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Biomedical subjects

D Eichelberg

Publications and source records attributed to D Eichelberg.

At least 19 recordsLinked to original sources
PubMed1989

Contact allergies induced by TTS-treatment.

The efficiency of a nicotine-containing transdermal therapeutic system (TTS) was investigated in a clinical study, the purpose of which was to help 183 heavy smokers give up their addiction by systematic and continuous nicotine application and simultaneous behavioral therapy. During the treatment period, 53% of the patients complained of pruritus and 39% developed erythemas that were almost exclusively confined to those areas where the patches had been applied. However, most symptoms appeared only in slight or moderate forms. In contrast to irritative cutireactions, 6 patients developed a genuine contact allergy (type IV, delayed type reaction) which proved in 5 cases to be induced by the nicotine contained in the patches. Presumably TTS-treatment may induce contact allergies to pharmaceutic agents, as has already been described in other observations on allergies to haptens.

Administration, Cutaneous↗
PubMed1988

[Desensitization ("hardening") in heat urticaria].

Heat contact urticaria, a very rare disease, is represented by the following pathogenetic entities: (1) forms provoked by histamine and (2) independent forms. Our case report deals with a temporary therapeutic success achieved by desensitization, as a result of local thermotherapy with rising temperatures and initially concomitant blocking of H1.

Benzhydryl Compounds↗
PubMed1988

Synthetic retinoids inhibit histamine release from isolated human mast cells.

In view of the immunomodulating properties of the synthetic retinoids etretinate and isotretinoin, their effects on isolated human mast cells were investigated. At concentrations of 10(-6) to 10(-5) M, isotretinoin and at 10(-6) M to 5 X 10(-5) M, etretinate inhibited concanavalin-A induced histamine release dose-dependently. Effective concentrations corresponded to achievable levels under therapeutic conditions in man. Without any additional stimulant, both drugs exhibited no appreciable effects with the exception of a toxic damage at very high levels.

Concanavalin A↗
PubMed1988

[Aerogenic contact dermatitis].

Airborne contact dermatitis is caused by hypersensitivity of the delayed type (cell-mediated allergy). This contact allergy is brought about by airborne plant particles, which affect the unclothed skin, especially outdoors. In 2 patients, we found strong reaction to different plants of the compositae family, their mutual allergens being sesquiterpene lactones.

Aged↗
PubMed1987

Study of the inhibition of histamine release by inosine pranobex.

The effects of Inosine pranobex and its parent compounds inosine and dimethylamino-2-propanol-p-acetamidobenzoic acid (DipPacBa) on the Concanavalin A (ConA)-induced histamine release from human adenoidal mast cells were investigated. Inosine pranobex inhibited the ConA-induced histamine release at concentrations greater than 10(-3) M. Inosine itself (10(-5)-10(-2) M) enhanced the ConA-induced histamine release whereas DipPacBa inhibited the release significantly at concentrations between 10(-6) and 10(-2) M. These results are consistent with the assumption that the effect of Inosine pranobex is due to the DipPacBa moiety.

Concanavalin A↗
PubMed1987

Seasonal variation of mast cell function in human adenoid tissues.

The number of mast cells which can be recovered from human adenoid tissues varies characteristically in the course of the year. The yield was found to be highest in May and lowest in July. The average histamine content was above average in April, June, July and September. Although the spontaneous histamine release remained relatively constant, the concanavalin A-stimulated histamine release was significantly reduced from June to September.

Adenoids↗
PubMed1985

The effects of adenosine and of some adenosine analogues on the concanavalin A-or acetylcholine-induced histamine release from human adenoidal mast cells.

Histamine release induced by concanavalin A (Con A) or acetylcholine is enhanced by adenosine or the adenosine analogues PIA and NECA. The enhancement is not affected by preincubation with adenosine deaminase. The degree of the Con A-induced histamine release decreases with increasing incubation time. Under these conditions, the enhancing effect of adenosine on histamine release is either abolished or even reversed to inhibition.

Acetylcholine↗
PubMed1985

The human adenoidal mast cell. Susceptibility to different secretagogues and secretion inhibitors.

Mast cells from adenoid tissues of man do not form a homogeneous population but differ in size and ultrastructure. They degranulate on stimulation with specific antigen, ionophore A 23187, Concanavalin A and, under certain conditions, antihuman IgE or acetylcholine. Compound 48/80, dextran, purified C3a or C5a are ineffective. Adenosine exerts either an enhancing or inhibiting effect on the stimulated histamine release, depending on the actual conditions of the mast cells. The study of a range of known mast cell degranulation inhibitors revealed important differences between human adenoidal mast cells and human basophils or animal mast cell systems. The efficacies of the drugs or drug combinations so far tested correspond well with the established therapeutic effects in man.

Adenoids↗
PubMed1984

Recognition of the 'calcium paradox' and the effects of verapamil and gallopamil in human adenoidal mast cells.

Human mast cells from adenoids show when resuspended in medium containing 10(-3) M CaCl2 after their temporary exposure to Ca2+-free saline for about 20 min an irreversible reduction of responsiveness to a variety of stimuli: The histamine release induced by concanavalin A or ionophore A 23187 is only 30-50% of the one obtained in cells which were kept in 10(-3) M Ca2+ throughout the experiment. This phenomenon called 'calcium paradox' can be almost entirely avoided if the cells are temporarily exposed to 10(-4) M Ca2+ instead of Ca2+-free saline. Number yields, average histamine contents of mast cells and the rate of the spontaneous histamine release are not affected by the transitory lack of Ca2+, nor is the histamine release enhancing effect of adenosine. At 10(-3) M Ca2+ concentration the calcium antagonists verapamil or gallopamil cause a significant inhibition of the Con A-induced histamine release only at concentrations much higher (10(-4) M than those effective in smooth muscle preparations. The actions of both calcium antagonists were not affected by the presence of added extracellular adenosine.

Adenoids↗
PubMed1983

[Pharmacological aspects of immunostimulants].

Immunostimulants are chemical substances capable of increasing the overall activity of a normal immune system as well as normalizing the function of an impaired immune system (immune restauration). This review is concerned with substances of microbial or chemical origin and excludes the so-called physiological inductors or regulators, e.g. thymic factors, interferon etc. During the last decade considerable progress has been achieved with respect to the isolation of effective compounds and the elucidation of their chemical structure. However, the knowledge of their mechanism of action and their effects in the living organism is still poor because of the complexity of the immune system, lack of appropriate standardization methods, lack of internationally agreed test conditions or diseases in intact animals or conditions for controlled clinical trials in man.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

[Pharmacological aspects of immunostimulation].

Immunostimulants are chemical substances capable of increasing the overall activity of a normal immune system as well as normalizing the function of an impaired immune system (immune restauration ). This review is concerned with substances of microbial or chemical origin and excludes the so-called physiological inductors or regulators, e.g. thymic factors, interferon etc. During the last decade considerable progress has been achieved with respect to the isolation of effective compounds and the elucidation of their chemical structure. However, the knowledge of their mechanism of action and their effects in the living organism is still poor because of the complexity of the immune system, lack of appropriate standardization methods, lack of internationally agreed test conditions or diseases in intact animals or conditions for controlled clinical trials in man.

Adjuvants, Immunologic↗