STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (3)
Translation Draft
I'll continue with the pustulous lesions.
I'll continue with the pustulous lesions.
Acneiform rashes and
folliculitis are the most common pustulous dermatosis. An
important consideration in the evaluation of perifolicular
pustules is the determination of the associated pathogen, for
example, normal flora, S. aureus, Pityrosporum. Non-infectious
forms of folliculitis include eosinophilic folliculitis and
secondary folliculitis induced by drugs such as glucocorticoids
and lithium.
Eosinophilic folliculitis can occur in HIV-infected individuals and is characteristic through multiple itchy lesions on the face and torso. The administration of high doses of oral glucocorticoids may cause a disseminated eruption of perifolicular pustules on the trunk, characterized by lesions at the same stage of development. As for underlying systemic diseases, pustules are a characteristic component of pustulous psoriasis and may occur in septic embolisms of bacterial or fungal origin. For example, skin lesions in disseminated gonococia often have a halo of erythema surrounding a central pustule.
Telangiectasis have several causes represented by: 1. primary skin conditions such as A. linear ones (a. rosacea, b. actinic damaged skin, c. venous hypertension and d. essential telangiectasis), B. poikilodermy (a. ionizing radiation and b. atrophied vascular poikilodermy), C. stelate angioma (a. idiopathic and b. of pregnancy) and 2. systemic conditions such as A. linear ones (a. carcinoid, b. ataxia-telangiectasis and c. mastocytosis), B. poikiloderma (a. dermatomyosis, b. xeroderma pigmentosum and c. T-cell skin lymphoma), C. reticular (scleroderma), D. periangle (a. lupus erythematosus, b. scleroderma and c. dermatomyosis), E. papulation (hereditary haemorrhagic telangiectasis) and F. stelate angioma (to cirrhosis).
In order to distinguish the different types of telangiectasis, it is important to examine the shape and configuration of dilated blood vessels. Linear telangiectasis are found on the faces of patients with actinic damage and rosacea and on the lower limbs of patients with venous hypertension and essential telangiectasis.
Telangiectasis are of two types: 1. linear (simple, red or blue line that disappears at diascopy/pressure, associated with a. rosacea, having as clinical characteristic the presence on the face, vasodilation-based pathogenicity, causing laser treatment/ pulsating coloration, b. actinic injured skin, having as clinical characteristics the presence on the face, arms, upper torso, associated with hypo or hyperpigmentation and keratosis, pathogenicity manifested by lesions of subacute connective tissue, laser treatment/ pulsating coloration, c. essential telangiectasis having clinical characteristics represented by the presence in the lower limbs that begins on the lower limbs and can be disseminated, more frequently in women, with unknown pathogenicity and treatment with sclerotherapy - ???) and 2. stellates/ star-level angiomas (with associated condition represented by idiopathic manifestations and pregnancy, having as clinical characteristics the presence on the anterior half of the body and halo of pallor secondary to the phenomenon of local theft, with pathogenicity represented by the proliferation of blood vessels, in combination with increased circulating estrogens, "inducing" laser treatment/ pulsating coloration).
Patients with an unusual form of mastocytosis (telangiectasia macalaris eruptiva pertans), carcinoid syndrome and ataxia-telangiectasis also have linear telangiectasis. In ataxia-telangiectasis, linear telangiectasis occur on the bulbar conjunctiva during childhood. Finally, damage to the ears, eyelids, cheeks and/ or flexural areas, such as antecubital and popliteal fossa, occurs. Finally, linear telangiectasis are found in areas of skin inflammation. For example, lesions of discoid lupus frequently have telangiectasis.
Poikiloderma is a term used to describe: 1. an area with reticulated hypo or hyperpigmentation, 2. secondary wrinkles to epidermal atrophy and 3. telangiectasis. Poikiloderma is not a unique condition, being found in skin damaged by ionizing radiation, in atrophican vascular poikiloderma (VA) and xeroderma pigmentosum, as in patients with connective tissue diseases, especially dermatomyositis (DM). PVA is a precursor lesion of THE CDCT, and poikilodermia regions begin in the flexural areas of the armpit and inguinal ones.
