Acne

From New World Encyclopedia

Acne is a group of skin rashes that have different causes.

  • Acne vulgaris - most commonly experienced around puberty, typically of the face and shoulders/chest
  • Acne rosacea - a red rash predominantly on the face
  • Acne keloidalis nuchae (Pseudofolliculitis nuchae) - a rash caused by shaving
  • Acne conglobata (Hidradenitis suppurativa) - chronic abscesses or boils of sweat glands and hair follicles; in the underarms, groin and buttocks, and under the breasts in women
  • Acne cosmetica - acne caused by cosmetics
  • Acne fulminans - an extreme form of acne conglobata
  • Acne medicamentosa - acne caused by starting or stopping a medicine
  • Baby acne - a rash seen on the cheeks, chin, and forehead of infants
  • Chloracne - an acne rash caused by exposure to chlorinated hydrocarbons such as dioxins or PCBs


Acne vulgaris

Acne
Akne-jugend.jpg

Acne of a 14 year old boy during puberty
ICD-10 L70.0
ICD-O: {{{ICDO}}}
ICD-9 706.1
OMIM {{{OMIM}}}
MedlinePlus 000873
eMedicine derm/2
DiseasesDB 10765
Different types of Acne Vulgaris: A: Cystic acne on the face, B: Subsiding tropical acne of trunk, C: Extensive acne on chest and shoulders.

Acne vulgaris is an inflammatory disease of the skin, caused by changes in the pilosebaceous units (skin structures consisting of a hair follicle and its associated sebaceous gland). Acne lesions are commonly referred to as pimples, spots or zits.

Acne affects a large percentage of humans at some stage in life. The condition is most common during puberty and is considered an abnormal response to normal levels of the male hormone testosterone. The response for most people diminishes over time and acne thus tends to disappear, or at least decrease, after one reaches his or her early twenties. However, there is no way to predict how long it will take for it to disappear entirely, as some individuals will continue to suffer from acne decades later into their thirties, forties,and beyond. [citation needed]

Symptoms

File:Acne face.jpg
Acne of an older teenager.

The most common form of acne is known as "acne vulgaris." Excessive secretion of oils from the sebaceous glands (mostly due to gland enlargement during puberty), accompanied by the plugging of the pores with naturally occurring dead skin cells (corneocytes), results in a blockade of the hair follicles. The accumulation of these corneocytes in the duct appears to be due to a failure of the normal keratinization process in the skin which usually leads to shedding of skin cells lining the pores. Once this defect in the keratinization process leads to these cells blocking the pore, the oil build up within the pore provides a favorable environment for the bacteria Propionibacterium acnes to multiply uncontrollably. In response to the bacterial populations, there is inflammation with attraction of white blood cells (neutrophils) to combat the bacteria, producing the visible lesion. The lesions have a propensity to affect the face, chest, back, shoulders and upper arms. The lesions occur as various forms and include: comedones, papules, pustules, nodules, and inflammatory cysts. Commonly, a pore that remains open (open comedo) but continues to distend with the keratinocytes, sebum oxidized by the bacteria, as well as the skin pigment melanin, is reffered to as a "blackhead". On the contrary, when a pore is occluded (closed comedo) by the dead skin cells, leading to accumulation of the materials below it, it is reffered to as a "whitehead." Cysts, pustules, papules, and nodules are severer lesions that usually form when the accumulations within the pore rupture into the surrounding skin. The level of the rupture determines the severity of these lesions. After resolution of acne lesions, prominent unsightly scars may remain. Hyperpigmentation of the skin around the lesion also has been noted, especially in darker skinned individuals. Aside from scarring, its main effects are psychological, such as reduced self-esteem [1] and depression or suicide.[2] Acne usually appears during adolescence, when people already tend to be most socially insecure. Early and aggressive treatment is therefore advocated to lessen the overall impact to individuals.[1]

Causes of acne

Exactly why some people get acne and some do not is not fully known. It is known to be partly hereditary. Several factors are known to be linked to acne:

  • Hormonal activity, such as menstrual cycles and puberty
  • Diet
  • Stress, through increased output of hormones from the adrenal (stress) glands.
  • Hyperactive sebaceous glands, secondary to the three hormone sources above.
  • Accumulation of dead skin cells.
  • Bacteria in the pores, to which the body becomes 'allergic'.
  • Skin irritation or scratching of any sort will activate inflammation.
  • Use of anabolic steroids.
  • Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
  • Exposure to high levels of chlorine compounds, particularly chlorinated dioxins, can cause severe, long-lasting acne, known as Chloracne.

