Allergic rhinosinusitis has three forms of therapy: pharmacotherapy, immunotherapy, and surgical therapy. Pharmacotherapeutically, there are six classes of drugs that give symptomatic relief: mucolytics, decongestants, anti-cholinergic agents, antihistamines, mast cell stabilizers, and corticosteroids. All six classes are discussed individually and in detail. For immunotherapeutic therapy of allergic rhinosinusitis, there are four types of skin testing in current use: scratch testing, prick testing, single intradermal testing, and skin end point titration testing. Only the latter is able to quantitate the antigenicity of each antigen, and thus the treatment vial made from only this type of skin testing can adequately treat all antigens to which the patient is sensitive. These differences in testing and vial mixing are explained. The last form of therapy is surgical therapy, which corrects the obstructive phenomenon caused by allergic rhinosinusitis. The procedures described are reduction inferior turbinectomies and endoscopic sinus surgery. It is felt by the authors that the specialist who is uniquely positioned to offer a patient suffering from allergic rhinosinusitis all three forms of therapy is the rhinologist.

Administration, Intranasal↗

PubMed1992

Treatment of refractory familial hypercholesterolemia by low-density lipoprotein apheresis using an automated dextran sulfate cellulose adsorption system. The Liposorber Study Group.

A subgroup of patients with familial hypercholesterolemia (FH) respond inadequately to standard diet and drug therapy, and are therefore at high risk for the premature development or progression of coronary artery disease. This study evaluated low-density lipoprotein (LDL) cholesterol and lipoprotein (a) removal in a multicenter, controlled trial with a new LDL apheresis procedure (Liposorber LA-15 System). The study comprised patients with FH who had not responded adequately to diet and maximal drug therapy. There were 54 patients with heterozygous FH (45 randomized to treatment and 9 control subjects) and 10 with homozygous FH (all of whom received LDL apheresis). The study included three 6-week treatment phases and a 4-week rebound phase. Treatments were administered at 7- to 14-day intervals. Mean acute reductions in LDL cholesterol were 76% in heterozygous FH patients and 81% in homozygous ones. Time-averaged levels of LDL cholesterol were reduced 41% (243 to 143 mg/dl) in heterozygous FH patients and 53% (447 to 210 mg/dl) in homozygous ones. The substantial acute reduction of lipoprotein (a) (means: 65%, heterozygous FH; 68%, homozygous FH) has not been reported with other therapies. The Liposorber LA-15 System represents an important therapeutic option in FH patients who respond inadequately to diet and drug therapy.

Adult↗

PubMed1992

Immunotherapy: rationale and mechanisms.

Immunotherapy is defined as the controlled exposure to known allergens to reduce the severity of the allergic response. Although available since 1910, its exact mechanisms of action is not known but may involve an increase in allergen-specific IgG antibodies, a decrease in IgE synthesis, and alteration in T-lymphocyte activity. Immunotherapy is indicated in patients with proven allergy who have significant symptoms. It may be used together with pharmacologic measures but is relatively contraindicated in patients receiving beta-blocker therapy. Immunotherapy may be continued during pregnancy and should not be initiated in patients with autoimmune diseases or in human immunodeficiency virus-positive patients. Selection of appropriate diagnostic tests is important. Before immunotherapy is considered, there are two recommended in vivo tests (combined prick and intradermal skin test, and skin end point titration) and two recommended in vitro tests (radioallergosorbent test [RAST] and enzyme-linked immunosorbent assays [ELISA]), all equally safe and sensitive. After appropriate test interpretation, treatment is initiated with slowly escalating doses of allergen. Effects are often apparent in 3 to 6 months and, after continuation for 3 to 5 years, patients usually achieve lasting benefit.

Contraindications↗

PubMed1992

Prevention and management of office allergy emergencies.

Acute anaphylaxis is a rare, potentially fatal, multisystem allergic reaction that every allergy office must be prepared to treat. Key points are reaction prevention, diagnosing the serious reaction, proper staff training, and keeping on hand (readily accessible and in functioning condition) adequate supplies to provide emergency treatment appropriate to the office locale. The diagnosis of, and treatment for, each common type of allergic reaction is discussed. Equipment and medicines suggested for office use are reviewed, and a sample allergy reaction management protocol is outlined. Office treatment of anaphylaxis is directed at stabilizing the patient for early transport to a hospital. Early administration of epinephrine is the most crucial step. The airway is maintained, circulation supported, and further mediator effects blocked. Cardiopulmonary resuscitation is used whenever respiration or circulation is insufficient. Stabilized patients should be transported as soon as possible by the most medically capable method available, preferably by ambulance with medical personnel in attendance. Because of the risk of subsequent delayed onset or late-phase reactions, and the possibility of multiorgan injury, anaphylaxis patients should be considered for admission to the hospital, extended observation, and appropriate specialist consultations.

Anaphylaxis↗

PubMed1990

Humoral immune response following extracorporeal immunoadsorption therapy of patients with hypercholesterolemia.