In scleroderma, dilated blood vessels have a unique configuration and are known as "networked" telangiectasis. The lesions are broad macles, which usually measure 2-7 mm in diameter (sometimes being larger). Reticular lesions have a polygonal or oval shape and their erythematous appearance may be uniform or the result of fine telangiectasis. The most common localizations of telangiectasis of this type are on the face, mouth and hands (peripheral regions susceptible to intermittent ischemia). CREST syndrome (calcinosus cutis, Raynaud phenomenon, oesophageal motility disorders, sclerodactyly and telangiectasis), a form of scleroderma, is associated with chronic evolution and anti-centromer antibodies.
Reticular telangiectasis is an important indication for the diagnosis of CREST syndrome, as well as systemic scleroderma, because they may be the only skin sign.
Periangle telangiectasis are pathognomonic signs for three major connective tissue diseases: 1. lupus erythematosus (LE), scleroderma and dermatomyolysis (DM). They are easy to view with the naked eye and occur in at least two-thirds of these patients. In DM and lupus there is an associated erythema of the nail fold, and in DM the erythema is often accompanied by "ragged" cuticles and sensitivity of the fingertips. Viewed at a 10x magnification, the blood vessels in the nail folds of patients with lupus are contorted and resemble "glomerules", while in scleroderma and dM there is a loss of capillary anises, and those that remain are intensely dilated.
In hereditary hemorrhagic telangiectasis (Rendu-Osler-Weber disease), lesions usually occur in adulthood and are most commonly found on the mucous membranes, compared to distal extremities, including the subangle. They represent arteriovenous malformations (AV) of dermal microvascularization, are dark-red and are usually slightly prominent. When the skin is stretched over an individual lesion, an eccentric point with radial extensions is highlighted. Although the degree of systemic impairment is variable in this dominant autosomal disease, major symptoms are recurrent epistaxis and gastrointestinal hemorrhage. The fact that these mucous telangiectasis are actually AV communications, helps explain their bleeding tendency.
The "time" of hypopigmentation has come. Hypopigmentation disorders are classified as diffuse and localized. The classic example of diffuse hypopigmentation is oculocutaneous albinism (AOC). The most common forms of the disease are due to mutations in the throsinase gene (type I) or the P gene (type II) (some patients with type I of AOC have a total lack of enzyme activity). At birth, different types of AOC may look similar to white hair, gray-blue eyes and white-pink skin.
However, patients without tyrosinasic activity maintain this phenotype, while those with low activity or mutations of the P gene will acquire a degree of pigmentation of the eyes, hair and skin with age. The degree of pigment formation is based on racial origin, but hypopigmentation is evident when compared to their first-degree relatives. Eye signs in AOC correlate with the degree of hypopigmentation and include low visual acuity, nystagmus, photophobia and monocular vision.
Generalized vitiligo, phenylcetonuria and homocystinuria are other unusual causes of diffuse depigmentation. In generalized vitiligo, melanocytes are not found in the affected skin, while in AOC they are present, but have low activity. Appropriate laboratory tests exclude other metabolism disorders.
Differential diagnosis of localized hypomelanosis includes the following primitive skin conditions: vitiligo, chemical leukoderma, piebaldism, nevus depigmentosus, post-inflammatory hypomelanosis and tinea versicolor. In the case of vitiligo, the clinical characteristics are represented by an acquired and progressive character, with symmetrical regions of complete loss of pigment, especially periorificial (around the mouth, nose, eyes, nipples, navel, anus but also in other regions such as the flexion area of the fist, the area of distal extension of the extremities), the segmental form being rarer , unilateral, dermatomal type. Examination with the Wood lamp shows a more obvious perception of these areas, with a white-cretos color.