Traditionally, attention has focused mostly on hormone-driven over-production of sebum as the main contributing factor of acne. More recently, more attention has been given to narrowing of the follicle channel as a second main contributing factor. Abnormal shedding of the cells lining the follicle, abnormal cell binding ("hyperkeratinization") within the follicle, and water retention in the skin (swelling the skin and so pressing the follicles shut) have all been put forward as important mechanisms. Several hormones have been linked to acne: the male hormones testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I). In addition, acne-prone skin has been shown to be insulin resistant [citation needed].

Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adults may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing's syndrome. Dermatologists are seeing more cases of menopause-associated acne as fewer women replace the natural anti-acne ovarian hormone estradiol whose production fails as women arrive at menopause.

Misconceptions about causes

There are many misconceptions and rumors about what does and does not cause the condition:

Diet

Diet. One study suggested that chocolate, french fries, potato chips and sugar, among others, affect acne. A high GI (glycemic index) diet that causes sharp rises in blood sugar worsens acne. This, however, has been refuted by dermatologists and has been accepted as myth.[3] If this study's conclusions are verified then a low GI diet may help acne, but a recent review of somewhat dated scientific literature cannot affirm either way.[4] A recent study, based on a survey of 47,335 women, did find a positive epidemiological association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese and cream cheese.[5] The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine IGF-I) present in cow milk. Although the association between milk and acne has been definitively shown, the ingredient in the milk responsible for the acne is still unclear. Most dermatologists are awaiting confirmatory research linking diet and acne but some support the idea that acne sufferers should experiment with their diets, and refrain from consuming such fare if they find such food affects the severity of their acne.[6]

Seafood, on the other hand, may contain relatively high levels of iodine. Iodine is known to make existing acne worse but there is probably not enough to cause an acne outbreak.[7]< Still, people who are prone to acne may want to avoid excessive consumption of foods high in iodine.

Hygiene

Deficient personal hygiene. Acne is not caused by dirt. This misconception probably comes from the fact that comedones look like dirt stuck in the openings of pores. The black color is simply not dirt but compact keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining the duct to separate and flow to the surface in the sebum created there by the body.

Sex

Sex. Common myths state that masturbation causes acne and, conversely, that celibacy or sexual intercourse can cure it. Though it has been widely accepted that these are not true due to lack of scientific study on the subject, it is also important to note sexual activity has been observed to result in hormonal spikes, which has been linked to acne.[8]

Treatments

Timeline of acne treatment

The history of acne reaches back to the dawn of recorded history. In Ancient Egypt, it is recorded that several pharaohs were acne sufferers. From Ancient Greece comes the English word 'acne' (meaning 'point' or 'peak'). Acne treatments are also of considerable antiquity:

  • Ancient Rome : bathing in hot, and often sulfurous, mineral water was one of the few available acne treatments. One of the earliest texts to mention skin problems is De Medicina by the Roman writer Celsus.
  • 1800s: Nineteenth century dermatologists used sulphur in the treatment of acne. It was believed to dry the skin.
  • 1920s: Benzoyl Peroxide is used
  • 1930s: Laxatives were used as a cure for what were known as 'chastity pimples'
  • 1950s: When antibiotics became available, it was discovered that they had beneficial effects on acne. They were taken orally to begin with. Much of the benefit was not from killing bacteria but from the anti-inflammatory effects of tetracycline and its relatives. Topical antibiotics became available later.
  • 1960s: Tretinoin (original Trade Name Retin A) was found effective for acne. This preceeded the development of oral isotretinoin (sold as Accutane and Roaccutane) since the early 1980s.
  • 1980s: Accutane is introduced in America
  • 1990s: Laser treatment introduced
  • 2000s: Blue/red light therapy

Some old treatments, like laxatives, have fallen into disuse but others, like spas, are recovering their popularity.

