7th June 2025

Sebaceous and sweat gland disorders

Acne

Acne vulgaris is a chronic inflammatory skin condition which predominantly affects the face, back and chest. It can present in any age group but peaks in adolescence, affecting 8 in 10 teenagers. Acne is characterised by blockage and inflammation of the pilosebaceous unit (the hair follicle, hair shaft and sebaceous gland) which manifests as comedones, papules, pustules, nodules, cysts and/or scarring. It can have a profound social and psychological impact on patients and hence there is a significant need for effective acne treatment.

Cause

Acne is a multifactorial disease with the following primary pathogenic factors:

Increased sebum production stimulated by androgens, within sebaceous follicles
Follicular hyperkeratinisation leading to follicular plugs (comedones)
Proliferation of Cutibacterium acnes within sebum in hair follicles
Release of inflammatory cells and mediators leading to development of papules, pustules, nodules and cysts.

Other factors that could contribute to acne pathogenesis include:

Genetic factors (high prevalence among identical twins)
High glycaemic index diets, dairy and meat products high in leucine
Hormonal factors (menstrual period related, hyperandrogenism, polycystic ovarian syndrome)
Mechanical trauma
Cosmetics
Topical corticosteroids
Oral medications (corticosteroids, lithium, iodides, antiepileptic medications)

Diagnosis

To diagnose acne vulgaris, a thorough history and examination are fundamental.

History and examination

Areas with increased pilosebaceous glands –face, chest, back
Clinical course – related to beginning puberty and women may note relation to menstrual cycle
Lesions:
- Closed comedones (‘whiteheads’ – non-inflammatory)
- Open comedones (‘blackheads’ – non-inflammatory)
- Papules and pustules – superficial raised lesions with or without pus (inflammatory)
- Nodules or cysts – deeper, palpable, >5mm (inflammatory)
  - Often tender
Pigmentation – post-inflammatory hyperpigmentation is very common in darker skin types
Scarring – various types including atrophic, ice-pick or hypertrophic; keloid scarring may result, usually on the torso
Severity
- Mild – mostly non-inflamed lesions (open and closed comedones) with few papules and pustules
- Moderate – more comedones, papules and pustules than in mild. Sometimes truncal involvement along with face.
- Severe – widespread comedones, papules, pustules, nodules, or cysts. Areas include face, chest and back. Scarring and hyperpigmentation may be present.
- Very severe – nodulocystic acne and acne conglobata with severe lesions; many large, painful nodulopustular lesions along with papules, pustules and comedones
Acne fulminans – rare acne subtype presenting with systemic features including fever, arthralgia, myalgia, hepatosplenomegaly and osteolytic bone lesions Image Source: Wikimedia Commons (2015). AcneVulgaris on a very Oily Skin, Licensed under a creative commons licence. Available for free at: https://en.m.wikipedia.org/wiki/File:Acne_vulgaris_on_a_very_oily_skin.jpg (Accessed 23 May 2025).

Management

Treatment is based on the severity and usually a combination of medications are needed to treat acne.

Mild to moderate acne:
- 12 week course of one of the following
  - Topical adapalene (retinoid) + topical benzoyl peroxide
  - Topical tretinoin (retinoid) + topical clindamycin
  - Topical benzoyl peroxide + topical clindamycin
- Topical benzoyl peroxide monotherapy if above contraindicated or patient preference
- Dry or sensitive skin – creams or lotions rather than gels
- Oily skin – consider less greasy gels
- If skin irritation occurs with treatment then modify concentration or frequency of application
Moderate to severe acne:
- 12 week course of one of the following
  - Topical adapalene (retinoid) + topical benzoyl peroxide
  - Topical tretinoin (retinoid) + topical clindamycin
  - Topical adapalene (retinoid) + topical benzoyl peroxide + oral lymecycline/ doxycycline
  - Topical azelaic acid + oral lymecycline/doxycycline
- Topical benzoyl peroxide monotherapy if above contraindicated or patient preference
- Trimethoprim/oral macrolide (erythromycin) if contraindication or not tolerated oral lymecycline/doxycycline.
- Combined oral contraceptive + topical agents (if systemic antibiotics not tolerated in women)
  - Useful in women with hormonal involvement for acne (acne related to menstrual periods, ovarian/adrenal hyperandrogenism and polycystic ovary syndrome)
  - Third and fourth generation combined oral contraceptives
  - Co-cyprindol or other ethinylestradiol/cyproterone acetate-containing products
  - Discontinue 3 months after acne controlled
- Spironolactone
  - Used for its anti-androgenic effects for women only
  - Useful to limit use of long-term antibiotics or for individuals who prefer not to take isotretinoin
  - Contraindicated in pregnancy
- Oral isotretinoin
  - Indicated in severe or scarring disease, or if insufficient response to other treatment or rapid relapse on stopping it; also in cases with marked psychosocial impact
  - Extremely effective
  - Potently teratogenic; women of child-bearing potential must be enrolled on to a pregnancy prevention programme
  - Common adverse effects comprise mucocutaneous dryness; reports of effects on mental health (e.g. depression, irritability) and sexual dysfunction
Pregnant women
- Safe topical agents – azelaic acid, benzoyl peroxide, clindamycin, erythromycin
- Erythromycin can be used in pregnancy if systemic treatment is clearly required