Skin biopsy reveals absence of melanocytes and minimal inflammation. From the point of view of pathogenicity, it is an autoimmune process that leads to the destruction of melanocytes (humoral and/ or cellular), the alternative hypothesis being the self-destruction of melanocytes and circulating antibodies to melanocytes, which appear as a secondary phenomenon. Treatment is represented by the administration of topical glucocorticoids, PUVA, transplants, skin depigmentation if the affected areas are extensive.
In the case of chemical leukoderma, the clinical characteristics are represented by similar appearance to vitiligo, often starting on the hands, with satellite lesions in regions not exposed to chemicals. When examining with the Wood lamp, a more obvious, white-cretos look is observed. Skin biopsy reveals low number or absence of melanocytes.
From the point of view of pathogenicity, exposure to substances that selectively destroy melanocytes, in particular phenols and catechlins (germicides, produced from the rubber industry) and the release of cellular antigens and activation of circulating lymphocytes that may explain satellite phenomena. Treatment is represented by avoiding exposure to the provoking agent, then treatment as in vitiligo. In the case of piebaldism, the clinical characteristics are represented by a dominant, congenital, stable autosomal mechanism with white mass, the regions of hypomelanosis containing normally pigmented and hyperpigmented maculas, of variable dimensions, symmetrical damage to the center of the forehead, ventral trunk and middle regions of the upper and lower extremities.
On examination with the Wood lamp, the emphasis of leucoderma and hyperpigmented macles is observed. Skin biopsy reveals hypomelanotic regions with few or no melanocytes. From the point of view of pathogenicity, there is a defect in the migration of melanoblasts from the neural crest to the ventral skin or the impossibility of melanoblas to survive or differentiate in these regions as well as mutations in protooncogen c-kit encoding the tyrosine-kinase receptor for the mast/stem cell growth factor.
Treatment does not exist or can sometimes be used for transplantation. Post-inflammatory hypomelanosis has as clinical characteristics hypopigmentation that can occur in active lesions, as in subacute lupus, or after the lesion is erased, as in dermatitis. In wood lamp analysis, elements can be found that depend on each condition, usually the intensity of depigmentation being lower than in vitiligo. Skin biopsy reveals that the type of inflammatory infiltration depends on the specific condition. From the point of view of pathogenicity, blockage in the transfer of melanin from melanocytes to keratinocytes may be secondary to edema or decreased contact time, as well as the destruction of melanocytes, if inflammatory cells attack the basal layer.
Treatment is focused on treating the underlying inflammatory disease. And, there would be the tinea versicolor which has as clinical characteristics the character of frequent affection, with distribution on the upper trunk and neck, in the scarf, especially in young adults, macles having fine white scars at the grating. Analysis with the Wood lamp reveals golden fluorescence. Skin biopsy reveals sprouting levs and hyfes in the corneal layer. Pathogenic is found the invasion of the corneal layer by the Pityrosporum levura, which is lipophilic and produces dicarboxylic acids C9 and C11, which inhibits vitro tyrosinease. Treatment is the administration of 2.5% selenium sulfide, topical imidazoles, imidazoles or triazoli per bone.
In this group of diseases, in the affected regions, maclets or areas that have a decrease or absence of pigmentation appear, and in the first four diseases mentioned, secondary changes such as crusts or swords are absent. Vitiligo patients have an increased incidence of autoimmune disorders, including hypothyroidism, Graves' disease, pernicious anemia, Addison's disease, uveitis, alopecia areata, chronic mucocutaneous candidiasis and autoimmune polyglandular syndromes (types I and II).
Thyroid gland diseases are the most common associated disorders, occurring in more than 30% of vitiligo patients. Circulating autoantibodies are often discovered, and the most common are anti-thireoglobulin, antimicrosomal and parietal anti-cell antibodies. There are three systemic diseases to be considered in a patient with clinical findings suggestive of vitiligo: 1. Vogt-Koyanagi-Harada syndrome, 2. scleroderma and 3. leucoderma associated with melanoma.
