DefinitionThis section has been translated automatically.
Hyperpigmentation in the broader sense is a pathological, congenital or acquired, brown coloration of the skin or mucous membrane (see below pigmentation, 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, localised or disseminated, in rare cases also generalised or universal, melanotic colour intensification (brown/black/blue colouring) of the skin/mucosa, caused by an increased number of melanocytes or an increased localised melanin formation, or by deposition of melanin formed at a distance from the focal point (e.g. in metastasised malignant melanoma) or by a combination of the various types of melanoma. mechanisms.
The opposite of hyperpigmentation is depigmentation (loss or absence of pigment cells).
If hyperpigmentation occurs as a consequence of inflammatory skin diseases, it is called inflammatory or post-inflammatory hyperpigmentation.
ClassificationThis section has been translated automatically.
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.
- inflammatory (post-inflammatory) hyperpigmentations
- non-inflammatory hyperpigmentations
- congenital hyperpigmentations (genodermatoses)
- acquired hyperpigmentations
- diffuse hyperpigmentations
- reticular hyperpigmentations
Classification according to underlying diseases/causes:
- 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)
- 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)
- Dowling-Degos disease
- Nelson Syndrome
- 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)
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EtiopathogenesisThis section has been translated automatically.
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).
TherapyThis section has been translated automatically.
Note(s)This section has been translated automatically.
LiteratureThis section has been translated automatically.
- Giehl K et al (2010) Genetically caused pigmentation disorders. Dermatologist 61:567-577
- Hallermann C et al (2011) Diffuse brown coloration of skin, mucosa and urine. Dermatologist 62: 51-54
Incoming links (58)Acromegaly; Acute radiodermatitis; Addison's disease; Amiodarone hyperpigmentation; Angiomatosis, diffuse corticomeningeal; Ataxia teleangiectatica; Azelaic acid; Bleaching agents; Café-au-lait stain; Camouflage; ... Show all
Outgoing links (48)Acanthosis nigricans (overview); Acropigmentation, so-called peak pigment; Addison's disease; Amiodarone hyperpigmentation; Amyloidosis macular cutaneous; Arsenic intoxication; Carcinoid syndrome; Cushing's syndrome (overview); Depigmentation; Dermatitis bullosa pratensis; ... Show all
Please ask your physician for a reliable diagnosis. This website is only meant as a reference.