status of macrophage-tumor cell and macrophage-microbe interaction. CrossrefMedlineGoogle Scholar7. REINHERZSCHLOSSMAN ES. Regulation of the immune response—inducer and suppressor T-lymphocyte subsets in human beings. N Engl J Med. 1980;303:370-3. The differentiation antigens of human thymocytes, the markers of mature inducer and cytotoxic/suppressor T-cell subsets and their immunologic functions are described. Emphasis is on the regulatory effects on the immune response. CrossrefMedlineGoogle Scholar8. ROSENTHAL A. Regulation of the immune response—role of the macrophage. N Engl J Med. 1980;303:1153-6. The role of the macrophage in antigen uptake and in antigen-specific T-cell proliferation, the mechanisms of the lymphocyte-macrophage interaction, and the histocompatibility restriction involved in macrophage-T-lymphocyte interaction are considered. CrossrefMedlineGoogle Scholar9. ATKINSNORMANWEINERZWEIMAN PMHB. Release of neutrophil chemotactic activity during immediate hypersensitivity reactions in humans. Ann Intern Med. 1977;86:415-8. Neutrophil chemotactic activity liberated during experimentally induced immunoglobulin E-mediated asthma is reported. Increased activity was found in serum 5 to 30 minutes after an antigen inhalation challenge. LinkGoogle Scholar10. AUSTEN K. The chemical mediators of immediate hypersensitivity reactions. In: SAMTER M, ed. Immunologic Disorders. Boston: Little, Brown; 1978:183-209. A discussion of the mast cell and the important mast cell mediators of inflammatory and allergic reactions. Emphasis is on the role of the mast cell in human disease. Google Scholar11. COHENDAVIDFELDMAN SJM. Current state of studies of mediators of cellular immunity: a progress report. Cell Immunol. 1977;33:233-44. Discusses the contribution of mediators of inflammation, characterization of mediators, and both helper and suppressor factors in immunity. The mechanism of action of lymphocyte mediators is discussed, with emphasis on cell receptors for mediators. CrossrefMedlineGoogle Scholar12. HOLEWISAUSTENORANGE PRKR. Mediators of immediate hypersensitivity. In: GUPTA S, GOOD RA, eds. Cellular, Molecular, and Clinical Aspects of Allergic Disorders (Comprehensive Immunology. Vol. 6). New York: Plenum Medical Books; 1979:179-229. Discusses physicochemical characteristics, metabolism, and pharmacologic action. Mast cell degranulation and biochemical mechanisms and controls are discussed; the interaction of the mediators of immediate hypersensitivity with humoral and cellular elements of the immune system is emphasized. CrossrefGoogle Scholar13. KOHLER P. Immune complexes and allergic disease. In: MIDDLETON E JR, REED CE, ELLIS EF, eds. Allergy: Principles and Practice. St. Louis: C.V. Mosby Co.; 1978:155-76. Serum sickness, immune complexes, and variables encountered in their detection are discussed. Tissues involved in immune complex disease are described, with clinical examples (kidneys, skin, joints, serous membranes). Google Scholar14. LICHTENSTEINMULLER-EBERHARD LH, eds. Effector mechanisms and mediators. In: New Initiatives in Immunology. U.S. Department of Health and Human Services; 1981; NIH publication no. 81-2215:210-55. Reviews the lymphokines, interferons, natural killer cells, mediators of allergic reactions, coagulation kinin system, chemotaxis, IgE receptors, and regulation of the IgE response. Mechanisms and pharmacology of allergic inflammation are discussed. Google Scholar15. MCFADDEN E. Beta-2 receptor agonists: metabolism and pharmacology. J Allergy Clin Immunol. 