Adult Acne Rosacea is a chronic and relapsing inflammatory skin condition commonly seen after age 30. It is characterized by either persistent or transient central facial erythema or flushing, small broken blood vessels (telangiectasias), and pustules or papules often along the cheeks. While there is no cure, there are a number of therapies to help suppress troublesome symptoms.


While there are a number of common triggers for adult acne rosacea, a definitive cause has yet to be determined. Considered possibilities include climactic change (extreme temperature changes, sun exposure, exercise), H. pylori infection, detrimental food habits (caffeine, spicy foods, alcohol), exercise, extreme mood changes (anger, embarrassment), irritation from applied topical products, and certain drugs (vasodilators, nicotinic acid from tobacco). Acne rosacea has a genetic predisposition for those with fairer skin types, particularly those of Northern European or Celtic origin; however, darker skinned individuals may also be afflicted. Furthermore, women appear to be affected in larger numbers than men.


Treatment is geared toward non-pharmacologic, often behavioral measures. These include avoidance of triggers, particularly those causing flushing, regular sun protection, and gentle skin care practices. Broken blood vessels may be treated with laser and light-based therapy (IPL). Those with inflammatory papules or pustules can be treated with topical medications, such as metronidazole cream or azelaic acid. For individuals suffering from more severe disease or extensive facial changes, oral medications such as tetracycline antibiotics or isotretinoin may be considered.


  • Abram K, Silm H, Maaroos HI, Oona M. Risk factors associated with rosacea. J Eur Acad Dermatol Venereol. 2010 May;24(5):565-71. doi: 10.1111/j.1468-3083.2009.03472.x. Epub 2009 Oct 23. PubMed PMID: 19874433.
  • Crawford GH, Pelle MT, James WD. Rosacea: I. Etiology, pathogenesis, and subtype classification. J Am Acad Dermatol. 2004 Sep;51(3):327-41; quiz 342-4. doi: 10.1016/j.jaad.2004.03.030. Review. PubMed PMID: 15337973.
  • Elewski BE, Draelos Z, Dréno B, Jansen T, Layton A, Picardo M. Rosacea – global diversity and optimized outcome: proposed international consensus from the Rosacea International Expert Group. J Eur Acad Dermatol Venereol. 2011 Feb;25(2):188-200. doi: 10.1111/j.1468-3083.2010.03751.x. Epub 2010 Jun 25. PubMed PMID: 20586834.




Early aging is a complex of skin changes including sunspots, wrinkles, sagging skin, dry or itchy skin, skin thinning, and hair loss.


As aging is not a homogenous process, there exists a multitude of factors contributing to early age changes. These include environmental exposures, socioeconomic stressors, lifestyle choices, and one’s own genetics. Those causes most commonly implicated in early aging of the skin include sun and UV light exposure, stress, drug use (particularly methamphetamine abuse and tobacco smoking), and air pollution.


Good lifestyle habits, including managing stress and sleeping regularly, weighs heavily in prevention of early aging. Additionally, abstaining from drugs and alcohol, eating a well-balanced diet with healthy fats and reduced simple carbohydrates and sugars, and drinking enough water is essential. This will fuel your body with the necessary components to build and maintain healthy skin as your cell activity slows down in this phase of life. Supplements, such as iron and vitamin D, can aid in this endeavor.

UV-protective strategies, including photoprotective clothing and mineral-based sunscreens (zinc, titanium dioxide) with SPF ≥ 30 and avoiding tanning beds is critical.

There are numerous medical treatments for early aging, depending upon the main cause. Topical medications, including retinoic acid derivatives, azelaic acid, and niacinamide, are treatment mainstays in reversing aging signs, such as fine lines and dark spots. Chemical peels and laser treatments, as well as various injectables (fillers and neurotoxins) also have a marked impact on improving overall appearance of aged skin.


  • Bayerl C. [Skin aging and evidence-based topical strategies]. Hautarzt. 2016 Feb;67(2):140-7. doi: 10.1007/s00105-015-3737-3. PubMed PMID: 26683808.
  • Yonei Y, Ichihashi M, Takabe W. Age-related diseases of the skin and anti-aging medicine. Nihon Rinsho. 2016 Sep;74(9):1541-1547. Review. PubMed PMID: 30557490.




Melasma is a common, asymptomatic condition of hyperpigmentation due to overactive pigment-producing skin cells (melanocytes) afflicting mostly women in their reproductive years. It is a chronic, recurring disorder affecting heavily sun-exposed areas, particularly the face.

Melasma lesions typically present as light brown-grey brown, irregularly-shaped macules and patches (small and big flat spots) symmetrically, usually along the nose bridge, upper lip, cheeks, forehead, and chin.


The pathogenesis of melasma is multifaceted; main triggers or predilections for its development include one’s UV light exposure, genetics, hormonal changes (pregnancy, oral contraceptives, hormonal treatments), and skin phototype. Additional factors contributing to the appearance of melasma include the use of photosensitizing drugs and zinc deficiency.


Treating melasma is challenging with frequent relapses commonplace. As causative factors are multifold, so, too, then must be the treatment plan. Caring for melasma starts with photoprotective strategies, such as sunscreen, sun avoidance, and sun-protective clothing. Topical therapy is then incorporated with the use of skin lighteners, such as hydroquinone, azelaic acid, niacinamide, kojic acid, and retinoids. Oral medications, such as Polypodium leucomotos and glutathione, are second-line agents. For those with extensive or refractory lesions, chemical peels and lasers may be considered.