Folliculitis

Folliculitis describes inflammation of the hair follicles, but the term is usually used in the context of bacterial infection, mostly commonly with Staphylococcus aureus. This presents with inflamed papules and pustules (see Figure). It often affects the back. It may occur on the legs or pubic area, as the infection may be spread via shaving or waxing.

Purulent rashes on the neck of a man. Allergy, acne

Image Source: Wikimedia Commons (2021). Purulent rashes on the neck of a Man – Allergy Acne Skin Disease, Licensed under a creative commons licence. https://www.istockphoto.com/photo/purulent-rashes-on-the-neck-of-a-man-allergy-acne-skin-diseases-gm1302757001-394401309?phrase=bacterial+folliculitis (Accessed 23 May 2025).

Investigations

Nasal swab to check for staphylococcal carriage
Swab of pus will typically show S. aureus; sensitivities may be helpful to guide treatment. Other potentially causative bacteria include Pseudomonas aeruginosa or other Gram negative organisms.
A biopsy is rarely indicated for refractory or atypical disease. Fungal/yeast infection is sometimes found mimicking bacterial infection (and should be treated accordingly).

Management

For very mild disease, no treatment may be necessary
Stop/minimise shaving or waxing the area (if relevant)
Antiseptic washes
Eradicate nasal staphylococcal carriage if found (as this is a potential source of recurrent disease)
Consider topical antibiotic for localised disease (e.g. clindamycin lotion)
Oral antibiotic, e.g. flucloxacillin, for 1-2 weeks for acute disease
Prolonged course (e.g. 3-6 months) of oral antibiotic, usually lymecycline or doxycycline, for chronic disease

Hyperhidrosis

Hyperhidrosis or excessive sweating is a common problem, with an estimated worldwide prevalence of 2-16%. It can occur in children and adults, with onset most often in the mid to late teens. It is usually a primary condition but can be secondary to an underlying cause. Hyperhidrosis can be generalised, or focal, mostly affecting the hands (palmar), feet (plantar), axillae or head (craniofacial). It may have serious social and emotional consequences impacting on patients’ quality of life.

Cause

The cause depends on whether it is primary or secondary hyperhidrosis.