1982;68:91-7. Synthesis of naturally occurring catecholamines and chemical structure of the catecholamine bronchodilators is emphasized. The adrenergic stimulants used in the treatment of obstructive airways disease (catecholamines, resorcinols, and salinigens) are described. CrossrefGoogle Scholar16. PLAUTLICHTENSTEIN ML. Cellular and chemical basis of the allergic inflammatory response. In: MIDDLETON E JR, REED CE, ELLIS EF, eds. Allergy: Principles and Practice. St. Louis: C.V. Mosby Co.; 1978:115-38. A review of inflammatory cells, including mast cells, eosinophils, platelets, neutrophils, lymphocytes, and mononuclear cells. Mediators of inflammatory response, both primary and secondary, and the mechanisms of pharmacologic control of mediator release are discussed. Google Scholar17. SULLIVANKULCZYCKI TA. Immediate hypersensitivity responses. In: PARKER CW, ed. Clinical Immunology. Vol. 1, Philadelphia: W.B. Saunders Co.; 1980:115-42. A review of IgE structure, physical and chemical properties, interaction of IgE with cell surface receptors, mast cells and basophils, and events leading to mediator release. Google Scholar18. TINGZWEIMANLAVKERDUNSKY SBRE. In vivo release of eosinophil chemoattractant activity in human allergic skin reactions. J Immunol. 1981;127:557-60. Low molecular weight factors in vivo, other than histamine, are probably responsible for late phase eosinophil accumulation in human allergic reaction sites. Much of the time lag between exposure and eosinophil accumulation is encompassed by local mediator release. MedlineGoogle Scholar19. TOMASILARSONCHALLICOMBEMCNABB TLSP. Mucosal immunity: the origin and migration patterns of cells in the secretory system. J Allergy Clin Immunol. 1980;65:12-9. Review of immune reactions on membranes and mucosal surfaces, cell migration patterns, cellular trafficing, the secretory system, and origins of secretory IgA. The possible functions of secretory immunity in preventing colonization of mucosal surfaces by pathogenic microorganisms are discussed. CrossrefMedlineGoogle Scholar20. WEISSMANNSMOLENKORCHACK GJH. Release of inflammatory mediators from stimulated neutrophils. N Engl J Med. 1980;303:27-34. A discussion of phagocytosis and concomitant events, the stimuli that activate neutrophils, neutrophilic membrane responses, generation of oxygen derivatives, and the role of ionic fluxes in the neutrophil's response to stimulation. CrossrefMedlineGoogle Scholar21. . Position Statements—Controversial Techniques. J Allergy Clin Immunol. 1981;67:333-8. Allergy techniques such as urine autoinjection, Rinkel immunotherapy, cytotoxic food testing, and sublingual or intracutaneous allergic provocation are controversial. There is no scientific basis for their use in diagnosis and management of patients with allergic disorders. CrossrefMedlineGoogle Scholar22. CORRAOBRAMANIRWIN WSR. Chronic cough as the sole presenting manifestation of bronchial asthma. N Engl J Med. 1979;300:633-7. Chronic cough without dyspnea or wheezing was associated with methacholine responsive airways. Therapy with bronchodilators was successful. CrossrefMedlineGoogle Scholar23. ERIKSSONAHLSTEDTLÖVHAGEN NSO. Immunotherapy in springtime hayfever: a clinical and immunological study comparing two different treatment extract compositions. Allergy 1979;34:233-47. A mixture of tree pollen antigens was effective in the treatment of specific allergic rhinitis. Relief of symptoms was associated with an increase in non-IgE antibody, and a decrease in specific IgE levels. CrossrefMedlineGoogle Scholar24. GERHARDSCHACHTER HE. Exercise-induced asthma. Postgrad Med. 1980;67(3):91-3, 96-9, 101-2. Exercise induced asthma is one of the forms of airway hyperreactivity, and can be diagnosed by sensitive sperometric techniques. This asthma responds well to prophylactic antiasthmatic agents. CrossrefMedlineGoogle Scholar25. MYERSCORRAOBRAMAN JWS. Clinical applicability of a methacholine inhalational challenge. JAMA. 1981;246:225-9. Bronchial inhalation challenge with methacholine may be of value in identifying hyperactive airways of asthma when pulmonary functions are normal. CrossrefMedlineGoogle Scholar26. NORMAN P. An overview of immunotherapy: implications for the future. J Allergy Clin Immunol. 