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Vitiligo is a syndrome characterized by acquired loss of pigmentation in a usually symmetrical but 'spotty distribution, commonly involving the central face and lips, genitalia, hands and extremities. Pigmentation in the skin is produced by melanin, a hetero-polymer synthesized in melanocytes by a complex biochemical pathway controlled by the rate-limiting Jarrett and Szabo first proposed that vitiligo was characterized by two stages that might be sequential type I vitiligo with decreased melanocyte tyrosinase activity, and type II vitiligo in which melanocytes were destroyed. In established vitiligo, cells with ultrastructural and immunohistochemical features of melanocytes are lost from the basal layer of the epidermis. Vacuolar damage to both basal layer melanocytes and keratinocytes can be found in association with infiltrates composed of monocytes and lymphocytes. Melanocytes and keratinocytes in the active border of vitiligo lesions show increased ICAM-1 expression, suggesting...
Vitiligo can be found in autoimmune families in association with Addison disease, alopecia areata, pernicious anemia, or mucocutaneous candidiasis, with an incidence 10-15 times higher than in the general population. Antibodies to thyroid, adrenal gland and gastric parital cells can be demonstrated in vitiligo patients using modern techniques, antibodies reactive with melanocytes have been consistently-found in vitiligo patients' sera. The levels of these antibodies are greatest in patients with actively progressing disease and in vitiligo patients with other autoimmune disease. Both melanocyte-specific antibodies and antibodies reactive to other cells in addition to melanocytes have been identified. Some of these antibodies are specific for proteins involved in melanization such as tyrosinase and tyrosinase-related protein 1. Antibodies to a melanocyte-specific 85 kDa antigen have been described in dogs, cats and horses with vitiligo. Similar antibodies are found in a chicken model...
Vitiligo is a syndrome of depigmentation of the skin caused by damage to epidermal melanocytes. This may occur as a component of autoimmune syndromes, as a polygenic disorder, or sporadically. Melanocyte damage in vitiligo is believed to be caused by a number of cytotoxic stimuli specific immune reactions, accumulation of toxic products of melanization, biochemical imbalances which favor cellular destruction, or neural stimuli.
The UK Vitiligo Society is unique in publishing a book,5 about to be revised and updated, on all aspects of vitiligo, its management and current research. Most self-help organisations have developed a raft of fact sheets, written in good lay language but with professional input where necessary to ensure accuracy. These help not only patients, but also professionals. Leaflets and fact sheets can be tailored to different groups, such as children, parents, teachers, health and other professionals, as well as to the general public.
Useful when wounds have been obscured by blood, thick hair, skin pigmentation, decomposition, medical alteration, and insect or animal activity (160,162,163). The presence of lead is confirmed by scanning electron microscopy energy-dispersive X-ray. Skull wounds owing to gunshots can have lead fragments deposited on the outer table of the cranium (16). Lead fragments also indicate the path of a wound track. Lead fragments can trace the path of an intracranial ricochet (see Subheading 19.4. and ref. 16).
Vitiligo is an acquired disorder of pigmentation affecting mainly the skin, where the loss of functioning melanocytes results in white patches. The hair and, rarely, the eyes or other organs and systems may be also affected. The most common form of vitiligo is symmetrical, usually affecting the skin around the orifices, the genitals, sun-exposed areas such as the face and hands, and friction areas such as extensor surfaces of the limbs. The rare segmental type affects only one area of the body.
We searched for randomised controlled trials (RCTs) or at least controlled trials of currently available medical and surgical treatments in the Cochrane Library and Cochrane Central Register of Controlled Trials, Medline and Embase, with the keywords vitiligo and treatment . We also searched for controlled trial , meta-analysis , systematic review , practice guideline , quality of life and prognosis . The search was completed in February 2002, and all the relevant papers found were critically appraised and included. Reference search of the key papers was performed. A protocol by Barrett and Whitton on Interventions for vitiligo is in the Cochrane Database of Systematic Reviews. Two systematic reviews and a meta-analysis from which practice guidelines for the treatment of vitiligo were developed, by Njoo and coworkers, were published in the Evidence-based Dermatology section of Archives of Dermatology.
