Gold Bond - The Pramoxine may be what helps

[Guest guest]

The active ingredients are pramoxine (hydrochloride) 1% and menthol

1%. Pramoxine is a Nonsteroidal antipruritic. I think that is what

helps rosacea. It's in gold bond, hemmorhoid, and other types of

creams. See below (pramoxine is discussed in last paragraph):

http://www.postgradmed.com/issues/1999/11_99/brodell.htm

Discussion

Topical corticosteroids have been the mainstay of dermatologic

treatment since they were introduced in the 1950s (1,2). Increasingly

strong preparations have led to more reports of side effects,

especially on the face, axillae, and groin, where corticosteroids

more easily penetrate the epidermis (1,3,4). These adverse effects

include cutaneous atrophy, striae formation, hypopigmentation,

fragility, and telangiectasia (1-9).

Perhaps the most pernicious side effect of topical corticosteroids is

perioral dermatitis, or corticosteroid-induced acne rosacea. Physical

dependence develops as attempts to discontinue corticosteroids lead

to ever-worsening flares, which prompt continued use (4,10). The

mechanism of this corticosteroid " addiction " has three phases: (1)

With initial use of topical corticosteroids, pustulation, pruritus,

erythema, and scaling diminish because of the anti-inflammatory

effect of the drugs. (2) With continued use of corticosteroids,

microbial growth increases because of local immunosuppression (1,4).

(3) On corticosteroid withdrawal, the immune response is no longer

suppressed, and rebound flares of itching, redness, pustulation, and

scaling result from the steadily worsening bacterial infection (4,10-

14).

This addictive cycle can be broken by use of three treatment

strategies. The first and most important is prompt discontinuation of

the offending topical corticosteroids (4). This strategy also

involves patient education about inevitable--although transient--

rebound flares so that patients accept and comply with treatment. The

second strategy is use of systemic antibiotics to suppress follicular

infection. Oral tetracycline hydrochloride, 500 mg twice a day for

several weeks, is the drug of choice; in young children, oral

erythromycin, 200 to 400 mg twice a day, may be substituted

(4,6,10,12,15). The third strategy is simultaneous use of emollients

and antipruritics to control symptoms. Clindamycin (Cleocin T lotion)

and erythromycin (Akne-Mycin ointment) are the topical antibiotics of

choice because of their emollient bases (4,16). Nonsteroidal

antipruritics such as pramoxine hydrochloride (Prax lotion) aid in

minimizing rebound symptoms so that a tapered course of low-potency

corticosteroids is not necessary (4). Systemic antihistamines may

also be useful in the control of pruritus.

[Guest guest]

I wrote the below message a while back. I found gold bond

ingredients by doing an internet search, but when I went to the drug

store to purchase and try it I noticed that the pramoxine (non

steriodal anti-pruitic) was only listed on the gold bond that comes

in the tube. This is confusing to me as I thought for sure the

pramoxine would have been the helpful ingredient. I really am

confused as to why the green bottle gold bond (without pramoxine)

would help SO much. I wonder if the pramoxine is in the green bottle

but not listed for some reason..

Patty

> The active ingredients are pramoxine (hydrochloride) 1% and menthol

> 1%. Pramoxine is a Nonsteroidal antipruritic. I think that is

what

> helps rosacea. It's in gold bond, hemmorhoid, and other types of

> creams. See below (pramoxine is discussed in last paragraph):

>

> http://www.postgradmed.com/issues/1999/11_99/brodell.htm

>

> Discussion

> Topical corticosteroids have been the mainstay of dermatologic

> treatment since they were introduced in the 1950s (1,2).

Increasingly

> strong preparations have led to more reports of side effects,

> especially on the face, axillae, and groin, where corticosteroids

> more easily penetrate the epidermis (1,3,4). These adverse effects

> include cutaneous atrophy, striae formation, hypopigmentation,

> fragility, and telangiectasia (1-9).

>

> Perhaps the most pernicious side effect of topical corticosteroids

is

> perioral dermatitis, or corticosteroid-induced acne rosacea.

Physical

> dependence develops as attempts to discontinue corticosteroids lead

> to ever-worsening flares, which prompt continued use (4,10). The

> mechanism of this corticosteroid " addiction " has three phases: (1)

> With initial use of topical corticosteroids, pustulation, pruritus,

> erythema, and scaling diminish because of the anti-inflammatory

> effect of the drugs. (2) With continued use of corticosteroids,

> microbial growth increases because of local immunosuppression

(1,4).