A history of aseptic meningitis, a non-traumatic, tinnitus, hearing loss and/ or suspected disease indicates the diagnosis of Vogt-Koyanagi-Harada syndrome. In these patients, the face and scalp are the most common localizations of pigment loss. Vitiligo-like leukoderma, found in patients with scleroderma, is clinically similar to idiopathic vitiligo that has begun to repigment as a result of treatment (normal perifolicular maculas are present in depigmentation areas).
The basis of this leukoderma is unknown, there are no signs of inflammation in the affected areas, but the condition can heal if the underlying connective tissue disease becomes inactive. Unlike idiopathic vitiligo, melanoma-associated leukoderma often begins on the trunk and its appearance must lead to the search for a metastatic disease. There is a possibility that the destruction of normal melanocytes may be the result of an immune response against malignant melanocytes.
There are two systemic conditions that have the skin signs of piebaldism: 1. Hirschsprung's disease and Waardenburg syndrome. One possible explanation for both conditions is an abnormal embryonic migration of two of the elements derived from the neural crest, one being melanocytes and the other cells of the myenteric ganglia (Hirschsprung's disease) or of the auditory nerve (Waardenburg syndrome).
This latter syndrome is characterized by congenital sensorineural hearing loss, dystopia canthorum (lateral displacement of internal cantus, but with normal interpupilal distance), heterochrome iris and a root of the wide nose, in addition to piebaldism.
Patients with Waardenburg syndrome have been shown to have mutations in two genes that encode DNA bonding proteins, PAX-3 and MITF, while some patients with Hirschsprung's disease and white spots have a mutation in one of the two endothelin receptors. In tuberous sclerosis, the most early skin sign is the stain in the "ash leaf".
These lesions are often present at birth and are often multiple (however, detection may require examination with the Wood lamp, especially in open-skin individuals). The pigment in them is reduced, but not absent. The average size is 1-3 cm and the common forms are oval, polygonal and lanceolate, while the uncommon forms are dermatomal and confetti-like. Examination of the patient in search of additional skin signs such as sebaceous adenomas (multiple angiofibromas on the face), nail and gum fibroids, fibrous plaques of the forehead and nevi of connective tissue (sagrin spots), is recommended.
It is important to remember that a stain in the "ash leaf" on the scalp will lead to a polyosis, which is a circumscribed macula of gray white hair. Internal manifestations include epileptic seizures, mental retardation, CNS and retinal hamartomas, renal angiomyolipomas and cardiac rhabdomyomas. The latter can be detected by ultrasound in up to 60% of children (less than 18 years of age) with tuberous sclerosis.
Nevus depigmentosum (depigmented nebula) is a stable, well circumscribed hypomelanosis that is present at birth. There is usually a single circular or rectangular lesion, but sometimes the nebula has a dermatomal or spiral distribution. It is important to differ this lesion from a macula in "ash leaf", especially when there are multiple lesions. In hypomelanosis Ito (incontinentia pigmenti achromians), swirls and stripes of hypopigmentation are arranged parallel to each other, in a form resembling a marbled cake.
Injuries can progress or regress over time and at least 1/3 of patients are found animals of the musculoskeletal system (asymmetry), CNS (epilepsy and mental retardation) and eyes (strabismus and hyperteleism). Chromosome mosaicism and diploid/ triploid mixoploidy have been reported in these patients (this supports the hypothesis that the skin design is the result of the migration of the two clones of primordial melanocytes, each with a different pigment potential). Localized regions of low depigmentation are usually encountered as a result of skin inflammation and have been observed in the skin covering active sarcoidosis lesions, as well as by LCCT.