1980;65:87-96. Controlled studies have confirmed most of the empirical observations on the clinical effects of immunization with allergenic extracts. Immunologic methods have provided clues as to the mechanisms of improvement after immunization. CrossrefMedlineGoogle Scholar27. ROCKLINSHEFFERGREINEDERMELMON RADK. Generation of antigen-specific suppressor cells during allergy desensitization. N Engl J Med. 1980;302:1213-9. Specific immunotherapy was administered to 20 patients with ragweed hay fever. Blood mononuclear cells showed in-vitro supressor activity against ragweed stimulation only when obtained after a course of immunotherapy with ragweed. CrossrefMedlineGoogle Scholar28. TAYLOROHMANLOWELL WJF. Immunotherapy in cat-induced asthma: double blind trial with evaluation of bronchial responses to cat allergen and histamine. J Allergy Clin Immunol. 1978;61(5):283-7. Trial of cat pelt immunotherapy in cat-sensitive persons was associated with decrease in skin reactivity and reduction in bronchial response after challenge with antigen. CrossrefMedlineGoogle Scholar29. WEBB D. Drug allergy in clinical practice. Postgrad Med. 1979;65(4):62-4, 67, 70-2. Adverse reactions to pharmacologic agents are becoming common. Allergic reactions are difficult to distinguish from idiosyncratic reactions. Diagnosis of allergic drug reactions can be difficult; often discontinuance and rechallenge with the drug are necessary. CrossrefMedlineGoogle Scholar30. BACONMCLEANMATHEWSBANAES JJKJ. Priming of the nasal mucosa by ragweed extract or by an irritant (ammonia). J Allergy Clin Immunol. 1981;67:111-6. Challenging the nasal mucosa with ragweed antigen results in a priming effect with increased nasal airway resistance; however, priming with an irritant (ammonia) does not produce this effect. CrossrefMedlineGoogle Scholar31. BLACKREMSEN MK. Rhinitis medicamentosa. Can Med Asso J. 1980;122:881-4. Discusses the history, types, and methods of intranasal vasoconstrictor overuse and pathophysiologic effects of sympathomimetic amines. MedlineGoogle Scholar32. BORUMMYGIND PN. Inhibition of the immediate allergic reaction in the nose by beta-2 adrenostimulant fenoterol. J Allergy Clin Immunol. 1980;66:25-32. Topical application of beta-2 adrenostimulants seems to have a mast-cell stabilizing effect in the airways; these drugs may be of use in treating allergic rhinitis. CrossrefMedlineGoogle Scholar33. BUSUTTILCHANDRACHUDKERRMEUDELL AHAG. Simple nasal polyps and allergic manifestations. J Laryngol Otol. 1978;92:477-88. Seventy-four patients with simple nasal polyposis were studied in detail using skin-testing and IgE evaluation. A specific subgroup of atopic patients with nasal polyposis was not found. CrossrefMedlineGoogle Scholar34. HAMORYSANDESYDNORSEALEGWALTNEY BMADJ. Etiology and antimicrobial therapy of acute maxillary sinusitis. J Infect Dis. 1979;139:197-202. Eighty-one patients were studied by aspiration of the maxillary sinus. Bacteriologic findings and therapy were discussed, and various antibiotic regimens were compared. CrossrefMedlineGoogle Scholar35. INCAUDOSCHATZYAMAMOTOMELLONCREPEAJOHNSON GMFMSJ. Intranasal flunisolide in the treatment of perennial rhinitis: correlation with immunological parameters. J Allergy Clin Immunol. 