  • Bak H, Lee HJ, Chang SE, Choi JH, Kim MN, Kim BJ. Increased expression of nerve growth factor receptor and neural endopeptidase in the lesional skin of melasma. Dermatol Surg. 2009 Aug;35(8):1244-50. doi: 10.1111/j.1524-4725.2009.01219.x. Epub 2009 May 12. PubMed PMID: 19438666.
  • Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. 1995 Dec;131(12):1453-7. doi: 10.1001/archderm.131.12.1453. Review. PubMed PMID: 7492140.
  • Passeron T. Melasma pathogenesis and influencing factors – an overview of the latest research. J Eur Acad Dermatol Venereol. 2013 Jan;27 Suppl 1:5-6. doi: 10.1111/jdv.12049. Review. PubMed PMID: 23205539.
  • Rajaratnam R, Halpern J, Salim A, Emmett C. Interventions for melasma. Cochrane Database Syst Rev. 2010 Jul 7;(7):CD003583. doi: 10.1002/14651858.CD003583.pub2. Review. PubMed PMID: 20614435.




Psoriasis is a common, immune-mediated, inflammatory skin disease with a strong polygenic component and multiple clinical subtypes. The most common of these subtypes is plaque psoriasis, which presents as sharply defined, erythematous (reddened), itchy plaques. The scalp, elbows, knees, and buttocks are most often affected. Additional subtypes less commonly seen are:

Guttate psoriasis: multiple smaller, erythematous plaques with a “rained-on” appearance along the torso and extremities
Pustular psoriasis: numerous tiny pustules develop superficially on the skin, often with accompanying erythema and/or fever. There are several pustular variants: von Zumbusch, annular pattern, exanthematic, localized patterns, and pustulosis of the hands and feet.
Erythrodermic psoriasis: extensive erythema, peeling, and scaling throughout the entire body. While uncommon, this condition makes patients more susceptible to complications due to their compromised skin barrier. They are often unable to properly regulate their body temperature or protect against infection or fluid loss.


Psoriasis has a strong polygenic component, meaning multiple genetic factors influence the development of the disease. These genetic predilections, when combined with environmental triggers, such as infections, medications, injury, and stress, result in the exacerbation of psoriatic lesions.


While there exists no cure for psoriasis, the goal of treatment is to maintain control of the disease and prevent widespread lesions. Limited disease can be treated with topical therapies, such as corticosteroids, vitamin D analogs, calcineurin inhibitors, and retinoids. More extensive disease may necessitate the use of phototherapy or systemic medications such as methotrexate, cyclosporine, oral retinoids, or biologic immune modifiers. These medications, while having the ability to clear lesions within several weeks, require informed consideration and prior lab work, due to their immunosuppressive effects.


  • Bolognia, J., Jorizzo, J. L., & Schaffer, J. V. (2012). Dermatology. Philadelphia: Elsevier Saunders.
  • Menter A, Griffiths CE. Current and future management of psoriasis. Lancet. 2007 Jul 21;370(9583):272-284. doi: 10.1016/S0140-6736(07)61129-5. Review. PubMed PMID: 17658398.
  • Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017 Feb;31(2):205-212. doi: 10.1111/jdv.13854. Epub 2016 Aug 30. Review. PubMed PMID: 27573025.




The most abundant protein in our skin is collagen, which provides a kind of scaffolding for our skin. Natural aging results in a breakdown of collagen and elastic fibers of the skin. This loss, combined with decreasing hyaluronic acid content, results in the formation of wrinkles, sagging skin, and an overall deflated appearance.


Collagen production naturally begins to slow after age 35, with loss directly attributable to hormonal changes accompanying the aging process. This process accelerates after menopause. However, the causes of premature collagen loss are multifactorial. They include sun and UV light exposure, tobacco smoking, air pollution, and an inflammatory diet.


Unfortunately, even though collagen loss can have a dramatic impact on the psycho-social health of individuals, these treatments are not typically considered medically necessary by insurance. As such, collagen loss therapy is considered cosmetic and incurs an out-of-pocket cost.

Hormone replacement therapy, such as estrogen and DHEA supplementation, can help reduce the rate of collagen loss. Injectable therapies, such as hyaluronic acid fillers (i.e., Juvederm and Restylane products), can be used to increase fullness in lips and cheeks, and for facial contouring to decrease the appearance of wrinkles and sagging skin. Fractionated lasers (Fraxel) and microneedling stimulate neocollagenesis (new collagen growth) through micro-injuries that promote the release of growth factors necessary to induce collagen production. There are a plethora of treatments to choose from, all of which should be discussed with a dermatology provider in order to choose the best treatment plan to meet your skincare goals.


  • Castelo-Branco C, Duran M, González-Merlo J. Skin collagen changes related to age and hormone replacement therapy. Maturitas. 1992 Oct;15(2):113-9. doi: 10.1016/0378-5122(92)90245-y. PubMed PMID: 1345134.
  • Fabbrocini, G., Mazzella, C., & D’Andrea, M. (2020). Microneedling for Neocollagenesis of the Face. In Minimally Invasive Aesthetic Procedures (pp. 625-630). Springer, Cham.
  • Moragas A, Castells C, Sans M. Mathematical morphologic analysis of aging-related epidermal changes. Anal Quant Cytol Histol. 1993 Apr;15(2):75-82. PubMed PMID: 8318130.
  • Varani, J., Dame, M. K., Rittie, L., Fligiel, S. E., Kang, S., Fisher, G. J., & Voorhees, J. J. (2006). Decreased collagen production in chronologically aged skin: roles of age-dependent alteration in fibroblast function and defective mechanical stimulation. The American journal of pathology, 168(6), 1861–1868.
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