Skin infections also exhibit hypopigmentation disorders, and in tuberculosis leprosy there are several asymmetric spots of hypomelanosis that are anesthetic, antihydrotic and alopecia. Biopsy of the palpable edge shows dermal granulomas in which Mycobacterium leprosy is missing.
Ready for today... tomorrow hyperpigmentation...
Eosinophilic folliculitis can occur in HIV-infected individuals and is characteristic through multiple itchy lesions on the face and torso. The administration of high doses of oral glucocorticoids may cause a disseminated eruption of perifolicular pustules on the trunk, characterized by lesions at the same stage of development. As for underlying systemic diseases, pustules are a characteristic component of pustulous psoriasis and may occur in septic embolisms of bacterial or fungal origin. For example, skin lesions in disseminated gonococia often have a halo of erythema surrounding a central pustule.
Telangiectasis have several causes represented by: 1. primary skin conditions such as A. linear ones (a. rosacea, b. actinic damaged skin, c. venous hypertension and d. essential telangiectasis), B. poikilodermy (a. ionizing radiation and b. atrophied vascular poikilodermy), C. stelate angioma (a. idiopathic and b. of pregnancy) and 2. systemic conditions such as A. linear ones (a. carcinoid, b. ataxia-telangiectasis and c. mastocytosis), B. poikiloderma (a. dermatomyosis, b. xeroderma pigmentosum and c. T-cell skin lymphoma), C. reticular (scleroderma), D. periangle (a. lupus erythematosus, b. scleroderma and c. dermatomyosis), E. papulation (hereditary haemorrhagic telangiectasis) and F. stelate angioma (to cirrhosis).
In order to distinguish the different types of telangiectasis, it is important to examine the shape and configuration of dilated blood vessels. Linear telangiectasis are found on the faces of patients with actinic damage and rosacea and on the lower limbs of patients with venous hypertension and essential telangiectasis.
Telangiectasis are of two types: 1. linear (simple, red or blue line that disappears at diascopy/pressure, associated with a. rosacea, having as clinical characteristic the presence on the face, vasodilation-based pathogenicity, causing laser treatment/ pulsating coloration, b. actinic injured skin, having as clinical characteristics the presence on the face, arms, upper torso, associated with hypo or hyperpigmentation and keratosis, pathogenicity manifested by lesions of subacute connective tissue, laser treatment/ pulsating coloration, c. essential telangiectasis having clinical characteristics represented by the presence in the lower limbs that begins on the lower limbs and can be disseminated, more frequently in women, with unknown pathogenicity and treatment with sclerotherapy - ???) and 2. stellates/ star-level angiomas (with associated condition represented by idiopathic manifestations and pregnancy, having as clinical characteristics the presence on the anterior half of the body and halo of pallor secondary to the phenomenon of local theft, with pathogenicity represented by the proliferation of blood vessels, in combination with increased circulating estrogens, "inducing" laser treatment/ pulsating coloration).
Patients with an unusual form of mastocytosis (telangiectasia macalaris eruptiva pertans), carcinoid syndrome and ataxia-telangiectasis also have linear telangiectasis. In ataxia-telangiectasis, linear telangiectasis occur on the bulbar conjunctiva during childhood. Finally, damage to the ears, eyelids, cheeks and/ or flexural areas, such as antecubital and popliteal fossa, occurs. Finally, linear telangiectasis are found in areas of skin inflammation. For example, lesions of discoid lupus frequently have telangiectasis.
Poikiloderma is a term used to describe: 1. an area with reticulated hypo or hyperpigmentation, 2. secondary wrinkles to epidermal atrophy and 3. telangiectasis. Poikiloderma is not a unique condition, being found in skin damaged by ionizing radiation, in atrophican vascular poikiloderma (VA) and xeroderma pigmentosum, as in patients with connective tissue diseases, especially dermatomyositis (DM). PVA is a precursor lesion of THE CDCT, and poikilodermia regions begin in the flexural areas of the armpit and inguinal ones.