1980;65:41-9. The safety and efficacy of intranasal flunisolide in allergic rhinitis were shown. Response was improved in those patients with strong atopic indicators as opposed to weak indicators. CrossrefMedlineGoogle Scholar36. KARMAJOKIPIISIPILÄLUOTONENJOKIPII PLPJA. Bacteria in chronic maxillary sinusitis. Arch Otolaryngol. 1979;105:386-90. Cultures from inflamed maxillary sinuses at surgery, compared with cultures from nasal secretions, did not correlate well. Presents a good case for intraoperative culture of antral mucosa as the best bacteriological indicator. CrossrefMedlineGoogle Scholar37. MOLONEY J. Nasal polyps, nasal polypectomy, asthma, and aspirin sensitivity: their association in 445 cases of nasal polyps. J LaryngoJ Otol. 1977;91:837-46. Helps dispel the myth that nasal polypectomy precipitates asthma. Nasal polypectomy on rare occasions may precipitate asthma but does not cause it. CrossrefGoogle Scholar38. MULLARKEY M. Clinical approach to rhinitis. Med Clin N Am. 1981;65:977-86. A systematic approach to diagnosis and management; anatomy, physiology, and classification of nasal disease are discussed. Recent advances in therapy as well as the relation between upper and lower airway disease, are presented. CrossrefMedlineGoogle Scholar39. MULLARKEY M. The classification of nasal disease: an opinion [Editorial]. J Allergy Clin Immunol. 1981;67:251-2. Allergic rhinitis is carefully classified and defined. Nonallergic rhinitis also is discussed, and nonallergic rhinitis with eosinophilia identified. Therapy of the rhinitis syndrome is reviewed. CrossrefMedlineGoogle Scholar40. RICEFISHMANBARTONHUTCHERSONEICHEL DSRRB. Cranial complications of frontal sinusitis. Am Fam Physician. 1980;22:145-9. Discussion of intracranial complications of sinusitis with review of antibiotic treatment. Bony, as well as intracranial, complications are discussed. Surgical indications are given. MedlineGoogle Scholar41. SPECTORLOTANENGLISHPHILPOT SAGI. Comparison between transillumination and the roentgenogram in diagnosing paranasal sinus disease. J Allergy Clin Immunol. 1981;67:22-6. Negates the usefulness of transillumination as compared with the roentgenogram in diagnosis. Transillumination in diagnosing 52 patients had limited diagnostic value. CrossrefMedlineGoogle Scholar42. TOSPOULSENBORCH MGJ. Etiologic factors in secretory otitis. Arch Otolaryngol. 1979;105:582-8. Dysfunction of the eustachian tube played a primary role in development of secretory otitis; allergy did not seem to be an etiologic factor. Screening tympanometry and medical history were used for this evaluation. CrossrefMedlineGoogle Scholar43. WHELAN C. Problems in the examination of nasal smears in allergic rhinitis. J Laryngol Otol. 1980;94:399-404. A concise description of techniques for obtaining nasal smears. Investigation of nasal smears is not a simple process and must be done properly for use in routine clinical practice. CrossrefMedlineGoogle Scholar44. WRAITHCUNNINGTONSEYMOUR DAW. The role and allergenic importance of storage mites in house dust and other environments. Clin Allergy. 1979;9:545-61. Dermatophagoides pteronyssinus is thought the most potent of house dust allergens; however, the skin testing of 210 patients with house dust allergy suggests that other mites also may be of some importance. CrossrefMedlineGoogle Scholar45. BACALPATTERSON RR. Long-term effects of beclomethasone dipropionate on prednisone dosage in the corticosteroid-dependent asthmatic. J Allergy Clin Immunol. 