Medical Literature - 1985

Munch EP, Weeke B. 2/1985 Allergy

Feb;40(2):92-97

Ten patients with frequent attacks of non-hereditary angioedema were treated with tranexamic acid or placebo in a double blind manner, each period lasting 3 months. During the tranexamic acid period nine patients became symptom-free, or substantially improved, while one was unaffected (P less than 0.05). In four patients itching was a major accompanying complaint which was relieved in three. Diarrhoea and abdominal discomfort were more pronounced during tranexamic acid treatment (P less than 0.05), but only necessitated dose reduction in one patient. Four years later contact was obtained with eight of the nine responders and six were still taking tranexamic acid regularly, while in two patients the attacks were so infrequent that the drug was not taken regularly.

Available online at: onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.1985.tb02666.x/abstract (small fee)

Farnam J, Grant JA. 1/1985 Dermatol.Clin.

Jan;3(1):85-95

Angioedema is characterized by a well-demarcated swelling on the skin, oropharyngolaryngeal tissue, or the gastrointestinal wall. Underlying mechanisms may include IgE-mediated reactions, complement activation, inhibition of the cyclo-oxygenase pathway of arachidonic acid metabolism, direct release of mediators from mast cells, and activation of the kinin-forming system. Foods, drugs, inhalants, insect bites, blood transfusion, collagen vascular disease, infections, physical factors, neoplasms, and hereditary factors can cause angioedema through one or more of these mechanisms. Chronic angioedema lasts more than 6 weeks or recurs during this period. Acute angioedema is a self-limited disorder and resolves spontaneously, or with simple therapy, in several days; the patient rarely requires a complete work-up. Chronic angioedema may necessitate a detailed history, physical examination, and limited clinical or laboratory tests to exclude serious underlying illnesses. The H1 antihistamines are used for the treatment of both acute and chronic angioedema. An H2 antihistamine, a second H1 antihistamine, or rarely even a low dose of corticosteroid may be added to the regimen if H1 antihistamine alone fails to control chronic angioedema. Hereditary angioedema is an autosomal dominant disease that is caused by C1INH deficiency. In patients with this disorder, swelling of the lip, pharynx, and extremities may follow trauma to soft tissue. Other clinical manifestations include abdominal pain, nausea, vomiting, and suffocation because of laryngeal swelling. Diagnosis can be confirmed by the finding of low levels of C4 and C2 and the absence of nonfunction of C1INH. Androgens reverse the biochemical defects.

Not available online.

Huber MM, Calliari D. 10/1985 American Journal of Nursing

Oct;85(10):1090-1092.

Not available online.

Black AK. 8/1985 American Journal of Industrial Medicine

8(4-5):297-303

Urticarial responses in skin may be elicited in different ways, viz, stroking (dermographism), after sustained pressure (delayed pressure urticaria), and after vibration (vibratory angio-oedema). Pressure may localise lesions of chronic idiopathic urticaria. Trauma may exacerbate hereditary angio-oedema. The extent of the morbidity caused by trauma-induced urticaria among workers is unknown.

Available online at: onlinelibrary.wiley.com/doi/10.1002/ajim.4700080408/abstract (small fee)

Synkowski DR 11/1985 Emergency Medicine Clinics of North America

Urticaria/angioedema is very common and usually not very serious. The main diagnostic task is the history, asking about pharmaceutical agents, foods, focuses of infection, physical agents, and psychogenic factors as well as inhalants, insect bites, internal diseases, immune complex diseases, contactants, and genetic factors. The main therapeutic tool is to eliminate the offending agent. If this cannot be done, therapy should begin with an H1 antihistamine pushed to tolerance or clearing. Life-threatening laryngeal edema and/or anaphylactic shock are extremely rare. Laryngeal edema is usually a component of hereditary angioedema. In such cases, subcutaneous epinephrine is the drug of choice. Laboratory investigation in chronic urticaria should include CBC, erythrocyte sedimentation rate, and a serum multiphasic analysis. A myriad of laboratory tests can be done in chronic urticaria, but some cost-yield effective ones are a test for antinuclear antibodies and x-rays of the sinuses and dentition.

Nov;3(4):737-745

Not available online.

Donaldson VH, Harrison RA, Rosen FS, Bing DH, Kindness G, Canar J, et al. 1/1985 The Journal of Clinical Investigation

Jan;75(1):124-132

C1(-)-inhibitor (C1(-)-INH) proteins from normal persons and members of eight different kindred with dysfunctional C1(-)-INH proteins associated with hereditary angioneurotic edema (HANE) were compared with respect to their inhibitory activity against purified preparations of C1s-, plasma kallikrein, activated forms of Hageman factor, and plasmin. Each dysfunctional C1(-)-INH protein showed a unique spectrum of inhibitory activity against these enzymes. Although none of the dysfunctional C1(-)-INH proteins significantly impaired amidolysis by plasmin, all but one inhibited activated Hageman factor. One purified dysfunctional C1(-)-INH (Ta) inhibited purified C1s- to a normal degree. Another C1(-)-INH (Za) had almost seven times as much inhibitory activity as normal C1(-)-INH against activated Hageman factor, but had decreased activity against C1s- and no activity against plasmin. Analyses of mixtures of plasmin and C1(-)-INH proteins in SDS gel electrophoresis revealed variability in the patterns of complex formation and cleavage of dysfunctional proteins after exposure to C1s- and plasmin. Some bound to plasmin and were cleaved, even though none significantly impaired the amidolytic activity of plasmin. Two were cleaved by C1s-, whereas neither normal or other dysfunctional C1(-)-INH were cleaved. Dysfunctional C1(-)-INH proteins from patients with HANE are thus heterogeneous in their inhibitory properties and there must be different structural requirements for the inhibition of the various plasma enzymes that can be regulated by normal C1(-)-INH. The data suggest that in addition to common sites of interactions between these proteases and C1(-)-INH, there are also points of contact that are specific for each protease. Genetic mutations leading to structural changes at some of these sites may have differing effects on the interaction between individual proteases and abnormal C1(-)-INH proteins. These alterations may allow these proteins to serve as probes for structural requirements for inhibitory actions of normal C1(-)-INH.

Available online at: ncbi.nlm.nih.gov/pmc/articles/PMC423417/