Pigmentation and hypopigmentation

Introduction The mechanism of pigment abnormalities is complicated. Some pigmented skin diseases are caused by genetic factors; others are caused by secondary factors; others are not clear.

Cause

The color of normal skin is mainly determined by the amount of melanin in the skin. Secondly, it is related to the content of melanin, carrot, and oxidative and reduced hemoglobin in skin blood. The abnormality of skin pigmentation is an abnormal color of the skin. In addition to the increase or decrease of the above factors, it can also be composed of drugs (Apipine, chlorpheniramine), metals (such as arsenic), foreign bodies (such as dyes, dust, tattoos), metabolites (such as scutellaria) and Caused by pathological changes in the skin.

an examination

Related inspection

Skin test, physical examination of skin diseases, determination of erythema

1. Pigmentation with increased melanocyte activity

1. The tyrosine is oxidized to form dopa, which in turn dehydrogenates to form dopamine. The catalysis of tyrosinase is required. Therefore, tyrosinase plays an important role in the synthesis of melanin. The formation of melanin in tyrosine requires several intermediate reaction processes and the need to reduce steel participation. Any factor affecting tyrosinase and its reaction process can cause abnormalities in the synthesis and metabolism of melanin. If the intradermal thiol group is deficient, the tyrosinase activity is increased, and the melanin formation is increased. The mechanism of pigmentation after inflammation is considered to be related to this.

2. Photosensitivity: Skin melanin has the ability to absorb ultraviolet rays to prevent UV damage to tissues. The skin protectively increases melanin formation after exposure to the sun or ultraviolet light. In addition to the genetics of freckles, photosensitivity promotes increased pigmentation.

3. The influence of neurological factors on melanin: such as the disorder of melanocyte stimulating factor produced by thalamus or the increase of melanocyte hormone in pituitary secretion, which stimulates the increase of melanocyte activity and increases melanin. Such as acromegaly.

4. The effect of endocrine on melanin: The gonads secrete estrogen and plenum, which can increase melanin. Such as pigmentation during pregnancy. Adrenal cortex hormones inhibit the action of melanocyte stimulating hormone, which can reduce melanin. When adrenal function is reduced, skin melanin can increase state Addison's disease. The thyroid gland promotes the production of melanin by melanocytes, so when the thyroid function is hyperthyroidism, the skin pigmentation can be deepened.

Second, pigmented skin disease with increased number of melanocytes

Most of the causes are unknown. May be related to genetic or innate factors. Some are born at birth, such as coffee spots, Mongolian spots, congenital color disease, oral sunspot disease.

Third, endogenous non-melanin pigmentation

1. Hemosiderin

It is due to varying degrees of skin bleeding spots. During the absorption recovery process, hemosiderin is deposited in the dermis and appears brownish yellow. Sometimes it is accompanied by melanin deposition due to local factors, such as pigmented purple epilepsy.

2. Yellow pigmentation

Caroteneemia is caused by excessive consumption of carrots and oranges, and elevated levels of carotene in the blood. Since carotene is a lipid pigment, normal skin can be rendered yellow. Astragalus is yellowed by the increase of bilirubin in the blood. The equality of the drug can make the skin yellow. The pathogenesis of yellow brown disease is abnormally metabolized by phenylalanine and tyrosine.

Fourth, exogenous pigmentation

The mechanism of metal pigmentation is due to the deposition of gold, silver, and secret metals in the skin or film. Foreign matter pigmentation is caused by foreign pigments or foreign matter entering the skin, and different pigmentation can be formed by different foreign matter colors.

Fifth, hypopigmentation or hypopigmentation

The mechanism is different. Albinism caused by genetic factors, pigmentation of nodular sclerosis, decreased or defective tyrosinase activity. There was no significant change in the structure of epidermal melanocytes, but the ability to synthesize melanin was inhibited by the lack of tyrosinase. Phenylketonuria inhibits the oxidation of tyrosine to melanin because phenylalanine cannot be oxidized to tyrosine.

Differential diagnosis

Symptoms of hypopigmentation and hypopigmentation need to be identified as follows:

1. Pigmentation based on the increase of melanin

(1) Genetic factors

Freckles, hereditary symmetrical pigment abnormalities, racial black skin disease, and pigmentation in skin diseases.

(two) endocrine factors

Pregnancy, chloasma, Addison's disease, hyperthyroidism, acromegaly, Cushing's syndrome, acanthosis nigricans, etc.

(3) Physical, mechanical and chemical stimulation

Pigmentation spots caused by sunburn, warmth, mechanical stimulation, tar blackness, Rare melanosis, arsenic blackening, drug-induced pigmentation, etc.

(4) Inflammation of pigmentation

Flat moss, chronic eczema, dermatitis, skin amyloidosis, fixed drug eruption, lupus erythematosus, cancerous dermatitis, acne, subcortical pyoderma, pigmentation and other measles, cosmetic dermatitis.

(5) Systemic diseases

1. Chronic infection: malaria, kala-azar, schistosomiasis, tuberculosis, etc.

2. Neoplastic diseases: lymphoma, dysentery, ectopic ACTH syndrome, melanoma, etc.

3. Nervous system diseases: diseases involving diencephalon and substantia nigra, hepatolenticular degeneration, ependymoma, schizophrenia, and the like.

4. Connective tissue disease: systemic scleroderma, dermatomyositis, systemic lupus erythematosus.

5. Chronic liver and kidney disease, anemia can show pigmentation.

6. Vitamin deficiency: vitamin A deficiency, vitamin B; and folic acid deficiency, acid deficiency, vitamin C deficiency.

Second, pigmentation based on the increase in the number of melanocytes

(1) Genetic factors

Black skin disease is affected by plaque, acral pigmentation, sunspot, and perioral medonia.

(2) Diseases

Color-derived juvenile melanoma, congenital color nevus nerve skin blackening disease, blue disease, animal skin and so on.

(3) Congenital or unexplained reasons

Albright syndrome, Mongolian plaque, Ota sinensis, malignant freckle-like clear, melanoma.

Third, endogenous non-melanin pigmentation

(a) bloody pigmentation purple epilepsy, red blood cells themselves sensitive, progressive pigmentation purple

Sexual skin disease, pigmented purple epilepsy moss-like skin disease, red group disease, acromegaly, reticular bluish.

(2) Yellow pigmentation

Caroteneemia, brownish yellow disease, jaundice.

Fourth, exogenous pigmentation

(1) Metal pigmentation

Pigmentation spots caused by gold, silver, lead, and mercury compounds.

(two) foreign matter pigmentation

Tattoos, explosive powdery stagnation.

Five, melanin decline

(1) Decrease in the number of melanocytes

White epilepsy, mottled disease, senile leukoplakia, Waardenburg syndrome.

(B) tyrosinase abnormal whitening disease, phenylketonuria.

(C) melanocyte activity decline

Post-inflammatory hypopigmentation, white pityriasis, leprosy, limited scleroderma, idiopathic punctate hypopigmentation, anemia.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.