Primary
- Complex over-reactivity or hyperexcitability of neurological circuits likely involving cortical, hypothalamic and autonomic nervous system interactions
- Usually focal hyperhidrosis: palmoplantar, axillary or craniofacial
- Positive family history
Secondary hyperhidrosis
- Systemic and neurological effects of organic conditions and their effect on thermoregulatory centres of hypothalamus
- Generalised hyperhidrosis (more common):
  - Anxiety
  - Physiological (pregnancy, menopause)
  - Cardiovascular (heart failure, endocarditis)
  - Infections (acute/chronic viral or bacterial infections)
  - Malignancy (Hodgkin’s disease, myeloproliferative disorders)
  - Endocrine or metabolic (hyperthyroid, diabetes mellitus, diabetes insipidus, phaeochromocytoma, acromegaly, carcinoid syndrome, hyperpituitarism, obesity and gout)
  - Neurological (Parkinson’s disease, epilepsy, hypothalamic lesions)
  - Drugs (e.g. cholinesterase inhibitors, antidepressants, pilocarpine eye drops, propranolol, proton pump inhibitors, ciprofloxacin, aciclovir, esomeprazole, opioids)
  - Drug or alcohol misuse or withdrawal (cocaine, heroin)
- Focal hyperhidrosis:
  - neurological (cerebrovascular disease, peripheral neuropathies, diabetic autonomic neuropathy, spinal cord lesions, complex regional pain syndrome)
  - intrathoracic lesions (mesothelioma, cervical rib)
  - Gustatory sweating, sweating caused by food or drink (diabetic neuropathy, preauricular herpes zoster, invasion of cervical sympathetic trunk by tumour, surgery/injury to parotid gland)
  - Compensatory hyperhidrosis (myelopathy, cerebrovascular disease, nerve trauma or post-surgery)
  - Others –Raynaud’s phenomenon, arteriovenous fistula, cold injury, rheumatoid arthritis, nail-patella syndrome Image Source: Wikimedia Commons (2018). Hyperhidrosis Treatment, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/w/index.php?search=Hyperhidrosis_Treatment.jpg&title=Special:MediaSearch&type=image (Accessed 23 May 2025).

Diagnosis

Diagnosis is based on the cause of hyperhidrosis; for primary, history and physical examination are enough. Investigations may be required to confirm or exclude secondary causes.

Diagnostic criteria for primary focal hyperhidrosis

Occurs in at least one of the following locations: axillae, palms, soles or craniofacial region AND
Lasted 6 months AND
No apparent cause AND
At least two of the following:
- Bilateral and relatively symmetrical
- Impairs daily activities
- At least one episode per week
- Onset before 25 years of age
- Positive family history
- Cessation of local sweating when sleeping
If symptoms less than 6 months or onset after 25 years, can be primary focal hyperhidrosis if other criteria are met, but clinically should exclude any underlying causes

Tests to consider for secondary hyperhidrosis depend on the clinical scenario

Urine analysis for substance abuse
Urine evaluation for metanephrines, catecholamines and 5-hydroxyindoleacetic acid
Bloods – FBC, ESR, CRP, U+E, LFT, TFT, HIV, TB
Blood film for malarial parasites, if indicated
Chest X-ray
ECG
CT scanning – thyroid, pituitary, diabetic, infectious, neoplastic disorders, as well as phaeochromocytoma and carcinoid tumours

Management

Treatment is dependent on the cause of hyperhidrosis. Secondary hyperhidrosis is managed by treating the underlying cause. For management of primary focal hyperhidrosis, it is as follows:

Minimise exposure to identified triggers
Self-care management strategies:
- Primary axillary hyperhidrosis – commercial antiperspirant, avoid tight clothing and man-made fabrics, white/black clothing to minimise sweating signs, armpit or sweat shield to absorb excess moisture
- Primary plantar hyperhidrosis – moisture wicking socks, absorbent soles, absorbent foot powder, alternate shoes daily, avoid occlusive footwear
20% aluminium chloride hexahydrate preparations as roll-on antiperspirant and spray for symptom relief (must be applied when skin is dry to minimise potential for irritation)
- If skin irritation occurs, reduce frequency of application, hydrocortisone 1% cream for 2 weeks, topical emollients and soap substitutes
- Review in 6 weeks and continue long-term if effective
Identify any anxiety and manage as needed
- Selective serotonin reuptake inhibitors and propranolol can worsen symptoms
Referral to dermatologist if above not effective or tolerated

Specialist treatment

Oral and topical treatment
- Topical glycopyrrolate (antimuscarinic) for primary craniofacial hyperhidrosis (off-label indication)
- Oral antimuscarinic (propantheline, oxybutynin, glycopyrronium bromide [off label indication; the latter may be difficult to procure])
  - Often limited by adverse effects such as dry mouth, blurred vision, constipation, urinary retention
Iontophoresis (for palmoplantar sweating)
- Hyperhidrosis site immersed in warm water through which weak electric current is passed
- Introduces charged ion into skin which inhibits function of sweat gland in that area
- If unsuccessful or in severe cases, glycopyrronium bromide added to water
- Every 1-4 weeks
- Adverse effects – transient discomfort, erythema, vesicle formation at treatment site
Botulinum A toxin (mostly used for axillae)
- Multiple intradermal injection to hyperhidrosis area
- Inhibiting acetylcholine release from sympathetic cholinergic nerve terminals that innervate sweat glands
- Lasts 6-9 months
- Adverse effects – pain during injection, compensatory sweating
Surgery
- Localised curettage or resection of axillary eccrine sweat glands under local anaesthesia
- Endoscopic thoracic sympathectomy if other measures unsuccessful
  - Division of sympathetic chain over the neck of the ribs in pleural cavity under general anaesthesia
  - Prevent transmission nerve signals from sympathetic ganglia to fibres innervating areas producing excess sweat
  - Indications – severe palmar, axillary or craniofacial hyperhidrosis
  - Complications – compensatory hyperhidrosis elsewhere, gustatory sweating, pneumothorax, atelectasis, significant bleeding, recurrence