1978;62:72-5. Topically-active corticosteroids are effective in the long-term management of bronchial asthma. Systemic steroids generally can be reduced of discontinued. CrossrefMedlineGoogle Scholar46. CORRAOBRAMANIRWIN WSR. Chronic cough as the sole presenting manifestation of bronchial asthma. N Engl J Med. 1979;300:633-7. Shows sensitivity of pulmonary function to methacholine challenge and response to bronchodilators in asthmatics experiencing chronic cough, but not wheezing. CrossrefMedlineGoogle Scholar47. FISCHLPITCHENIKGARDNER MAL. An index predicting relapse and need for hospitalization in patients with acute bronchial asthma. N Engl J Med. 1981;305:783-9. The presence of seven signs highly correlated with relapse and need for hospitalization in patients seeking emergency room care. Careful assessment of these signs may permit better planning for proper management of these patients. CrossrefMedlineGoogle Scholar48. FRASERVENTERKALINER CJM. Autonomic abnormalities and autoantibodies to beta-adrenergic receptors. N Engl J Med. 1981;305:1165-70. Patients with allergic asthma had serum antibodies to beta-adrenergic receptors that correlated with increased responsiveness to alpha-adrenergic and cholinergic stimulation and decreased response to beta-adrenergic stimulation in vivo. CrossrefMedlineGoogle Scholar49. FRIGASLOEGERINGSOLLEYFARROWGLEICH EDGGG. Elevated levels of the eosinophil granule major basic protein in the sputum of patients with bronchial asthma. Mayo Clin Proc. 1981;56:345-53. The function of eosinophils is unknown, but these cells are frequently recovered from the sputum of asthmatic patients; eosinophils may damage airway epithelium. MedlineGoogle Scholar50. KANGVELLODYHOMBURGERYUNGINGER BDHJ. Cockroach cause of allergic asthma: its specificity and immunologic profile. J Allergy Clin Immunol. 1979;63:80-6. Initial evaluation of persons with bronchial asthma may not show an allergic cause; this frequent cause of asthma in urban environments is described. CrossrefMedlineGoogle Scholar51. KARRLEHRERBUTCHERSALVAGGIO RSBJ. Coffee worker's asthma: a clinical appraisal using the radioallergosorbent test. J Allergy Clin Immunol. 1978;62:143-8. Pulmonary disease is often thought related to the work environment. Antigens and immune mechanisms in one type of occupational asthma are identified. CrossrefMedlineGoogle Scholar52. KNAUERLICHTENSTEINADKINSONFISH KLNJ. Platelet activation during antigen-induced airway reactions in asthmatic subjects. N Engl J Med. 1981;304:1404-7. The mechanisms involved in allergic asthma are now being discovered; platelets may participate in the pathogenesis of allergic asthma. CrossrefMedlineGoogle Scholar53. KULCZYKI A. Role of immunoglobulin E and immunoglobulin E receptors in bronchial asthma. J Allergy Clin Immunol. 1981;68:5-14. IgE antibodies are often implicated in allergic asthma; the immune mechanisms in this syndrome are reviewed. CrossrefMedlineGoogle Scholar54. LICHTENSTEIN L. An evaluation of the role of immunotherapy in asthma [Editorial]. Am Rev Respir Dis. 1978;117:191-7. Immunotherapy is an established technique for management of allergic rhinitis. Clinical studies of injection therapy in bronchial asthma are reviewed. MedlineGoogle Scholar55. MCFADDENKISERDEGROOT ERW. Acute bronchial asthma: relations between clinical and physiologic manifestations. N Engl J Med. 1973;288:221-5. A classic description of the relationship between symptoms and pulmonary function measurements, and of the persistence of airway abnormalities even after an asthmatic patient becomes asymptomatic. CrossrefMedlineGoogle Scholar56. MYERSCORRAOBRAMAN JWS. Clinical applicability of a methacholine inhalation challenge. JAMA. 1981;246:225-9. Discusses a useful clinical test to identify persons with bronchial asthma who may have only