bubble_chart Overview

Acne, also known as acne, is a chronic inflammatory disease of the hair follicle sebaceous glands. It commonly occurs in young people, mainly on the face, chest, and back. Symptoms include acne, papules, pustules, nodules, and cysts.

bubble_chart Etiology

Acne has multiple disease causes, and its mechanism of disease is not yet fully understood. Endocrine factors, the role of sebum, and microorganisms within hair follicles are the main contributors to acne development.

Acne is closely related to sexual endocrine functions. It rarely occurs before puberty, and individuals with lost or diminished sexual function, such as eunuchs in ancient courts, do not develop acne. In people with reduced sexual function, the use of testosterone can promote beard growth and the onset of acne. When treating diseases with adrenocorticotropic hormone or corticosteroids, acne-like rashes often appear. Women frequently experience acne flare-ups before menstruation, while symptoms may alleviate during pregnancy. Both men and women have androgens and estrogens. The organs secreting sex hormones in males are the testes and adrenal glands, while in females, they are the ovaries, placenta, and adrenal glands. The varying ratios of androgens and estrogens in the bodies of men and women may lead to acne when these ratios change. The development of sebaceous glands and sebum secretion are also linked to increased androgen levels, with testosterone having the strongest effect on sebaceous gland activity. Progesterone and dehydroepiandrosterone (DHA) from the adrenal cortex also play a role, with the latter potentially being significant in the initial stage [first stage] of acne. Testosterone is converted into the more active 5-α dihydrotestosterone by the enzyme 5-α reductase in the skin, stimulating sebaceous gland cell turnover and lipid synthesis, leading to increased sebum production. This thick and abundant sebum cannot be fully excreted, gradually accumulating at the hair follicle opening. Simultaneously, the hair follicle duct undergoes excessive keratinization due to androgen action, thickening the follicle wall and obstructing sebum excretion. The increased shedding of epithelial cells from the follicle wall mixes with the thick sebum, forming a cheese-like substance that plugs the follicle opening, creating acne. The exposed tip of the plug eventually dries out and, through oxidation, melanin deposition, and contamination by dust, changes color to form acne. The presence of *Propionibacterium acnes*, *Staphylococcus albus*, and *Pityrosporum ovale* in hair follicles, particularly *P. acnes*, which contains lipase that breaks down sebum, leads to the production of more free fatty acids within the follicle. These free fatty acids can cause nonspecific inflammatory reactions around the follicle. When microscopic ulcers form on the acne wall and free fatty acids enter the nearby dermis, combined with the squeezing of adjacent cells, their antibacterial resistance declines, making them more susceptible to bacterial infection and inflammation. As a result, patients develop papules, pustules, hard nodules, and abscesses.

In recent years, some have suggested that this condition is related to immunity. Patients show elevated serum IgG levels in humoral immunity, which increase with disease severity. *P. acnes* produces antibodies in patients, and circulating antibodies reach local sites, contributing to the early inflammatory disease process.

Regarding the relationship between trace elements and acne, recent studies have shown that low zinc levels in acne patients may impair vitamin A utilization, promoting keratinization of hair follicles and sebaceous glands, while low copper weakens the body's resistance to bacterial infections. In summary, reduced levels of zinc, copper, and iron, along with elevated manganese in acne patients, may affect fat metabolism and sex hormone secretion, coupled with weakened skin resistance, potentially playing a role in acne development.

Additionally, genetics is an important factor in the occurrence of this condition. Beyond the aforementioned factors, a diet high in animal fats and sugars, digestive issues or constipation, mental stress, dampness-heat climates, and other environmental factors can adversely affect acne patients. Contact with mineral oils or ingestion of iodides, bromides, and certain other medications may also exacerbate acne.

bubble_chart Pathological Changes

Acne is composed of cells with sebaceous keratinization and parakeratosis, which are packed within enlarged hair follicles, surrounded by inflammatory changes. In suppurative lesions, the affected tissue contains abscesses with numerous lymphocytes and polymorphonuclear leukocytes, and sometimes staphylococci can be found. If the lesion has persisted for a long time, plasma cells, foreign body giant cells, and proliferating fibroblasts may also be observed. In larger lesions, the sebaceous glands may be partially or completely destroyed, sometimes forming large cysts.

bubble_chart Clinical Manifestations

Skin lesions mainly occur on the face, but can also appear on the upper chest, back, and shoulders, and occasionally in other areas. The skin around the eyes is never affected. Initially, patients almost always have acne and oily seborrhea, often accompanied by papules, nodules, pustules, abscesses, sinuses, or scars. The size and depth of the lesions vary, with one or two types usually predominating. The course is prolonged, and most cases are asymptomatic, though significant inflammation can cause pain and tenderness, with symptoms fluctuating in severity. After adolescence, most patients recover naturally or experience symptom relief. Clinically, based on the main manifestations of skin lesions, the following types can be distinguished:

1. **Comedonal acne**: Comedones are the primary lesions of acne, consisting of a cheese-like semi-solid plug in the pilosebaceous duct. The exposed end appears black, and when squeezed, a black-headed, yellowish-white translucent sebaceous plug can be expelled.
2. **Papular acne**: The lesions are primarily inflammatory small papules, ranging from millet to pea-sized, firm, and light red to deep red. The center of the papule may contain a comedone or a sebaceous plug with an unblackened tip.
3. **Pustular acne**: Characterized by pustules, which are grain- to mung bean-sized, follicular pustules or papules with pustular tops. Upon rupture, the pus is thick, and shallow scars may remain after healing.
4. **Nodular acne**: When inflammation is deep-seated, pustular acne can develop into thick-walled nodules of varying sizes, appearing light red or purplish-red. Some are deeply situated, forming hemispherical or conical protrusions. They may persist for a long time or gradually resolve, and some may suppurate and ulcerate, leaving prominent scars.
5. **Atrophic acne**: Papular or pustular lesions destroy the glands, leading to pitted atrophic scars. Ruptured pustules or naturally absorbed papules and pustules can cause fibrosis and atrophy.
6. **Cystic acne**: Forms sebaceous cysts of varying sizes, often complicated by secondary purulent infections. Upon rupture, bloody jelly-like pus is discharged, though inflammation is usually mild, eventually forming sinuses and scars.
7. **Acne conglobata**: The most severe form, presenting with polymorphic lesions, including numerous comedones, papules, pustules, abscesses, cysts, sinuses, scars, and keloids clustered together.
8. **Acne fulminans**: Lesions are millet- to broad bean-sized, bluish-red or purplish-red papules, pustules, or nodules, soft to the touch, containing pus and blood. They persist for a long time and heal with minimal scarring, causing little pain or infiltration. This type is more common in debilitated patients.

bubble_chart Treatment Measures

1. Pay attention to regulating digestive function, reduce intake of animal fats, sweets, and irritating foods. Wash the affected area frequently with warm water and soap containing sulfur or other lipid-reducing and anti-inflammatory ingredients.
2. Do not pick or squeeze acne, and avoid using oily cosmetics or corticosteroids.
3. Avoid bromine and iodine medications.
4. Explain to patients that acne is a common phenomenon caused by endocrine changes during adolescence, primarily due to fluctuations in sex hormones. Treatment can alleviate skin lesions but may not completely eliminate them, as symptoms may periodically worsen or improve with endocrine changes.
5. Oral Therapy

   (1) Antibiotics: Broad-spectrum antibiotics can control inflammation. For infection-dominated cases, antibiotics should be the first choice, with tetracyclines being the most effective. Tetracycline may inhibit Propionibacterium acnes and leukocyte chemotaxis, significantly reducing the concentration of free fatty acids in sebum. Tetracycline can be administered in low doses over a long course: start with 0.25g, four times daily for one month, then reduce by 0.25g every two weeks until reaching 0.25g daily, which should be maintained for another month. Erythromycin dosage and duration are the same as tetracycline. For cases resistant to other antibiotics, minocycline (50mg twice daily) can be used, reducing to 50mg once daily after 2–3 weeks. Clindamycin is the best alternative to tetracycline, suitable for severe inflammation or tetracycline-resistant cases. Start with 0.15g twice daily, reducing to once daily after symptoms are controlled. The average course is about three months. However, it may cause severe diarrhea and pseudomembranous colitis, so it should only be used for severe dermatitis in patients without intestinal diseases.

   (2) Sex Hormones: Not for routine use.

   1) Diethylstilbestrol: Severe cases may take 1mg daily for 10 days as one course. For female patients, start five days after menstruation. For those with premenstrual worsening, take 0.25–0.5mg daily for two to three weeks after menstruation begins. Contraindicated in patients with thromboembolic diseases, hemiplegia, liver disease, or abnormal uterine bleeding.

   2) Chorionic Gonadotropin: Some administer 500–1000U intramuscularly once weekly to female patients, avoiding use 5–10 days before menstruation.

   3) Progesterone: For severe cases or premenstrual worsening in female patients, inject 10mg intramuscularly 10 days before menstruation and another 5mg five days before menstruation.

   (3) Anti-Androgens: Anti-androgen therapy reduces free fatty acids and bacterial counts on the skin surface, thereby preventing or mitigating follicular and perifollicular inflammatory reactions.

   1) Spironolactone: 20mg three times daily.

   2) Ketoconazole: 200mg daily, taken orally for one month, then reduced to 100mg daily.

   3) Cimetidine: 400mg three times daily, reduced to 200mg three times daily after one month.

   The above three drugs are highly effective for female acne.

   4) Compound Norethisterone: Males take one tablet daily for four weeks; females start with 0.625mg on the fifth day of menstruation and continue for 22 days.

   5) Cimetidine: Take 0.2g orally three times daily before meals for four weeks as one course. It is believed to have anti-androgenic effects, blocking dihydrotestosterone binding to follicular receptors, inhibiting sebum secretion, and reducing inflammation.