> (3) On corticosteroid withdrawal, the immune response is no longer

> suppressed, and rebound flares of itching, redness, pustulation,

and

> scaling result from the steadily worsening bacterial infection

(4,10-

> 14).

>

> This addictive cycle can be broken by use of three treatment

> strategies. The first and most important is prompt discontinuation

of

> the offending topical corticosteroids (4). This strategy also

> involves patient education about inevitable--although transient--

> rebound flares so that patients accept and comply with treatment.

The

> second strategy is use of systemic antibiotics to suppress

follicular

> infection. Oral tetracycline hydrochloride, 500 mg twice a day for

> several weeks, is the drug of choice; in young children, oral

> erythromycin, 200 to 400 mg twice a day, may be substituted

> (4,6,10,12,15). The third strategy is simultaneous use of

emollients

> and antipruritics to control symptoms. Clindamycin (Cleocin T

lotion)

> and erythromycin (Akne-Mycin ointment) are the topical antibiotics

of

> choice because of their emollient bases (4,16). Nonsteroidal

> antipruritics such as pramoxine hydrochloride (Prax lotion) aid in

> minimizing rebound symptoms so that a tapered course of low-potency

> corticosteroids is not necessary (4). Systemic antihistamines may

> also be useful in the control of pruritus.

[Guest guest]

I wrote the below message a while back. I found gold bond

ingredients by doing an internet search, but when I went to the drug

store to purchase and try it I noticed that the pramoxine (non

steriodal anti-pruitic) was only listed on the gold bond that comes

in the tube. This is confusing to me as I thought for sure the

pramoxine would have been the helpful ingredient. I really am

confused as to why the green bottle gold bond (without pramoxine)

would help SO much. I wonder if the pramoxine is in the green bottle

but not listed for some reason..

Patty

> The active ingredients are pramoxine (hydrochloride) 1% and menthol

> 1%. Pramoxine is a Nonsteroidal antipruritic. I think that is

what

> helps rosacea. It's in gold bond, hemmorhoid, and other types of

> creams. See below (pramoxine is discussed in last paragraph):

>

> http://www.postgradmed.com/issues/1999/11_99/brodell.htm

>

> Discussion

> Topical corticosteroids have been the mainstay of dermatologic

> treatment since they were introduced in the 1950s (1,2).

Increasingly

> strong preparations have led to more reports of side effects,

> especially on the face, axillae, and groin, where corticosteroids

> more easily penetrate the epidermis (1,3,4). These adverse effects

> include cutaneous atrophy, striae formation, hypopigmentation,

> fragility, and telangiectasia (1-9).

>

> Perhaps the most pernicious side effect of topical corticosteroids

is

> perioral dermatitis, or corticosteroid-induced acne rosacea.

Physical

> dependence develops as attempts to discontinue corticosteroids lead

> to ever-worsening flares, which prompt continued use (4,10). The

> mechanism of this corticosteroid " addiction " has three phases: (1)

> With initial use of topical corticosteroids, pustulation, pruritus,

> erythema, and scaling diminish because of the anti-inflammatory

> effect of the drugs. (2) With continued use of corticosteroids,

> microbial growth increases because of local immunosuppression

(1,4).

> (3) On corticosteroid withdrawal, the immune response is no longer

> suppressed, and rebound flares of itching, redness, pustulation,

and

> scaling result from the steadily worsening bacterial infection

(4,10-

> 14).

>

> This addictive cycle can be broken by use of three treatment

> strategies. The first and most important is prompt discontinuation

of

> the offending topical corticosteroids (4). This strategy also

> involves patient education about inevitable--although transient--

> rebound flares so that patients accept and comply with treatment.

The

> second strategy is use of systemic antibiotics to suppress

follicular

> infection. Oral tetracycline hydrochloride, 500 mg twice a day for

> several weeks, is the drug of choice; in young children, oral

> erythromycin, 200 to 400 mg twice a day, may be substituted

> (4,6,10,12,15). The third strategy is simultaneous use of

emollients

> and antipruritics to control symptoms. Clindamycin (Cleocin T

lotion)

> and erythromycin (Akne-Mycin ointment) are the topical antibiotics

of

> choice because of their emollient bases (4,16). Nonsteroidal

> antipruritics such as pramoxine hydrochloride (Prax lotion) aid in

> minimizing rebound symptoms so that a tapered course of low-potency

> corticosteroids is not necessary (4). Systemic antihistamines may

> also be useful in the control of pruritus.