Available treatments

There are many products sold for the treatment of acne, many of them without any scientifically-proven effects. Generally speaking successful treatments give little improvement within the first week or two; and then the acne decreases over approximately 3 months, after which the improvement starts to flatten out. Treatments that promise improvements within 2 weeks are likely to be largely disappointing. Short bursts of cortisone, quick bursts of antibiotics and many of the laser therapies offer a quick reduction in the redness, swelling and inflammation when used correctly, but none of these empty the pore of all the materials that trigger the inflammation. Emptying the pores takes months.

Modes of improvement are not necessarily fully understood but in general treatments are believed to work in at least 4 different ways (with many of the best treatments providing multiple simultaneous effects):

  • normalising shedding into the pore to prevent blockage
  • killing P. acnes
  • antinflammatory effects
  • hormonal manipulation

A combination of treatments can greatly reduce the amount and severity of acne in many cases. Those treatments that are most effective tend to have greater potential for side effects and need a greater degree of monitoring, so a step-wise approach is often taken. Many people consult with doctors when deciding which treatments to use, especially when considering using any treatments in combination. There are a number of treatments that have been proven effective:

Cotton pads soaked in salicylic acid solution can be used to exfoliate the skin.
Exfoliating the skin

This can be done either mechanically, using an abrasive cloth or a liquid scrub, or chemically. Common chemical exfoliating agents include salicylic acid and glycolic acid, which encourage the peeling of the top layer of skin to prevent a build-up of dead skin cells which combine with skin oil to block pores. It also helps to unblock already clogged pores.[citation needed] Note that the word "peeling" is not meant in the visible sense of shedding, but rather as the destruction of the top layer of skin cells at the microscopic level. Depending on the type of exfoliation used, some visible flaking is possible. Moisturizers and anti-acne topicals containing chemical exfoliating agents are commonly available over-the-counter. Mechanical exfoliation is less commonly used as many benefits derived from the exfoliation are negated by the act of mechanically rubbing and irritating the skin.

Benzoyl peroxide cream.
Topical Bactericidals

Widely available OTC bactericidal products containing benzoyl peroxide may be used in mild to moderate acne. The gel or cream containing benzoyl peroxide is rubbed, twice daily, into the pores over the affected region. Bar soaps or washes may also be used and vary from 2 to 10% in strength. In addition to its therapeutic effect as a keratolytic (a chemical that dissolves the keratin plugging the pores) benzoyl peroxide also prevents new lesions by killing P.acnes. Unlike antibiotics, benzoyl peroxide has the advantage of being a strong oxidizer (essentially a mild bleach) and thus does not appear to generate bacterial resistance. However, it routinely causes dryness, local irritation and redness. A sensible regimen may include the daily use of low-concentration (2.5%) benzoyl peroxide preparations, combined with suitable non-comedogenic moisturisers to help avoid overdrying the skin.[9] This has occasioned widespread editorial comment.[10]

Phototherapy
Blue and red light

It has long been known that short term improvement can be achieved with sunlight. However, studies have shown that sunlight worsens acne long-term, presumably due to UV damage. [citation needed] More recently, visible light has been successfully employed to treat acne (Phototherapy) - in particular intense blue light generated by purpose-built fluorescent lighting, dichroic bulbs, LEDs or lasers. Used twice weekly, this has been shown to reduce the number of acne lesions by about 64%;[11] and is even more effective when applied daily. The mechanism appears to be that a porphyrin (Coproporphyrin III) produced within P. acnes generates free radicals when irradiated by blue light.[12] Particularly when applied over several days, these free radicals ultimately kill the bacteria.[13] Since porphyrins are not otherwise present in skin, and no UV light is employed, it appears to be safe, and has been licensed by the U.S. FDA.[14] The treatment apparently works even better if used with red visible light (660 nanometer) resulting in a 76% reduction of lesions after 3 months of daily treatment for 80% of the patients;[15] and overall clearance was similar or better than benzoyl peroxide. Unlike most of the other treatments few if any negative side effects are typically experienced, and the development of bacterial resistance to the treatment seems very unlikely. After treatment, clearance can be longer lived than is typical with topical or oral antibiotic treatments; several months is not uncommon. The equipment or treatment, however, is relatively new and reasonably expensive.