In scleroderma, dilated blood vessels have a unique configuration and are known as "networked" telangiectasis. The lesions are broad macles, which usually measure 2-7 mm in diameter (sometimes being larger). Reticular lesions have a polygonal or oval shape and their erythematous appearance may be uniform or the result of fine telangiectasis. The most common localizations of telangiectasis of this type are on the face, mouth and hands (peripheral regions susceptible to intermittent ischemia). CREST syndrome (calcinosus cutis, Raynaud phenomenon, oesophageal motility disorders, sclerodactyly and telangiectasis), a form of scleroderma, is associated with chronic evolution and anti-centromer antibodies.
Reticular telangiectasis is an important indication for the diagnosis of CREST syndrome, as well as systemic scleroderma, because they may be the only skin sign.
Periangle telangiectasis are pathognomonic signs for three major connective tissue diseases: 1. lupus erythematosus (LE), scleroderma and dermatomyolysis (DM). They are easy to view with the naked eye and occur in at least two-thirds of these patients. In DM and lupus there is an associated erythema of the nail fold, and in DM the erythema is often accompanied by "ragged" cuticles and sensitivity of the fingertips. Viewed at a 10x magnification, the blood vessels in the nail folds of patients with lupus are contorted and resemble "glomerules", while in scleroderma and dM there is a loss of capillary anises, and those that remain are intensely dilated.
In hereditary hemorrhagic telangiectasis (Rendu-Osler-Weber disease), lesions usually occur in adulthood and are most commonly found on the mucous membranes, compared to distal extremities, including the subangle. They represent arteriovenous malformations (AV) of dermal microvascularization, are dark-red and are usually slightly prominent. When the skin is stretched over an individual lesion, an eccentric point with radial extensions is highlighted. Although the degree of systemic impairment is variable in this dominant autosomal disease, major symptoms are recurrent epistaxis and gastrointestinal hemorrhage. The fact that these mucous telangiectasis are actually AV communications, helps explain their bleeding tendency.
The "time" of hypopigmentation has come. Hypopigmentation disorders are classified as diffuse and localized. The classic example of diffuse hypopigmentation is oculocutaneous albinism (AOC). The most common forms of the disease are due to mutations in the throsinase gene (type I) or the P gene (type II) (some patients with type I of AOC have a total lack of enzyme activity). At birth, different types of AOC may look similar to white hair, gray-blue eyes and white-pink skin.
However, patients without tyrosinasic activity maintain this phenotype, while those with low activity or mutations of the P gene will acquire a degree of pigmentation of the eyes, hair and skin with age. The degree of pigment formation is based on racial origin, but hypopigmentation is evident when compared to their first-degree relatives. Eye signs in AOC correlate with the degree of hypopigmentation and include low visual acuity, nystagmus, photophobia and monocular vision.
Generalized vitiligo, phenylcetonuria and homocystinuria are other unusual causes of diffuse depigmentation. In generalized vitiligo, melanocytes are not found in the affected skin, while in AOC they are present, but have low activity. Appropriate laboratory tests exclude other metabolism disorders.
Differential diagnosis of localized hypomelanosis includes the following primitive skin conditions: vitiligo, chemical leukoderma, piebaldism, nevus depigmentosus, post-inflammatory hypomelanosis and tinea versicolor. In the case of vitiligo, the clinical characteristics are represented by an acquired and progressive character, with symmetrical regions of complete loss of pigment, especially periorificial (around the mouth, nose, eyes, nipples, navel, anus but also in other regions such as the flexion area of the fist, the area of distal extension of the extremities), the segmental form being rarer , unilateral, dermatomal type. Examination with the Wood lamp shows a more obvious perception of these areas, with a white-cretos color.
