Acne vulgaris
MedicalConditionA chronic inflammatory disease of the pilosebaceous unit producing follicular hyperkeratinisation, seborrhoea, C. acnes phylotype dysbiosis, and immune activation.
26 entities in this category
A chronic inflammatory disease of the pilosebaceous unit producing follicular hyperkeratinisation, seborrhoea, C. acnes phylotype dysbiosis, and immune activation.
Progressive genetic hair loss where follicles gradually miniaturise, shortening growth phases and producing finer, thinner hairs.
Chapped lips — dryness, flaking, and fissuring of the vermilion — are the most common lip complaint and reflect the structural vulnerability of lip tissue.
Dermatitis is a broad term for inflammatory skin conditions characterised by barrier dysfunction, immune activation, and varying degrees of erythema, pruritus, scaling, and vesiculation.
Compulsive eating pattern with addiction-like features including tolerance, withdrawal, and loss of control; distinct from restriction-induced issues.
Umbrella term for conditions causing increased hair shedding or thinning, ranging from temporary telogen effluvium to progressive androgenetic alopecia.
Hyperpigmentation describes the localised or diffuse overproduction or abnormal distribution of melanin in the skin. It is not a single condition but three mechanistically distinct presentations.
A state of reduced insulin responsiveness driven by DAG–PKC signalling and impaired fuel switching, linking metabolic overload to systemic glucose dysregulation.
Lips requiring external lipid sources and protective barriers due to lacking oil-producing glands found elsewhere on the face.
A feedback loop in which sensory neurons and immune cells amplify each other via neuropeptides and cytokines, driving vasodilation, itch, and escalating inflammatory sensitivity.
Excess adipose tissue volume. A chronic low-grade inflammatory state with specific, measurable consequences for skin biology, barrier function, wound healing, and treatment response.
Obstructive sleep apnoea is repeated airway collapse during sleep, causing fragmented rest, daytime fatigue, and metabolic stress; common in obesity, and often missed.
Paradoxical adipose hyperplasia (PAH) is a rare adverse event following cryolipolysis in which the treated area develops an increase in fat volume rather than the expected reduction.
Perimenopausal skin changes describe the cascade of biological alterations across every layer of the skin that accompany declining oestrogen during the menopausal transition.
A T-cell-mediated autoimmune skin disease driven by the IL-23/Th17 axis, producing keratinocyte hyperproliferation and systemic inflammatory burden extending to joints and cardiovascular tissue.
Psychological stress produces measurable, mechanistically defined changes in skin biology, including accelerated collagen degradation, DNA damage, and inflammageing.
A chronic inflammatory condition driven by a self-amplifying KLK5/LL-37 feedback loop, neurovascular sensitisation, and barrier dysfunction — not simply reactive or vascular skin.
The pro‑inflammatory secretory programme of senescent cells, releasing cytokines and MMPs that degrade collagen, suppress regeneration, and drive chronic tissue inflammation.
Barrier dysfunction describes the full spectrum of stratum corneum failure, from the earliest detectable impairment of moisture retention to the self-perpetuating inflammatory cycle.
A state of microbial community imbalance on the skin surface, characterised by loss of commensal species, reduced diversity, and conditions that permit pathogenic overgrowth.
The accumulation of disorganised, non-functional elastotic material in the upper dermis, representing the defining histological marker of photoaged skin.
A reactive hair loss condition in which a significant proportion of scalp follicles are simultaneously shifted into the resting phase by a systemic stressor.
Condition affecting hair growth cycles, worth investigating when experiencing unexplained hair changes.
A drug‑related dermatosis in which prolonged topical steroid use leads to burning, erythema, and severe barrier dysfunction after withdrawal, often misdiagnosed as worsening eczema.
Metabolic condition characterised by insulin resistance and elevated blood glucose, for which Mounjaro is an approved treatment.
Discontinuation of GLP-1 receptor agonists produces rapid, substantial weight regain driven by the reassertion of the biological mechanisms the drug was suppressing.