In patients with the adrenogenital syndrome, a single intramuscular injection of 40 mg every two weeks may be adequate. For maintenance of patients with rheumatoid arthritis , the weekly intramuscular dose will vary from 40 to 120 mg. The usual dosage for patients with dermatologic lesions benefited by systemic corticoid therapy is 40 to 120 mg of methylprednisolone acetate administered intramuscularly at weekly intervals for one to four weeks. In acute severe dermatitis due to poison ivy, relief may result within 8 to 12 hours following intramuscular administration of a single dose of 80 to 120 mg. In chronic contact dermatitis, repeated injections at 5 to 10 day intervals may be necessary. In seborrheic dermatitis, a weekly dose of 80 mg may be adequate to control the condition.
As others have noted, effective treatment of keloids can be very difficult. The reason for this is that keloids are an abnormal response to injury, and area of scar tissue that grows beyond its natural boundaries. On examination of a piece of Keloid tissue under a microscope, it looks substantially different than the average scar. The initial phase of treatment is to slow the inflammation, ergo the use of several spaced injections. The next option is to excise the scar surgically (50% recurrence rate) or to treat with radiation. After excision, the area can be radiated and/or re-injected with steroid. Some Surgeons advocate placement of topical mitomycin and/or topical 5 flurouracil at the time of excision. Despite all of these options, keloids can and do recur.
We hypothesize that the fibroblast, or the myofibroblast, or both are the key cells responsible for keloid and hypertrophic scar formation. These cell types produce the bulk of extracellular matrix components during normal wound healing. In fact, experimental evidence suggests that hypertrophic scars and keloids result from excessive amounts of collagen and proteoglycan production or from lack of remodeling of these moieties.''-" We also hypothesize that wound tension is a major factor in the formation of both the hypertrophic scar and the keloid, which occurs secondary to direct biochemical changes induced by this mechanical factor. Most likely these changes are a direct result of the effect of wound tension on the metabolism of the fibroblast or myofibroblast. Fibroblasts have been shown to increase cell proliferation in response to mechanical tension in Mechanical stretch alone has been shown to raise the number of myofibroblasts in mouse dermis in Presumably, mechanical tension is also responsible for a positive balance in the collagen and proteoglycan production-degradation cycle in the wound healing under excessive tension. We are currently studying the effects of mechanical tension on wound healing at the biochemical level. The cause-effect relationship between hypertrophic scar and keloid formation as well as other etiologic factors, such as the age and race of the patient, remain more highly speculative and are not discussed here.