Skin biopsy reveals absence of melanocytes and minimal inflammation. From the point of view of pathogenicity, it is an autoimmune process that leads to the destruction of melanocytes (humoral and/ or cellular), the alternative hypothesis being the self-destruction of melanocytes and circulating antibodies to melanocytes, which appear as a secondary phenomenon. Treatment is represented by the administration of topical glucocorticoids, PUVA, transplants, skin depigmentation if the affected areas are extensive.
In the case of chemical leukoderma, the clinical characteristics are represented by similar appearance to vitiligo, often starting on the hands, with satellite lesions in regions not exposed to chemicals. When examining with the Wood lamp, a more obvious, white-cretos look is observed. Skin biopsy reveals low number or absence of melanocytes.
From the point of view of pathogenicity, exposure to substances that selectively destroy melanocytes, in particular phenols and catechlins (germicides, produced from the rubber industry) and the release of cellular antigens and activation of circulating lymphocytes that may explain satellite phenomena. Treatment is represented by avoiding exposure to the provoking agent, then treatment as in vitiligo. In the case of piebaldism, the clinical characteristics are represented by a dominant, congenital, stable autosomal mechanism with white mass, the regions of hypomelanosis containing normally pigmented and hyperpigmented maculas, of variable dimensions, symmetrical damage to the center of the forehead, ventral trunk and middle regions of the upper and lower extremities.
On examination with the Wood lamp, the emphasis of leucoderma and hyperpigmented macles is observed. Skin biopsy reveals hypomelanotic regions with few or no melanocytes. From the point of view of pathogenicity, there is a defect in the migration of melanoblasts from the neural crest to the ventral skin or the impossibility of melanoblas to survive or differentiate in these regions as well as mutations in protooncogen c-kit encoding the tyrosine-kinase receptor for the mast/stem cell growth factor.
Treatment does not exist or can sometimes be used for transplantation. Post-inflammatory hypomelanosis has as clinical characteristics hypopigmentation that can occur in active lesions, as in subacute lupus, or after the lesion is erased, as in dermatitis. In wood lamp analysis, elements can be found that depend on each condition, usually the intensity of depigmentation being lower than in vitiligo. Skin biopsy reveals that the type of inflammatory infiltration depends on the specific condition. From the point of view of pathogenicity, blockage in the transfer of melanin from melanocytes to keratinocytes may be secondary to edema or decreased contact time, as well as the destruction of melanocytes, if inflammatory cells attack the basal layer.
Treatment is focused on treating the underlying inflammatory disease. And, there would be the tinea versicolor which has as clinical characteristics the character of frequent affection, with distribution on the upper trunk and neck, in the scarf, especially in young adults, macles having fine white scars at the grating. Analysis with the Wood lamp reveals golden fluorescence. Skin biopsy reveals sprouting levs and hyfes in the corneal layer. Pathogenic is found the invasion of the corneal layer by the Pityrosporum levura, which is lipophilic and produces dicarboxylic acids C9 and C11, which inhibits vitro tyrosinease. Treatment is the administration of 2.5% selenium sulfide, topical imidazoles, imidazoles or triazoli per bone.
In this group of diseases, in the affected regions, maclets or areas that have a decrease or absence of pigmentation appear, and in the first four diseases mentioned, secondary changes such as crusts or swords are absent. Vitiligo patients have an increased incidence of autoimmune disorders, including hypothyroidism, Graves' disease, pernicious anemia, Addison's disease, uveitis, alopecia areata, chronic mucocutaneous candidiasis and autoimmune polyglandular syndromes (types I and II).
Thyroid gland diseases are the most common associated disorders, occurring in more than 30% of vitiligo patients. Circulating autoantibodies are often discovered, and the most common are anti-thireoglobulin, antimicrosomal and parietal anti-cell antibodies. There are three systemic diseases to be considered in a patient with clinical findings suggestive of vitiligo: 1. Vogt-Koyanagi-Harada syndrome, 2. scleroderma and 3. leucoderma associated with melanoma.