Less widely used treatments

  • Azelaic acid (brand names Azelex, Finevin, Skinoren) is suitable for mild, comedonal acne.[16]
  • Zinc. Orally administered zinc gluconate has been shown to be effective in the treatment of inflammatory acne, although less so than tetracyclines.[17][18]
  • Tea Tree Oil (Melaleuca Oil) has been used with some success, and has been shown to be an effective anti-inflammatory in skin infections [19]
  • Heat therapy - Zeno product uses heat at a specific temperature to kill bacteria and to treat mild to moderate acne.[citation needed]
  • Niacinamide, (Vitamin B3) used topically in the form of a gel, has been shown in a 1995 study to be more effective than a topical antibiotic used for comparison, as well as having less side effects.[20] Topical niacinamide is available both on prescription and over-the-counter. Some users choose to make their own at home, mixing together crushed niacinamide pills with aloe vera gel.[citation needed] The property of topical niacinamide's benefit in treating acne seems to be it's anti-inflammatory nature. It is also purported to result in increased synthesis of collagen, keratin, involucrin and flaggrin.[citation needed]
  • In some cases, people found that bathing in salt water (pure from the ocean) noticed lessened redness and decreased size in their acne.

Future treatments

Laser surgery has been in use for some time to reduce the scars left behind by acne, but research is now being done on lasers for prevention of acne formation itself. The laser is used to produce one of the following effects:

  • to burn away the follicle sac from which the hair grows
  • to burn away the sebaceous gland which produces the oil
  • to induce formation of oxygen in the bacteria, killing them

Since lasers and intense pulsed light sources cause thermal damage to the skin there are concerns that laser or intense pulsed light treatments for acne will induce hyperpigmented macules (spots) or cause long term dryness of the skin. As of 2005, this is still mostly at the stage of medical research rather than established treatment.

Because acne appears to have a significant hereditary link, there is some expectation that cheap whole-genome DNA sequencing may help isolate the body mechanisms involved in acne more precisely, possibly leading to a more satisfactory treatment. (Crudely put, take the DNA of large samples of people with significant acne and of people without, and let a computer search for statistically strong differences in genes between the two groups). However, as of 2005, DNA sequencing is not yet cheap, and all this may still be decades off. It is also possible that gene therapy could be used to alter the skin's DNA.

Phage therapy has been proposed to kill P. acnes, and has seen some use, particularly in Georgia.[21]

Preferred treatments by types of acne vulgaris

  • Comedonal (non-inflammatory) acne: local treatment with azelaic acid, salicylic acid, topical retinoids, benzoyl peroxide.
  • Mild papulo-pustular (inflammatory) acne: benzoyl peroxide or topical retinoids, topical antibiotics (such as erythromycin).
  • Moderate inflammatory acne: benzoyl peroxide or topical retinoids combined with oral antibiotics (tetracyclines). Isotretinoin is an option.
  • Severe inflammatory acne, nodular acne, acne resistant to the above treatments: isotretinoin, or contraceptive pills with cyproterone for females with virilization or drospirenone.
  • Most physicians state that topical retinoids are the preferred treatment for all forms of acne vulgaris.
  • There are also certain treatments for acne mentioned in Ayurveda using herbs such as Aloevera, Aruna, Haldi, and Papaya.[22]

Acne scars

Severe acne often leaves small scars where the skin gets a "volcanic" shape. Acne scars are difficult and expensive to treat, and it is unusual for the scars to be successfully removed completely. Acne scars generally fall into two categories: physical scars and pigmented scars. Physical acne scars are often referred to as "Icepick" scars. This is because the scars tend to cause an indentation in the skins surface. Pigmented scars are usually the result of nodular or cystic acne. They often leave behind an inflamed red mark. Often, the pigmentation scars can be avoided simply by avoiding aggravation of the nodule or cyst. When sufferers try to 'pop' cysts or nodules, pigmentation scarring becomes significantly worse, and may even bruise the affected area. The treatment for severe scarring is usually surgical in nature.

