Molecular and clinical pharmacology of psoriasis.

نویسندگان

  • J J Voorhees
  • E A Duell
  • M Stawiski
  • E R Harrell
چکیده

Psoriasis appears in most cases to be a genetic disease in which stratified squamous epithelium (epidermis) of skin in involved versus normal-appearing uninvolved areas has the following prototypic features: (1) excessive cell proliferation and an accelerated cell cycle of the proliferating cells '; (2) incomplete epidermal specialization (keratinization) for tissue function; and (3) marked increase in glycogen content. 7 It has been widely held that the relative lack of epidermal specialization is due to the rapid transit of cells through the epidermis (i.e., the cells are shed from the patient without sufficient time for normal keratinization to occur). However, an alternate explanation is that the excessive cell proliferation is the result of an inability of differentiated basal cells to make the commitment of specialization. For this reason we have listed incomplete specialization as one of the three characteristic findings in psoriasis lesions. We developed the concept that increased proliferation, decreased specialization, and increased glycogen content in psoriasis lesions might be associated with diminished levels of epidermal cyclic adenosine monophosphate (cAMP).1O This concept was derived from earlier observations that epinephrine inhibits epidermal mitosis in

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عنوان ژورنال:
  • Clinical pharmacology and therapeutics

دوره 16 5 Part 2  شماره 

صفحات  -

تاریخ انتشار 1974