A history of aseptic meningitis, a non-traumatic, tinnitus, hearing loss and/ or suspected disease indicates the diagnosis of Vogt-Koyanagi-Harada syndrome. In these patients, the face and scalp are the most common localizations of pigment loss. Vitiligo-like leukoderma, found in patients with scleroderma, is clinically similar to idiopathic vitiligo that has begun to repigment as a result of treatment (normal perifolicular maculas are present in depigmentation areas).
The basis of this leukoderma is unknown, there are no signs of inflammation in the affected areas, but the condition can heal if the underlying connective tissue disease becomes inactive. Unlike idiopathic vitiligo, melanoma-associated leukoderma often begins on the trunk and its appearance must lead to the search for a metastatic disease. There is a possibility that the destruction of normal melanocytes may be the result of an immune response against malignant melanocytes.
There are two systemic conditions that have the skin signs of piebaldism: 1. Hirschsprung's disease and Waardenburg syndrome. One possible explanation for both conditions is an abnormal embryonic migration of two of the elements derived from the neural crest, one being melanocytes and the other cells of the myenteric ganglia (Hirschsprung's disease) or of the auditory nerve (Waardenburg syndrome).
This latter syndrome is characterized by congenital sensorineural hearing loss, dystopia canthorum (lateral displacement of internal cantus, but with normal interpupilal distance), heterochrome iris and a root of the wide nose, in addition to piebaldism.
Patients with Waardenburg syndrome have been shown to have mutations in two genes that encode DNA bonding proteins, PAX-3 and MITF, while some patients with Hirschsprung's disease and white spots have a mutation in one of the two endothelin receptors. In tuberous sclerosis, the most early skin sign is the stain in the "ash leaf".
These lesions are often present at birth and are often multiple (however, detection may require examination with the Wood lamp, especially in open-skin individuals). The pigment in them is reduced, but not absent. The average size is 1-3 cm and the common forms are oval, polygonal and lanceolate, while the uncommon forms are dermatomal and confetti-like. Examination of the patient in search of additional skin signs such as sebaceous adenomas (multiple angiofibromas on the face), nail and gum fibroids, fibrous plaques of the forehead and nevi of connective tissue (sagrin spots), is recommended.
It is important to remember that a stain in the "ash leaf" on the scalp will lead to a polyosis, which is a circumscribed macula of gray white hair. Internal manifestations include epileptic seizures, mental retardation, CNS and retinal hamartomas, renal angiomyolipomas and cardiac rhabdomyomas. The latter can be detected by ultrasound in up to 60% of children (less than 18 years of age) with tuberous sclerosis.
Nevus depigmentosum (depigmented nebula) is a stable, well circumscribed hypomelanosis that is present at birth. There is usually a single circular or rectangular lesion, but sometimes the nebula has a dermatomal or spiral distribution. It is important to differ this lesion from a macula in "ash leaf", especially when there are multiple lesions. In hypomelanosis Ito (incontinentia pigmenti achromians), swirls and stripes of hypopigmentation are arranged parallel to each other, in a form resembling a marbled cake.
Injuries can progress or regress over time and at least 1/3 of patients are found animals of the musculoskeletal system (asymmetry), CNS (epilepsy and mental retardation) and eyes (strabismus and hyperteleism). Chromosome mosaicism and diploid/ triploid mixoploidy have been reported in these patients (this supports the hypothesis that the skin design is the result of the migration of the two clones of primordial melanocytes, each with a different pigment potential). Localized regions of low depigmentation are usually encountered as a result of skin inflammation and have been observed in the skin covering active sarcoidosis lesions, as well as by LCCT.
Skin infections also exhibit hypopigmentation disorders, and in tuberculosis leprosy there are several asymmetric spots of hypomelanosis that are anesthetic, antihydrotic and alopecia. Biopsy of the palpable edge shows dermal granulomas in which Mycobacterium leprosy is missing.
Ready for today... tomorrow hyperpigmentation...
Have a good day!
Dorin, Merticaru