minimal symptoms of pulmonary distress. CrossrefMedlineGoogle Scholar57. NASSIFWEINBERGERTHOMPSONHUNTLEY EMRW. The value of maintenance theophylline in steroid-dependent asthma. N Engl J Med. 1981;304:71-5. Regular administration of theophylline to 33 children led to significant clinical improvement compared with placebo. CrossrefMedlineGoogle Scholar58. ROSSINGFANTAMCFADDEN TCE. A controlled trial of the use of single versus combined-drug therapy in the treatment of acute episodes of asthma. Am Rev Respir Dis. 1981;123:190-4. Intravenous aminophylline added to adrenergic drugs significantly improved the response during the first hour without greater toxicity. MedlineGoogle Scholar59. STRAUSSMCFADDENINGRAMDEALJAEGERSTEARNS REREJD. Influence of heat and humidity on the airway obstruction induced by exercise in asthma. J Clin Invest. 1978;61:433-40. Dyspnea after exercise frequently limits the performance of asthmatic subjects. Bronchospasm is related to the amount of heat loss from the lungs. CrossrefMedlineGoogle Scholar60. TURNERGREENBERGERPATTERSON EPR. Management of the pregnant asthmatic patient. Ann Intern Med. 1980;93:905-18. The choice of safe drugs for management of asthma during pregnancy is reviewed. Most bronchodilators, and even corticosteroids, have been administered with little evidence of adverse effects on the fetus. LinkGoogle Scholar61. WILLIAMS M. Beclomethasone dipropionate. Ann Intern Med. 1981;95:464-7. Reviews the use of topical steroids for therapy of bronchial asthma. LinkGoogle Scholar62. WOLFETASHKINCLAVERESESIMMONS JDBM. Bronchodilator effects of terbutaline and aminophylline alone and in combination in asthmatic patients. N Engl J Med. 1978;298:363-7. Both adrenergic agonists and xanthines are widely used as bronchodilators. An additive clinical effect was seen with two commonly used drugs from each class. CrossrefMedlineGoogle Scholar63. HELMERALPERINYUNGINGERGRANT RJJJ. Anaphylactic reactions following infusion of factor VIII in a patient with classic hemophilia. Am J Med. 1980;69:953-7. Describes an IgE-mediated drug reaction. Reviews diagnostic techniques and the results of antiallergic drugs and attempted desensitization. CrossrefMedlineGoogle Scholar64. HUNTVALENTINESOBOTKABENTONAMODIOLICHTENSTEIN KMAAFL. A controlled trial of immunotherapy in insect hypersensitivity. N Engl J Med. 1978;299:157-61. Controlled study showing the efficacy of insect venom for desensitization of patients experiencing anaphylaxis after insect stings. Whole body insect extracts were no more effective than placebo. CrossrefMedlineGoogle Scholar65. JACOBSRAKEFOURNIERCHILTONCULVERBECKMANN RGDRWC. Potentiated anaphylaxis in patients with drug-induced beta-adrenergic blockade. J Allergy Clin Immunol. 1981;68:125-7. Propranolol seemed to block the therapeutic response to epinephrine. Bradycardia was thought related to unopposed cholinergic action. Beta-adrenergic blockers may increase the severity of anaphylactic reactions and limit the effectiveness of standard therapy for reversing anaphylaxis. CrossrefMedlineGoogle Scholar66. LEVINELOCKEY MR, eds. Insect Allergy. Milwaukee: American Academy of Allergy; 1981. Allergic reactions after insect stings are common, although fatalities are rare. This syndrome and the proper use of insect venoms for diagnosis and treatment are reviewed. Google Scholar67. LIEBERMANTAYLOR PW. Recurrent idiopathic anaphylaxis. Arch Intern Med. 1979;139:1032-4. Description of 18 patients with recurrent anaphylaxis in whom no identifiable cause could be established. CrossrefMedlineGoogle Scholar68. SHEFFERAUSTEN AK. Exercise-induced anaphylaxis. J Allergy Clin Immunol. 