Pigmentation abnormalities
Introduction
Introduction 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 caused by drugs (Apipine, chlorpheniramine), metals (such as arsenic, antimony), foreign bodies (such as dyes, dust, tattoos), metabolites (such as jaundice). And caused by pathological changes in the skin.
Cause
Cause
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. This chapter has several explanations for its etiology classification.
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.
Depigmentation of vitiligo and mottled disease is due to the absence of epidermal melanocytes. The cause of the defect of the melanocytes is still unclear, and the latter is autosomal dominant. The mechanism of the occurrence of vitiligo is generally believed to have a genetic background; it is thought to be autoimmune or melanocyte destruction; there is also a hypothesis of neurochemical factors. At present, according to its clinical, pathological, physiological, biochemical, and immunological studies, it is difficult to explain with one factor.
Hypopigmentation after inflammation, hypopigmentation of white pityriasis is due to a decrease in the ability of epidermal cells at the lesion to receive melanocytes from melanocyte transfer. The hypopigmentation of psoriatic lesions may be due to the rapid proliferation of epidermal cells and the inability of melanocytes to transfer melanin. The hypopigmentation of spotted mites is thought to be a pathogen that blocks UV rays or releases certain toxins that interfere with melanocyte activity.
Leukopenia caused by leprosy, it is generally believed that cell infiltration interferes with the function of melanocytes, neurotrophic dysfunction, local blood flow reduction and M. leprae inhibits the activity of dopa, causing the competitive effects of melanocytes, making black The combined results of the synthetic barriers.
Examine
an examination
Related inspection
Skin color filtered UV inspection
First, medical history
To learn more about the medical history. Such as onset time, age, location, extent, development of pigment abnormalities; whether there are local symptoms or systemic symptoms; the onset factors are primary or secondary; previous treatment, the effect; whether there is family history, genetic history and so on.
Second, physical examination
Check the area of the pigment abnormality to determine the color of the pigment abnormality. If the yellow-brown plaque occurs on the face, it is found in chloasma; reddish brown is found in the erythema erythema of the face and neck; blue-brown is found in Ota disease; light black is seen in Riel melanosis; porcelain white is found in white epilepsy; There are fine sputum in the white pity. For pigment abnormalities that occur in the trunk, brown spots are found in coffee spots; blue-brown spots are found in Mongolian spots; pale brown is found in pigmented measles; pigmentation in exposed parts of the extremities is associated with contact allergy and light sensitivity. Pigment abnormalities with limited physical appearance above the skin surface are found in mites. Generalized pigmentation is seen in systemic diseases. Such as systemic scleroderma, dermatomyositis, Addison's disease, skin black fever and so on. Generalized skin whitening is seen in albinism, and limited white spots are seen in white epilepsy.
Third, laboratory inspection
Histopathological examination is important for the diagnosis of pigment abnormalities. In particular, pigmentation damage becomes darker and darker in the short term, and pathological examination is required to prevent malignant transformation. Pigment abnormalities caused by systemic diseases can be checked in the laboratory for the primary disease.
Diagnosis
Differential diagnosis
Depigmentation: Vitiligo is a common acquired pigmented mucosal disease. According to the depigmentation, it is acquired, milky white, peripheral pigmentation zone and no symptoms. It can be diagnosed.
Increased melatonin: melatonin, an endogenous substance secreted by the pineal gland, is a regulating hormone that affects the secretion of all other hormones almost directly or indirectly. It has a wide range of physiological activities and can enhance the function of the immune system. Regulates the endocrine system, has anti-oxidation, protects cells from free radicals, delays aging and prolongs lifespan, but increased melatonin secretion may cause seasonal depression. Decreased light leads to increased melatonin secretion, while excessive melatonin inhibits the synthesis of serotonin, and reduced serotonin synthesis leads to depression.
Pigmentation: 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.
