Hyperpigmentation L81.89

Hyperpigmentation in the broader sense is a pathological, congenital or acquired, brown coloration of the skin or mucous membrane (see below pigment, pigmentation, melanosis) as a result of pathological accumulation of an endogenous or exogenous pigment.

Hyperpigmentation in the narrower sense (melanotic hyperpigmentation, see also melanosis) is a pathological, clinical colour symptom caused by a congenital or acquired, solitary or multiple, localized or disseminated, in rare cases also generalized or universal, melanotic color intensification (brown/black/blue coloration) of the skin/mucous membrane, caused by an increased number of melanocytes or increased localized melanin formation, or by the deposition of melanin formed remotely from the heart (e.g. in metastatic malignant melanoma) or by a combination of the various mechanisms. mechanisms.

The opposite of hyperpigmentation is depigmentation/hypopigmentation(absence, reduction or loss of function of the melanocytes).

If hyperpigmentation occurs as a result of inflammatory skin diseases, it is referred to as inflammatory or post-inflammatory hyperpigmentation.

It is difficult to classify the different disease patterns, whose only common feature is the phenomenon of "hyperpigmentation". The term "hyperpigmentation" describes a pathological brown discoloration of the skin or mucous membrane. Physiological pigmentation of the skin, e.g. caused by the influence of the sun, is not called hyperpigmentation but generally called "tanning".

Basically one can distinguish between:

• localized hyperpigmentations
• generalized hyperpigmentations.

Furthermore between:

• inflammatory (post-inflammatory) hyperpigmentations
• non-inflammatory hyperpigmentations

Furthermore between:

• congenital hyperpigmentations (genodermatoses)
• acquired hyperpigmentations

Furthermore between:

• diffuse hyperpigmentations
• reticular hyperpigmentations

Classification according to underlying diseases/causes:

• Drugs
  • Antibiotic therapy(tetracyclines)
  • Antihypertensive therapy(amiodarone hyperpigmentation)
  • cytostatic therapy (e.g. bleomycin, melanodermia factitia
• Postinflammatory hyperpigmentations
  • Melasma (Chloasma)
  • Melanodermatitis toxica (Hoffmann-Habermann)
  • Melanosis perioralis et peribuccalis (Brocq)
  • Periocular hyperpigmentation (atopic diathesis, chronic contact dermatitis)
  • Actinic hyperpimentation (e.g. in erythrosis interfollicularis colli)
  • lichen planus
  • Mechanical hyperpigmentation (under continuous mechanical load)
  • Thermal hyperpigmentation (repetitive infrared irradiation, heating pad: hyperpigmentation caloric)
  • Traumatic hyperpigmentation (after abrasions, after other injuries)
  • Chemical hyperpigmentation (e.g. furocoumarins in meadow grass dermatitis)
  • Poikiloderma
• Other hyperpigmentations
  • Acanthosis nigricans (hyperpigmentation and flat acanthosis)
  • Amyloidosis macular
  • Acropigmentation (so-called peak pigment)
  • renal insufficiency, chronic terminal
  • M. Addison
  • Arsenic intoxications
  • Graves' disease
  • Cushing's Syndrome
  • Dyschromatosis universalis hereditaria
  • Hyperpigmentation familial progressive (mutation in KITLG)
  • Epidermolysis bullosa simplex with spotted hyperpigmentation
  • Hepatolenticular degeneration(M. Wilson)
  • Fanconi Syndrome
  • incontinentia pigmenti
  • Carcinoid syndrome
  • Keratosis palmoplantaris with mutations in connexin 26 (KID syndrome)
  • Metastatic malignant melanoma (so-called melanosis diffusa acquisita)
  • Melanoerythroderma
  • Dowling-Degos disease
  • Nelson Syndrome
  • Pellagra
  • Porphyria cutanea tarda
  • Riehl melanosis
  • Pregnancy pigmentation
  • Systemic Scleroderma
  • Transitory neonatal pustular melanosis
  • Cirrhosis, biliary (e.g. Chloasma hepaticum (biliary cirrhosis); see below liver diseases skin alterations)

Hyperpigmentation in the broader sense is caused by the inclusion of exogenous or endogenous pigments.

• Endogenous pigments: Increased melanin deposition, increased deposition of hemosiderin, bile dyes, carotene, etc.
• Exogenous pigments: deposition of carbon (tattoo) and various substances which are administered by medication. These include: silver and gold particles, bismuth, tetracyclines, amiodarone, clofazimine, phenacetin, carotene, levodopa, phenothiazines
• The main stimulus of (melanotic) hyperpigmentation in the narrower sense is mainly UV radiation. However, hormones, mediators of inflammation such as interleukin-1, prostaglandins, mechanical factors (constant local irritation) or chemical photosensitizers (see phototoxic dermatitis below) can also lead to an increase in melanocyte activity (see post-inflammatory hyperpigmentation below).

From a clinical-etiological point of view, the following classification is made:

• genetic (congenital or acquired)
• numerical (solitary or multiple)
• Localization (light accentuated, inverse)
• extension (localized, disseminated, generalized or universal) and
• Patterning of hyperpigmentations (segmental, nevoid following the Blaschko lines, random)
• etiological (post-inflammatory, drug-induced; physical: caloric, mechanical; endocrine; chemical)
• Location of pigments (epidermal or superficial: brown; dermal: greyish blue to deep blue and blue-black; combination of epidermal and dermal: brown-black).

1. Giehl K et al (2010) Genetically caused pigmentation disorders. Dermatologist 61:567-577
2. Hallermann C et al (2011) Diffuse brown coloration of skin, mucosa and urine. Dermatologist 62: 51-54