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Thread: Should type 1 rosacea people use metrogel,soolantra,finacea etc?

  1. #21
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    Quote Originally Posted by Brady Barrows View Post
    Did you actually get a diagnosis of subtype 1 from your physician or did you self diagnose yourself? Either way, you or your physician are not keeping up with the latest classification of rosacea. Depending on the phenotype determines the treatment.

    One of the many theories on the cause of rosacea is sun damage and you should have your physician rule out photosensitivity diseases from rosacea.

    "When a patient presents with a rash on sun-exposed areas, a thorough history must be taken that includes exposure to sunlight, use of medication, and prior personal and family history of manifestations of dermatologic disease. The dermatologic examination further delineates the photosensitive dermatosis. Correctly diagnosing the specific condition associated with a photosensitive rash makes it possible to provide adequate treatment and, depending on the diagnosis, avoid future outbreaks. Clinicians must be aware of the spectrum of photosensitivity diseases because these conditions are common and can be associated with systemic diseases, although they are rarely life-threatening."

    https://www.jwatch.org/na37452/2015/04/21/rosacea-or-photodamage

    The redness of erythematotelangiectatic rosacea appears to be caused by inflammation and vasodilation rather than vasodilation alone.

    The diagnosis of erythematotelangiectatic rosacea (ETR) is complicated by its resemblance to photodamage in light-skinned individuals. To better define the clinical, histologic, and molecular differences, investigators conducted a case-controlled observational study of visible facial telangiectasia and erythema in patients with ETR, telangiectatic photoaging (TP), and 11 controls.

    Clinically, ETR patients had erythema and telangiectases primarily on the central face and less photodamage overall than TP patients. A chromometer failed to detect a significant difference in erythema between TP and ETR patients but did detect differences from controls. Significantly more inflammation was observed in ETR patients. Gene expression of matrix metalloproteinase-3 was greater in the ETR patients compared with controls and patients with TP, as were gene transcripts for the neuropeptides calcitonin gene-related peptide and substance P. Expression of gene transcripts for collagen types I and III, decorin, and matrix metalloproteinases 1, 3, and 9 were increased in ETR compared with TP and control patients. Counts of mast cells did not differ, but quantitative image analysis of histologic sections stained with mast cell tryptase showed 4-fold greater staining in TP and 25-fold greater staining in ETR. Levels of cytokines such as TNFα and CXCL12 were increased; levels of defensin were elevated, but levels of other antimicrobial peptides were not elevated in ETR skin compared with controls.

    COMMENT
    Clinical, histological, immunochemical, ultrastructural, and gene-control parameters differed between ETR skin and TP skin, but no finding was a definitive marker. Because clinical findings overlap, some patients may have been inappropriately assigned. Centrofacial location of redness, flushing, sensory change, and involvement of the nose help point to a diagnosis of ETR over TP.

    This study adds evidence that the redness of ETR consists of inflammation and vasodilation rather than vasodilation alone. This inflammation may account for barrier impairment, burning sensations, “dryness” of facial skin, and response to anti-inflammatory agents. Why the skin inflames is speculative. The study and the accompanying editorial present lots of data to ponder and raise many questions.

    Interesting article
    Last edited by LawrenceK; 19th March 2020 at 04:29 AM.

  2. #22
    Senior Member Brady Barrows's Avatar
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    Quote Originally Posted by LawrenceK View Post
    https://www.jwatch.org/na37452/2015/04/21/rosacea-or-photodamage
    The redness of erythematotelangiectatic rosacea appears to be caused by inflammation and vasodilation rather than vasodilation alone.
    The diagnosis of erythematotelangiectatic rosacea (ETR) is complicated by its resemblance to photodamage in light-skinned individuals. To better define the clinical, histologic, and molecular differences, investigators conducted a case-controlled observational study of visible facial telangiectasia and erythema in patients with ETR, telangiectatic photoaging (TP), and 11 controls.
    Clinically, ETR patients had erythema and telangiectases primarily on the central face and less photodamage overall than TP patients. A chromometer failed to detect a significant difference in erythema between TP and ETR patients but did detect differences from controls. Significantly more inflammation was observed in ETR patients. Gene expression of matrix metalloproteinase-3 was greater in the ETR patients compared with controls and patients with TP, as were gene transcripts for the neuropeptides calcitonin gene-related peptide and substance P. Expression of gene transcripts for collagen types I and III, decorin, and matrix metalloproteinases 1, 3, and 9 were increased in ETR compared with TP and control patients. Counts of mast cells did not differ, but quantitative image analysis of histologic sections stained with mast cell tryptase showed 4-fold greater staining in TP and 25-fold greater staining in ETR. Levels of cytokines such as TNFα and CXCL12 were increased; levels of defensin were elevated, but levels of other antimicrobial peptides were not elevated in ETR skin compared with controls.
    COMMENT
    Clinical, histological, immunochemical, ultrastructural, and gene-control parameters differed between ETR skin and TP skin, but no finding was a definitive marker. Because clinical findings overlap, some patients may have been inappropriately assigned. Centrofacial location of redness, flushing, sensory change, and involvement of the nose help point to a diagnosis of ETR over TP.
    This study adds evidence that the redness of ETR consists of inflammation and vasodilation rather than vasodilation alone. This inflammation may account for barrier impairment, burning sensations, “dryness” of facial skin, and response to anti-inflammatory agents. Why the skin inflames is speculative. The study and the accompanying editorial present lots of data to ponder and raise many questions.
    Interesting article
    I tried to find the full text of the article but couldn't. If you have a link to the full article that would be appreciated. I have added your link above to this post about photosensitivity diseases. Good find LawrenceK.
    Brady Barrows
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  3. #23
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    Quote Originally Posted by LawrenceK View Post
    So I have type 1 rosacea which basically just gives me baseline redness 24/7 with visible spider veins down the side of my nose. I do flush occasionally but that doesn't really bother me. I also have zero spots, acne etc. I'm like 99% sure my Rosacea was caused by sun damage it appeared during last summer and hasn't left. So I'm thinking in my case it's not so much an inflammatory problem as much as blood vessel/capillary damage.

    I'm wondering before I try for last resort and go for a v beam. Would any of these -metrogel,soolantra,finacea/azelaic gel, rozex, efacea; help me out? Or are these medications for people that have type 2-3 and gut/inflammation issues?
    Mine was popping white heads whilst getting sunburnt on my nose.

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