Detection of R576 interleukin-4 receptor an allele gene, serum interleukin-4, and eosinophilic cationic protein in atopic dermatitis patients.

Atopic dermatitis (AD) is a chronic pruritic skin disease. It results from a complex interplay between strong genetic and environmental factors. The aim of this work was to study some biochemical markers of the dermatosis. This included detection of R576 interleukin-4 receptor alpha allele gene. Twenty five patients with AD and 25 controls participated in this study.

The effect of ivomec super on dogs experimentally infested with Sarcoptes scabiei isolated from a patient.

Scabies infestation is a community health problem worldwide. This is particularly true in overcrowded and unhygienic areas. Seven dogs were experimentally infested with Sarcoptes scabiei freshly recovered from a patient. The dogs after infestation were treated with a mixture of ivermectin and clorsulon (Ivomec Super). The dose given to a single dog was 1 ml/50 kg body weight. This is equivalent to 200 mcg ivermectin and 2 mg clorsulon per Kg body weight. Five of the dogs (71.43%) were completely cured with 1 ml/50 Kg body weight. The remaining two dogs needed each, another injection of the same dose two weeks later. So, ivomec super is effective against the human strain of Sarcoptes scabiei in experementally infested dogs. A general discussion was given.

Suppression of vascular injury at the Arthus reaction site by a complement inhibitor, 5,5',5''-(1,3,6-naphthalene-triyl-tris[sulfonylimino])-tris (1,3-benzene disulfonic acid) hexasodium salt.

A novel polyanionic complement inhibitor 5,5,5''-(1,3,6-naphthalene-triyl-tris[sulfonylimino])-tris(1 ,3-benzene- disulfonic acid) hexasodium salt (compound IIb) was tested for its ability to suppress vascular injury at the site of the Arthus reaction (AR). In control animals in which AR was evoked without drug treatment, venules at AR sites ranged from normal (arbitrarily defined as stage I) to destroyed (stage V). Between these two ends of the spectrum were venules with an accumulation of cells and deposits of electron dense material (stage II), accumulations of cells and deposits and small endothelial gappings (stage III), and accumulations of cells and depositions which had spread into perivascular tissue and small gappings (stage IV). In animals treated with compound IIb, the AR stopped at stage III or IV depending on the dose, it never reached stage V. In other words compound IIb treatment resulted in protection of endothelium, basal lamina and other structures from the destruction which is characteristically observed in the AR. The effect of high doses of compound IIb was similar to that described before for suramin.

Inhibition of cellular infiltration at the site of Arthus reaction by chlorpromazine. Use of a new area integration technique.

Chlorpromazine, an inhibitor of the complement (C) system, inhibited the cellular infiltration at the site of Arthus reaction (AR), as assessed by a newly developed computerized area integration technique (CAIT). This inhibition was rather strong (mean value 92%) and statistically significant according to the classical quotient estimator. This may, at least in part, explain the protection of vessel wall destruction by chlorpromazine in AR, as observed in a previous study. CAIT estimated cellular infiltration in H & E stained skin biopsy sections quantitatively and reliably.

Suppression of complement-mediated vascular injury at Arthus reaction sites by complement inhibitors.

Certain complement inhibitors, namely chlorpromazine, suramin, 2-hydroxystilbamidine and chlorophenothiazine sulphonate were tested for their ability to suppress complement deposition and vascular injury at the site of an Arthus reaction. Deposition of complement was suppressed in the order 2-hydroxystilbamidine greater than suramin greater than chlorpromazine. All the above mentioned four compounds strongly protected vascular injury as observed by electron microscopic studies. At Arthus reaction sites prepared without drug treatment venules ranged from normal to severely altered and damaged. Discontinuities in endothelial linings varied from small to longer stretches. In the latter situation remaining endothelial cells were degenerated and endothelial remnants did not have an intact basal lamina. After treatment with the above complement inhibitors, at arthus reaction sites some venules appeared normal, whereas others were altered but in all cases the endothelium and its basal lamina remained intact.