1980;66:106-11. A new syndrome especially of interest because of the recent emphasis on physical conditioning. The scope of the syndrome is described, as well as potential causes. CrossrefMedlineGoogle Scholar69. SMITHKAGEY-SOBOTKABLEECKER PAE. Physiologic manifestations of human anaphylaxis. J Clin Invest. 1980;66:1072-80. Hypotension was associated with peripheral vasodilation and increased plasma histamine. Standard therapy was only partially effective with the most severe anaphylactic shock. Hemodynamic recovery was gradual and not directly related to therapy. CrossrefMedlineGoogle Scholar70. ELIASLEVINSON JA. Hypersensitivity reactions to ethylenediamine in aminophylline. Am Rev Respir Dis. 1981;123:550-2. Patients can have severe exfoliative erythroderma after intravenous administration of aminophylline. The reaction is likely a cell-mediated hypersensitivity to the drug's ethylenediamine components. MedlineGoogle Scholar71. GRANTFINDLAYTHUESONFINEKRUEGER JSDDG. Local heat urticaria/angioedma; evidence for histamine release without complement activation. J Allergy Clin Immunol. 1981;67:75-7. Exposure of the forearm to water at 44° C can produce a localized lesion. Venous blood from the extremity shows a transient rise in plasma histamine levels without significant change in hemolytic complement activity, C3, C4, or factor B. CrossrefMedlineGoogle Scholar72. HOSEASANTAELLABROWNBERGERKATUSHAFRANK SMEMKM. Long-term therapy of hereditary angioedema with danazol. Ann Intern Med. 1980;93:809-12. Danazol is very effective for long-term treatment ( 1 to 6 years). Significant dose-related adverse reactions, alterations tions in menstrual function, and occasional masculinizing side effects may occur. LinkGoogle Scholar73. KAPLANROSENBERG RE. Atopic dermatitis: clinical and immunologic aspects and treatment. Postgrad Med. 1978;64:52-6. Emphasizes chronicity, onset, exacerbations and precipitating factors. Treatment primarily consists of using mild topical agents to reduce inflammation and pruritus. Long-term systemic therapy with corticosteroid is not recommended. CrossrefMedlineGoogle Scholar74. MARDERBURCHSCHMIDZEISSGEWURZ RFFCH. Low molecular weight Clq-precipitins in hypocomplementemic vasculitis-urticaria syndrome: partial purification and characterization as immunoglobulin. J Immunol. 1978;121:613-8. A lupus-like syndrome of chronic urticaria, cutaneous vasculitis, systemic symptoms, hypocomplementemia, preferential depletion of Clq, and low molecular weight (7S) Clq-precipitins can occur. The Clq-precipitin activity represents a diagnostic marker of disease. MedlineGoogle Scholar75. MATHEWS K. Management of urticaria and angioedema. J Allergy Clin Immunol. 1980;66:347-57. Review stressing the role of the mast cell, IgE, clinical assessment, diagnostic procedures, and therapy. Genetic types of urticaria are listed and the roles of histamine and complement abnormalities are discussed. CrossrefMedlineGoogle Scholar76. MONROECOHENKALBFLEISCHSCHULZ ESJC. Combined H1 and H2 antihistamine therapy in chronic urticaria. Arch Dermatol. 1981;117:404-7. Human skin blood vessels possess H2 receptors, as well as the commonly recognized H1 receptors. Combined H1 (hydroxyzine) and H2 (cimetidine) therapy is statistically more effective than H1 antihistamines alone in controlling symptoms. CrossrefMedlineGoogle Scholar77. O'LOUGHLINSCHROETERJORDON SAR. Chronic urticaria-like lesions in systemic lupus erythematosus: a review of 12 cases. Arch Dermatol. 1978;114:879-83. Patients may have nonpruritic, urticaria-like lesions. Skin biopsy often shows necrotising vasculitis; laboratory and clinical data suggest a positive association between lesions and disease severit