Low-density lipoprotein apheresis (LDL-apheresis) is an extracorporeal procedure that preferentially removes LDL cholesterol from the blood. One of the primary techniques for performing this procedure uses immunoadsorption columns containing monospecific polyclonal sheep antibodies to human LDL covalently coupled to a gel filtration medium. LDL-apheresis has generally been well-tolerated, with chills, fever, or flushing occurring rarely. The possibility of an immune reaction was investigated as a basis for these reactions observed in 12 of the 1312 procedures performed. Antibodies to sheep IgG developed in 12 of the 15 patients treated with LDL-apheresis as a result of the shedding of small quantities of the sheep immunoglobulin from the columns. A column acid-washing procedure minimized the quantity of shed antibody but did not prevent immunization of the patient. The clinical reactions were probably unrelated to shedding and immunization, as the reactions occurred even in patients who were not immunized to the sheep IgG. Immunization to ethylene oxide was not the cause, as determined by a radioallergosorbent test. The reactions were more likely related to the activation of complement, as indicated by the generation of C3a des Arg by the columns and an increase in C3a des Arg levels systemically.

Antibody Formation↗

PubMed1990

Allergy skin tests and immunotherapy: comparison of methods in common use.

Scratch, prick, single dilution intradermal, and skin endpoint titration skin testing techniques are compared and contrasted. The use of these skin testing methods for safely initiating and advancing allergy immunotherapy treatment is discussed. Concepts of low-dose, symptom-relieving dose, and maximally-tolerated dose immunotherapy are described, and common factors in all allergy techniques are stressed.

Humans↗

PubMed1989

Plasmin catalyzes binding of lipoprotein (a) to immobilized fibrinogen and fibrin.

Lipoprotein (a) [Lp(a)] is a plasma component whose concentration is related to the development of atherosclerosis, although the underlying mechanisms are not known. Lp(a) contains a unique structure, apolipoprotein (a), that shares partial homology with plasminogen. We now report that plasmin catalyzes the binding of Lp(a) to both immobilized fibrinogen and fibrin in a manner analogous to our previously reported studies with plasminogen. Plasmin treatment of immobilized fibrinogen induces a 3.7-fold increase in Lp(a) binding. Low density lipoprotein, molecules similar to Lp(a) but lacking apolipoprotein (a), bind poorly to immobilized fibrinogen and binding is not increased by plasmin. Trypsin but not neutrophil elastase also increases the binding of Lp(a) to fibrinogen. Lp(a) also complexes to plasmin-fibrinogen digests, and binding increases in proportion to the time of plasmin-induced fibrinogen degradation. Lp(a) binding is lysine-binding site dependent as it is inhibited by epsilon-aminocaproic acid. Lp(a) inhibits the binding of plasminogen to plasmin-modified immobilized fibrinogen, indicating that both molecules compete for similar lysine-binding sites. These findings demonstrate an affinity between Lp(a) and protease-modified fibrinogen or fibrin and thereby provide a potential mechanism to explain the association between thrombosis, coronary atherosclerosis, and increased blood concentrations of Lp(a).

Arteriosclerosis↗

PubMed1989

Extracorporeal LDL cholesterol removal: role of LDL-pheresis in combination with other hypolipidemic therapy to regress vascular disease.

The direct relationship between hypercholesterolemia and atherosclerosis has resulted in formal cholesterol-lowering recommendations for patients at increased risk. The incomplete response to therapy of some forms of hypercholesterolemia as well as not uncommon drug intolerance prompted the development of extracorporeal techniques to reduce serum cholesterol levels. Nonhuman primate data and an analysis of human cholesterol epidemiology and reduction trials were used to establish guidelines that would maximize the likelihood of stabilizing or regressing established coronary artery atherosclerosis. These goals are a total cholesterol (TC) level of less than or equal to 150 mg/dL (3.9 mmol/L) and a ratio of TC to high-density lipoprotein cholesterol (HDL) of less than 2.8. Selective, extracorporeal removal of LDL cholesterol (LDL-pheresis) was combined with diet and hypolipidemic drugs in a pilot study at The Rogosin Institute to achieve these lipid end-points. Technical aspects of LDL-pheresis, the background rationale for its use as part of a combined hypolipidemic therapy, the initial experience at The Rogosin Institute, and plans for future studies and applications are presented.

Animals↗

PubMed1988

A rationale for setting target plasma lipid levels to reverse atherosclerosis.

Explore the source record for details and available documents.

Animals↗

PubMed1987

Topical cocaine nasal anesthesia.

Explore the source record for details and available documents.

Anesthesia, Local↗

PubMed1986

Removal of low-density lipoproteins in patients by extracorporeal immunoadsorption.

A new technique called LDL-pheresis was used in patients to lower low-density lipoprotein cholesterol levels. This procedure combines continuous extracorporeal plasma separation with immunoadsorption of low-density lipoprotein on columns containing monospecific antibody to human apolipoprotein B. Six patients underwent a total of 164 procedures without significant side effects or nonspecific protein depletion. Acutely, LDL-pheresis lowered plasma cholesterol levels by removing up to 82 percent of the circulating low-density lipoprotein. Weekly LDL-pheresis combined with a portacaval shunt in a patient with homozygous familial hypercholesterolemia resulted in normalization of plasma cholesterol levels and rapid regression of skin xanthomata. Three of four patients with atherosclerotic coronary artery disease have noted improvement in their angina. LDL-pheresis appears to be a promising new technique capable of safely and efficiently lowering plasma low-density lipoprotein cholesterol levels.

Adult↗