Anhidrosis

Anhidrosis is an acquired disorder of sweating where there is a reduction in or complete loss of sweat production in response to a thermal or pharmacological stimulus.

Cause

Idiopathic
Peripheral alteration in eccrine gland
Neuropathic disease or medication that disrupt neural inputs from anterior hypothalamus to the gland

Diagnosis

Symptoms
- Heat intolerance
- Fatigue
- Drowsiness
- Inability to concentrate in warm environments
- Ptosis and miosis in Horner syndrome (neuropathic anhidrosis)
Investigation
- Sweat test – decreased sweat production
- Skin biopsy – identify sweat gland abnormality

Management

Remove underlying cause
- Remove offending medication (e.g., anticholinergic agents)
- Treatment of lung carcinoma if it is causing Horner syndrome
Cool environments
Frequent and gentle exfoliations

Rosacea

Rosacea is a common, chronic, and relapsing inflammatory skin condition that primarily affects the central face. In the UK around 1 in 20 people are affected and onset is between 30-50 years of age. Rosacea cannot be cured and is characterised by episodes of remission and recurrence. Treatment is targeted at controlling symptoms.

Cause

Pathogenesis is thought to be multifactorial involving genetic and environmental factors. Potential causes include factors that affect inflammatory or immune response, including various microbes, or vascular dysfunction.

Certain factors may trigger or worsen rosacea:

Ultraviolet radiation exposure
Increasing age
Photosensitive skin types
Smoking
Hot or cold ambient temperature
Spicy foods and hot beverages
Alcohol
Emotional stress and exercises
Medication (calcium channel blockers, topical corticosteroid)

Diagnosis

Rosacea is a clinical diagnosis, but the findings can mimic other diseases, so other conditions may need to be excluded. Rosacea is sometimes divided into erythematotelangiectatic versus papulopustular subtypes. In most cases, features of both occur. Phymatous rosacea, in which there is soft tissue overgrowth usually affecting the nose, is more unusual. Some people with rosacea have ocular involvement, which may be more severe than the skin disease.

Symptoms and signs

Central face predominantly affected, including cheeks, chin, nose and mid-forehead
Facial flushing
Burning or stinging sensation from skin (not pruritus)
Facial erythema with prominent telangiectasia
Inflammatory papules and pustules
Rhinophyma
Ocular manifestations including blepharitis, chalazia, conjunctivitis and keratitis
Facial oedema

Investigations

Usually a clinical diagnosis
Occasionally, lupus antibodies or skin biopsy may be helpful in atypical cases Image Source: Wikimedia Commons (2014). Acne Rosacea, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Acne_rosacea.jpg (Accessed 23 May 2025).

Management

High sun protection factor (SPF) sunscreen on face regularly (SPF 30-50)
Minimise triggers that could worsen skin and flushing, such as:
- Ultraviolet light exposure
- Temperature extremes
- Alcohol
- Heavy exercise
- Stressful situations
- Spicy food
- Hot beverages
Treatment of erythematotelangiectatic component
- Brimonidine (alpha agonist) gel – produces temporary vasoconstriction for a few hours after application but rebound erythema can be problematic
- Camouflage cream
- Laser therapy
Treatment of papulopustular component
- Topical azelaic acid/ivermectin/metronidazole
- Oral lymecycline or doxycycline for moderate-to-severe disease
Management of ocular disease
- May require ophthalmology input
- Lid hygiene
- Lubricants +/- topical anti-inflammatories
- Oral lymecycline or doxycycline

Hidradenitis suppurativa

Hidradenitis suppurativa (HS) is a chronic inflammatory disease occurring in the apocrine follicles causing painful, inflamed nodules and sterile abscesses. In Europe it has an estimated prevalence of 1%. Early diagnosis and treatment aim to minimise progression and scarring.