Grading scale

There are multiple grading scales for grading the severity of acne vulgaris,[23] three of these being: Leeds acne grading technique: Counts and categorises lesions into inflammatory and non-inflammatory (ranges from 0-10.0). 'Cook's acne grading scale: Uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). Pillsbury scale: Simple classifies the severity of the acne from 1 (least severe) to 4 (most severe).


==

Acne cosmetica

Acne cosmetica is a term refering to acne caused by or made worse by cosmetics. The mechanism was presumably a chemically induced plugging of the pilosebaceous orifice. This was a significant problem for dermatologists in the 1970s and 1980s, but with the improved formulations produced by cosmetic chemists over the past thirty years, this is now a relatively rare diagnosis in daily practice.

The terms "non-comedogenic" and "non-acne(i)genic" appeared on moisturizers and other cosmetic compounds as re-formulations were introduced, sometimes associated with claims that the products were oil-free or water-based. Although early work produced lists of comedogenic chemicals in various strengths and vehicles, it became apparent that the actual comedogenicity of a product could not be predicted from its contents; rather the finished product itself needed to be use-tested.

The production of a low-grade folliculitis by some components of the cosmetic product has led to misdiagnosis on occasion.


Acne fulminans

Acne fulminans, also known as Acne Maligna, is a rare severe form of acne.

Acne medicamentosa

Acne medicamentosa is acne that is caused or aggravated by medication. Because acne is generally a disorder of the pilosebaceous units caused by hormones, the medications that trigger acne medicamentosa most frequently are hormones.

Although the male's hormone testosterone is most often blamed, and although men with acne secondary to bodybuilding hormones is seen from time to time, the major hormonal medication that causes acne is the progestin / progestagen present in birth control pills. Other medications can produce 'acneiform' eruptions (usually pimply bumps and pustules that look like acne).

Some conditions mimic acne medicamentosa. The most common mimic is the yeast folliculitis produced by an overgrowth of the Malassezia species, often secondary to oral or systemic corticosteroids, or secondary to broad-spectrum antibiotics such as the tetracycline family used in acne. This is often misinterpreted as 'tetracycline-resistant acne'.

Baby acne

Baby acne, also known as acne neonatorum, is a condition that affects roughly 20% of newborn babies. Lesions appear at around 2 weeks postpartum and commonly disappear after 3 months. Lesions include small, red, papules, which mainly affect the cheeks, as well as the nasal bridge of infants. Infants usually develop neonatal acne because of stimulation of the baby's sebaceous glands by lingering maternal hormones after delivery. These hormones cross the placenta into the baby and after delivery they cause the oil glands on the skin to form bumps that look like pimples.[1] Baby acne usually clears up within a few weeks, but it can linger for months.

Tiny bumps on a baby's face after birth that disappear within a few weeks are called milia and are unrelated to baby acne.

Baby acne has recently been described to be caused by saprophytic yeast of the Malassezia species, which cause a primary skin infection leading to the appearance of acne-like pustules. Initially it was believed to be the common yeast species, Malassezia furfur, which also causes 'cradle-cap' in infants. However, new publications have pointed to another species, Malassezia sympolais. Treatment options are still the same for both species, which includes low dose topical antifungals.

Chloracne

Acne
Classification and external resources
An example of chloracne on Viktor Yushchenko
ICD-10 L70.8
DiseasesDB 31706
eMedicine topic/620 
(Acneiform Eruptions)

Chloracne is an acne-like eruption of blackheads, cysts, and pustules associated with over-exposure to certain halogenic aromatic hydrocarbons, such as chlorinated dioxins and dibenzofurans. The lesions are most frequently found on the cheeks, behind the ears, in the armpits and groin region.