   (4) Corticosteroids themselves can cause acneiform lesions. For severe cystic acne and conglobate acne, small doses can reduce inflammatory reactions, but the effect is only temporary. Long-term use can lead to many side effects, so they are generally avoided when possible. Commonly used is prednisone 10mg, taken 2-3 times daily. The dose should be gradually reduced once effectiveness is achieved, and the duration should not be too long. Side effects should be monitored. Currently, it is often recommended to combine corticosteroids with female hormones or anti-androgens for better results.

   (5) Retinoids - Inhibit retained hyperkeratosis, prevent new blockages and inflammation, reduce sebum secretion and acne formation, and are effective for nodular and cystic lesions. 13-cis-retinoic acid 1-2mg/kg, divided into two doses, taken for 2-3 weeks. If a second course is needed, it should be repeated after an 8-week break. Lesions may continue to improve after discontinuation, but side effects include dry skin, cheilitis, gastrointestinal symptoms, and teratogenicity. Women of childbearing age should use contraception during treatment and for six months after discontinuation.

   (6) Dapsone (DDS) - May have anti-inflammatory effects and is suitable for cystic and nodular lesions. Take 50mg orally twice daily for 1-2 months. Monitor for hematologic and liver side effects.

   (7) Zinc preparations - Inhibit follicular keratinization or inflammation. Take zinc gluconate 70mg three times daily for 4 weeks, or zinc sulfate 0.2g 2-3 times daily for 4-12 weeks. May cause gastrointestinal side effects.

   (8) Vitamins

   1) Vitamin B2, B6, and B complex.

   2) Vitamin A 150,000 U daily for 4-8 weeks.

   3) Vitamin A 150,000 U and vitamin E 50mg daily for 4-8 weeks.

6. Topical treatment - The goal is to reduce inflammation, kill bacteria, remove excess oil, unclog pores, and promote sebum flow. Maintain skin cleanliness and control infection. Wash face 1-3 times daily with hot water and soap, preferably sulfur-containing medicated soap.

   (1) Antibiotics - 1% chloramphenicol tincture (chloramphenicol + salicylic acid), 2% erythromycin alcohol, 1% lincomycin solution, etc.

   (2) Benzoyl peroxide - Has antibacterial, keratolytic, and sebum-reducing effects, decreasing free fatty acids. However, some patients may develop contact dermatitis. Perform a patch test before use. Studies show 3.5% benzoyl peroxide lotion or cream is effective. Apply 1-2 times daily.

   (3) Retinoids - Have keratolytic effects, such as 0.05%-0.1% retinoic acid cream or solution. Apply 1-2 times daily. If local irritation, erythema, or peeling occurs, pause for 1-2 days before resuming or start with a lower concentration until skin tolerance is achieved. Can be used for 1-2 months.

   (4) White lotion (zinc sulfate 4.5, potassium sulfide 4.0, rose water or water up to 100) - Reduces sebum, inhibits infection, and dilates follicular openings to facilitate sebum excretion. Apply 1-2 times daily.

7. Physical therapy

   (1) Face masks - Include Chinese medicinal masks and plaster masks. Cleanse skin before application, then apply medication, spray, and massage to integrate physiotherapy, massage, and medication for therapeutic and cosmetic purposes.

   1) Chinese medicinal mask - Mix mask powder with a small amount of honey and water to form a paste, then apply to the face while spraying and massaging along meridians and acupoints following blood circulation directions.

   2) Plaster mask - Add various medications to a base to create creams, then apply to the face while spraying and massaging for several minutes. Cover eyes, nose, mouth, and beard with cotton, then apply gypsum mixed with water in a thin paste, leaving nostrils and mouth exposed. Once the gypsum hardens, heats up, and cools, remove it.

   (2) Intralesional injection - Inject 0.05-1ml of triamcinolone acetonide suspension (10mg/ml diluted with saline) into severe nodular or cystic lesions weekly for 3-4 sessions.

bubble_chart Differentiation

The diagnosis can be made based on the fact that patients are mostly young and the condition commonly occurs on the face, upper chest, and back, with the presence of acne. However, it should be differentiated from the following diseases:

1. Acne-like drug rash caused by bromine or iodine: There is a history of medication use, no typical acne, the rash is generalized, and there is no age restriction for onset.
2. Occupational acne: Workers exposed to compounds such as coal tar, machine oil, petroleum, paraffin, or chloronaphthalene may develop acne-like rashes. This is usually occupation-related, and colleagues often develop similar lesions. The lesions are often dense and typically occur in contact areas, such as the back of the hands, forearms, elbows, etc.
3. Rosacea: More common in middle-aged individuals, the rash occurs only on the face, predominantly in the central area, often accompanied by telangiectasia.
4. Lupus miliaris disseminatus faciei: The lesions are mostly dark red or brownish-yellow papules and small nodules. On the lower eyelid margin, the lesions are arranged in a ridge-like pattern. Diascopy reveals an apple-jelly color change, and the lesions are not consistent with hair follicles.