Cause

The aetiology is not fully understood, but proposed contributors and associations include:

Immune factors – immune system activation from occluded hair follicles forming painful nodules and abscess rupture leading to sinus tracts, scarring and tissues destruction; complex interactions with the skin microbiome.
Genetics – family history is seen in 30% of cases.
Hormones – clearly more common in women in Western populations but this may not be reflected elsewhere; can vary with menstrual cycle and pregnancy.
Smoking – thought to be due to hair follicles being more likely to be blocked.
Obesity – friction and sweating in skin folds with hormonal and pro-inflammatory changes may promote HS.
Other diseases – co-existing metabolic syndrome, type 2 diabetes mellitus, atherosclerosis, spondyloarthropathy, inflammatory bowel disease, depression and cardiovascular disease commonly seen. Can be part of a rare autoinflammatory syndrome, e.g. PASH (pyoderma gangrenosum, acne, suppurative hidradenitis), PAPASH (pyogenic arthritis, pyoderma gangrenosum, acne, suppurative hidradenitis).

Diagnosis

History and Examination

Onset
- 18-39 years of age usually
Site
- Intertriginous skin of axillary, groin, perianal, perineal and inframammary regions
Double- headed open comedones
Inflamed nodules
- Solitary lesion initially before multiple sites affected
- Recurrences common
- Develop into pustules and rupture with purulent discharge
Abscesses
Sinus tracts or fistulae (draining skin tunnels)
- Chronic as recurrence in same regions
Scar formation
- Due to healing with dense fibrosis
Discomfort or pain which can be severe
Malodour
Disfigurement
Reduced quality of life

Image Source: Wikimedia Commons (2012). Lesions from Hidradenitis Suppurativa, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Lesions_from_hidradenitis_suppurativa.jpg (Accessed 23 May 2025).

Classification

Severity of HS can be classified using Hurley staging which can help guide the type of treatment.

Hurley Stage 1 (mild) – single or multiple, discrete abscesses and inflammatory nodules. There is no scarring or sinus tract formation.
Hurley Stage 2 (moderate) – single or multiple, discrete abscesses and inflammatory nodules. There is scarring and widely separated sinus tracts.
Hurley Stage 3 (severe) – multiple and extensive interconnected scars with or without active inflamed lesions.

Investigation

Hidradenitis suppurativa is a clinical diagnosis based on symptoms and signs. However, the following investigations may be useful:

Bacterial swab – usually negative
Blood tests if secondary infection is suspected or to exclude diabetes mellitus
Skin biopsy – occasionally undertaken to exclude squamous cell carcinoma and differentiate from other inflammatory diseases such as Crohn’s disease.
MRI scan – used in severe disease to check sinus tract path and plan surgery.

Management

Management depends on the severity of disease and impact on quality of life. Treatment is split into general advice, medical and surgical treatment. The main aim is to reduce new and existing lesions, sinus tracts and scarring. However, there is a lack of curative treatment.

General advice

Good hygiene – antiseptic cleansers are often recommended
Antiperspirants
Loose-fitting cotton clothing
Avoid shaving affected areas
Minimise heat, humidity, sweating, trauma, friction and irritation
Weight reduction if overweight or obese
Smoking cessation

Medical treatment (high-quality evidence is limited)

Intralesional corticosteroid
- Sometimes used for acute, painful lesions
Antibiotics
- Topical
  - For mild disease
  - Clindamycin lotion
- Systemic
  - Lymecycline, doxycycline or macrolide, usually used for prolonged durations such as 3-6 months
  - Clindamycin and rifampicin, usually for 10-12 weeks
Biological therapies
- For moderate to severe, refractory HS
  - Anti-TNF (adalimumab or infliximab)
  - Anti-interleukin-17A (secukinumab)
Anti-androgens (for women)
- Combined oral contraceptive pill
- Spironolactone
Dapsone
Metformin
Retinoid (acitretin – unsuitable for women of child-bearing potential)