The condition was first described in German industrial workers in 1897 by Von Bettman, and was initially believed to be caused by exposure to toxic chlorine (hence the name "chloracne"). It was only in the mid-1950s that chloracne was associated with aromatic hydrocarbons[24]. The substances that may cause chloracne are now collectively known as "chloracnegens".

Chloracne is particularly linked to toxic exposure to dioxins (byproducts of many chemical processes, including the manufacture of herbicides such as Agent Orange) — so much so that it is considered a clinical sign of dioxin exposure. The severity and onset of chloracne may follow a typical asymptotic dose response curve.

Etiology and progression

Chloracne normally results from direct skin contact with chloracnegens, although ingestion and inhalation are also possible causative routes.

Chloracnegens are fat-soluble, meaning they persist in the body fat for a very long period following exposure. Chloracne is a chronic inflammatory condition that results from this persistence, in combination with the toxin's chemical properties. It is believed, at least from rodent models, that the toxin activates a series of receptors promoting macrophage proliferation, inducing neutrophilia and leading to a generalised inflammatory response in the skin. This process may also be augmented by induction of excess tumor necrosis factor in the blood serum.

The inflammatory processes lead to the formation of keratinous plugs in skin pores, forming yellowish cysts and dark pustules. The skin lesions occur mainly in the face, but in more severe cases they involve the shoulders and chest, the back, and the abdomen. In advanced cases, the lesions appear also on the arms, thighs, legs, hands and feet.

In some instances, chloracne may not appear for three to four weeks after toxic exposure; however in other cases - particularly in events of massive exposure - the symptoms may appear within days [24][25].

Treatment

Once chloracne has been identified, the primary action is to remove the patient and all other individuals from the source of contamination. Further treatment is symptomatic.

Severe or persistent lesions may be treated with oral antibiotics or isotretinoin. However, chloracne may be highly resistant to any treatment.

The course of the disease is highly variable. In some cases the lesions may resolve within two years or so; however, in other cases the lesions may be effectively permanent (mean duration of lesions in one 1984 study was 26 years, with some workers remaining disfigured over three decades after exposure [26]).

Recent research by groups at University of Cincinnati School of Medicine in Ohio and the University of Western Australia indicated that PCB poisoning, including chloracne symptoms, can be treated with fat substitute olestra.

Related conditions

Chloracne is very often seen in combination with hyperhidrosis (clammy, sweaty skin) and porphyria cutanea tarda (a skin condition of increased pigmentation, hair coarsening and blistering).

Notable cases

  • 193 cases of chloracne occurred in Seveso, Italy in 1976 following the Seveso disaster in which several kilograms of TCDD were released into the atmosphere.
  • Hundreds of individuals suffered chloracne after chronic exposure to PCBs and PCDFs in central Taiwan in 1979.
  • Ukrainian President Viktor Yushchenko suffered from extremely prominent facial chloracne after being diagnosed with dioxin poisoning in late 2004. His diagnosis of chloracne was put forth by prominent toxicologist John Henry.

