Purpura corticosteroids

IT SHOULD BE EMPHASIZED THAT DOSAGE REQUIREMENTS ARE VARIABLE AND MUST BE INDIVIDUALIZED ON THE BASIS OF THE DISEASE UNDER TREATMENT AND THE RESPONSE OF THE PATIENT. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached. Situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient’s individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment. In this latter situation it may be necessary to increase the dosage of the corticosteroid for a period of time consistent with the patient’s condition. If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly.

The proportion of patients who achieved an overall initial response was higher in the group that received HD-DXM (% vs. % in the prednisone group, P = .044) and the rate of complete response also favored HD-DXM (% vs. %; p=). Additionally, patients on the HD-DXM arm responded more quickly. The likelihood of achieving a sustained response was similar: 40 percent in the HD-DXM arm and percent in the prednisone arm (P = ). While the frequency of some adverse effects (., mood disorder or insomnia) was similar in both groups, weight gain and/or Cushingoid appearance affected more than 10 percent of the prednisone-treated patients (vs. none of the patients treated with HD-DXM).

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics , American Society of Nephrology , International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Horizon Pharmaceuticals); ; Dicerna, Jannsen Pharmaceuticals.

Parameters No. treated 40 Females 23 Males 17 No. with Atopic Dermatitis 15 No. with Psoriasis vulgaris 25 Mean age (years) 43 (range 22-57) Mean duration of treatment with Group III or IV topical steroids (years) 16 (range 6-25) Localization of skin atrophy:   Extremities 40 Face 28 Trunk 12 Concomitant Diseases:   Arthritis 7 Hypertonia 6 Rhinitis allergica 4 Concomitant medication:   Antiflogistica 6 Antihistamines 2 Antihypertensive drugs 5 Table 2.
Clinical evaluation of severity of symptoms and signs of skin atrophy at baseline and at end of treatment.

Clinical parameters Mean severity at baseline Mean severity at end of treatment Decreased thickness of skin (range 2-3) Laxity (range 2-3) Purpura/Echymoses (range 1-3) Dryness Teleangiectasia (range 2-3) (range 1-2) Table 3.
Mean epidermal and dermal thickness, skin elasticity, erythemal and moisture indexes at baseline and after 8 months of treatment with Vivida of 40 patients with corticosteroid induced skin atrophy.
Parameters Baseline 8 months Epidermal thickness (mm) (-) (-) Dermal thickness (mm) (-) (-) Elasticity Index 44 (39-53) 74 (65-78) Erythemal Index (-) (-) Moisture Index (11-37) (75-97)

In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone. [46] The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field. [47] The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.

Purpura corticosteroids

purpura corticosteroids

Parameters No. treated 40 Females 23 Males 17 No. with Atopic Dermatitis 15 No. with Psoriasis vulgaris 25 Mean age (years) 43 (range 22-57) Mean duration of treatment with Group III or IV topical steroids (years) 16 (range 6-25) Localization of skin atrophy:   Extremities 40 Face 28 Trunk 12 Concomitant Diseases:   Arthritis 7 Hypertonia 6 Rhinitis allergica 4 Concomitant medication:   Antiflogistica 6 Antihistamines 2 Antihypertensive drugs 5 Table 2.
Clinical evaluation of severity of symptoms and signs of skin atrophy at baseline and at end of treatment.

Clinical parameters Mean severity at baseline Mean severity at end of treatment Decreased thickness of skin (range 2-3) Laxity (range 2-3) Purpura/Echymoses (range 1-3) Dryness Teleangiectasia (range 2-3) (range 1-2) Table 3.
Mean epidermal and dermal thickness, skin elasticity, erythemal and moisture indexes at baseline and after 8 months of treatment with Vivida of 40 patients with corticosteroid induced skin atrophy.
Parameters Baseline 8 months Epidermal thickness (mm) (-) (-) Dermal thickness (mm) (-) (-) Elasticity Index 44 (39-53) 74 (65-78) Erythemal Index (-) (-) Moisture Index (11-37) (75-97)

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