Footnotes

  1. 1.0 1.1 Goodman G (2006). Acne and acne scarring - the case for active and early intervention. Aust Fam Physician 35 (7): 503-4. PMID 16820822.
  2. Purvis D, Robinson E, Merry S, Watson P (2006). Acne, anxiety, depression and suicide in teenagers: a cross-sectional survey of New Zealand secondary school students. J Paediatr Child Health 42 (12): 793-6. PMID 17096715.
    One study has estimated the incidence of suicidal ideation in patients with acne as 7.1% :
    * Picardi A, Mazzotti E, Pasquini P (2006). Prevalence and correlates of suicidal ideation among patients with skin disease. J Am Acad Dermatol 54 (3): 420-6. PMID 16488292.
  3. CHOICE - Citizens for Healthy Options In Children's Education (Nov 2003). Acne Has Nothing to Do with Diet - Wrong!.
  4. Magin P, Pond D, Smith W, Watson A (2005). A systematic review of the evidence for 'myths and misconceptions' in acne management: diet, face-washing and sunlight. Fam Pract 22 (1): 62-70. PMID 15644386.
  5. Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD (2005). High school dietary dairy intake and teenage acne. J Am Acad Dermatol 52 (2): 207-14. PMID 15692464.
  6. Fries JH (1978). Chocolate: a review of published reports of allergic and other deleterious effects, real or presumed. Ann Allergy 41 (4): 195-207. PMID 152075.
  7. Danby FW (2007). Acne and iodine: Reply. J Am Acad Dermatol 56 (1): 164-5. PMID 17190637.
  8. Endocrine effects of masturbation in men.
  9. The iPLEDGE Program - Guide to Best Practices for Isotretinoin - "The resource to help the prescriber prepare, plan treatments, and prevent pregnancies during the course of isotretinoin therapy" (PDF) (2005).
  10. Bernadine Healy. "Pledging for Accutane", US News Best Health, 2005-05-09.
  11. Kawada A, Aragane Y, Kameyama H, Sangen Y, Tezuka T (2002). Acne phototherapy with a high-intensity, enhanced, narrow-band, blue light source: an open study and in vitro investigation. J Dermatol Sci 30 (2): 129-35. PMID 12413768.
  12. Kjeldstad B (1984). Photoinactivation of Propionibacterium acnes by near-ultraviolet light. Z Naturforsch [C] 39 (3-4): 300-2. PMID 6730638.
  13. Ashkenazi H, Malik Z, Harth Y, Nitzan Y (2003). Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light. FEMS Immunol Med Microbiol 35 (1): 17-24. PMID 12589953.
  14. "New Light Therapy for Acne" U.S. Food and Drug Administration, FDA Consumer magazine, November-December 2002 Notice
  15. Papageorgiou P, Katsambas A, Chu A (2000). Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris.. Br J Dermatol 142 (5): 973-8. PMID 10809858.
  16. MedlinePlus (2001-07-24). Azelaic Acid (Topical).
  17. Dreno B, Amblard P, Agache P, Sirot S, Litoux P (1989). Low doses of zinc gluconate for inflammatory acne. Acta Derm Venereol 69 (6): 541-3. PMID 2575335.
  18. Dreno B, Moyse D, Alirezai M, Amblard P, Auffret N, Beylot C, Bodokh I, Chivot M, Daniel F, Humbert P, Meynadier J, Poli F (2001). Multicenter randomized comparative double-blind controlled clinical trial of the safety and efficacy of zinc gluconate versus minocycline hydrochloride in the treatment of inflammatory acne vulgaris. Dermatology 203 (2): 135-40. PMID 11586012.
  19. Koh KJ; Pearce AL; Marshman G; Finlay-Jones JJ; Hart PH Department of Dermatology, Flinders Medical Centre, Bedford Park, South Australia, Australia (2002). Tea tree oil reduces histamine-induced skin inflammation. Dermatology: 147. ISSN 0007-0963.
  20. Shalita A, Smith J, Parish L, Sofman M, Chalker D (1995). Topical nicotinamide compared with clindamycin gel in the treatment of inflammatory acne vulgaris.. Int J Dermatol 34 (6): 434-7. PMID 7657446.
  21. The star ledger- Germs that fight germs
  22. Ayurveda Encyclopedia, "Acne Treatment"
  23. Leeds, Cook's and Pillsbury scales obtained from here
  24. 24.0 24.1 Williams, D.E.; Wolfe, W.H.; Lustik, M.B. et al. (1995). An Epidemiologic Investigation of Health Effects in Air Force Personnel Following Exposure to Herbicides. Vol. 4.
  25. De Marchia, B, and Ravetzb, J.R. (1999). Risk management and governance: a post-normal science approach. Futures 31:743–757.
  26. Moses, M. et al. (1984). American Journal of Industrial Medicine 5(3):161-82.


References
ISBN links support NWE through referral fees

  • James W (April 7 2005). Clinical practice. Acne.. N Engl J Med 352 (14): 1463-72. PMID 15814882.
  • Webster G (31 August 2002). Acne vulgaris.. BMJ 325 (7362): 475-9. PMID 12202330.


External links


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