The prevalence of vitamin D insufficiency is increasing in western societies. The major source of vitamin D in healthy individuals of normal mobility is through the action of sunlight on the skin, but increased skin pigmentation or behaviours that reduce sun exposure, such as increased time spent indoors or extensive skin covering while outdoors, predispose to vitamin D insufficiency in the absence of dietary supplementation. Although vitamin D has been classically associated with bone mineralization, the wide distribution of vitamin D receptors provides the basis for a more extensive role for vitamin D. Thus, there is accumulating evidence for an involvement of vitamin D in the regulation of cell proliferation and differentiation, brain development, immune responses, the renin-angiotensin system and cardiovascular function. A recent disturbing recognition of startlingly low vitamin D levels amongst women of reproductive age, and indeed, in pregnant women, places in sharp focus our...
An increase in skin pigmentation and zenith angle of the sun (change in latitude, season, and time of day) and the topical application of a sunscreen can markedly diminish or even prevent the production of vitamin D3 in the skin. Over the age of 65 years, there is a three- to fourfold decline in the synthetic capacity of the skin to produce vitamin D3. Excessive exposure to sunlight cannot cause vitamin D3 intoxication because once previta-min D3 and vitamin D3 are made in the skin, excessive quantities are rapidly destroyed by sunlight (Figure 3).
There is compelling evidence from epidemiological, clinical and scientific studies of a link between vitamin D and blood pressure in adults. There is an inverse relationship between blood pressure and UV B exposure. Data from the INTERSALT study indicated a positive association between the prevalence of hypertension and distance north or south of the equator.56 There is also seasonal variation in blood pressure, with higher blood pressures reported in winter and lower blood pressures in summer, corresponding with changes in UV B levels.27'56'57 Skin pigmentation influences the efficiency of producing vitamin D, as melanin is capable of absorbing UV B photons and thus reducing the amount available for converting 7-dehydroc-holesterol to previtamin D3. Dark skinned individuals require between 10 to 50 times the exposure to sunlight than white skinned individuals to produce similar amounts of 25 (OH Dj 1 Thus, it is not surprising that dark skinned individuals living at greater latitudes...
Several theories have been proposed to explain the functional inhibition and melanocyte destruction in vitiligo the autocytotoxic hypothesis, the neural hypothesis and the autoimmune hypothesis. In the autocytotoxic hypothesis, toxic melanin intermediates are produced in excess or imbalance, causing autocytotoxicity. The neural hypothesis is based on a proposed adrenergic cholinergic imbalance in some vitiligo patients, and was promoted as a cause for segmental vitiligo. Schallreuter and Wood have proposed a variant of this hypothesis, that vitiligo is a disease of the entire epidermis in which heightened adrenergic responses lead to biochemical imbalances which inhibit melanization, but do not necessarily destroy melanocytes. They have demonstrated a number of biochemical abnormalities which induce decreases in antioxidant defenses and increases in tetrahydrobiopterin, which are proposed to inhibit melanization or to bleach melanin. The autoimmune hypothesis is based on the...
The characteristic appearance of the vulva is white, atrophic, and finely wrinkled. Ulcerations, blisters, excoriations, and inflammation are seen over the vulva, perineum, and perianal area, often giving rise to the terms hourglass or figure-eight to describe the pattern of skin involvement. Secondary infection is possible. Progression of the disease leads to distortion, thickening, and scarring of vulvar and perineal architecture. The condition is differentiated from vitiligo by absence of inflammation or atrophy in the latter. The diagnosis of lichen sclerosis atrophica is made on clinical grounds and may be confirmed histologically from biopsy specimen in atypical cases.
Measurements of height and weight, signs of other illnesses, and evidence of cachexia should be assessed. The skin, breasts, and genital tissues should be evaluated for estrogen deficiency. The breasts should be palpated, including an attempt to express galactorrhea. The skin should be examined for hirsutism, acne, striae, acanthosis nigricans, vitiligo, thickness or thinness, and easy bruisability.
Cobalamin deficiency is suspected in individuals who display the typical manifestations of deficiency of the vitamin as described in the section above on the effects of deficiency. In addition to the symptoms that may be experienced by individuals that are related to anemia (easy fatigue, shortness of breath, palpitations) and neuropathy (sensory and motor disturbances and memory loss) there are features that may be detected by a physician, including skin pallor (from anemia), abnormalities in neurological examination (sensory loss, abnormal balance and reflexes, mental changes), and epithelial changes (skin pigmentation, smooth tongue). On the basis of any combination of such changes, cobalamin
Clinically the patient presents with truncal obesity, moon face, hypertension, diabetes, abdominal striae, acne and a buffalo hump, and experiences profound weakness. Pituitary ACTH-producing tumours tend also to produce skin pigmentation as ACTH has a similar molecular structure to melanocyte-stimulating hormone (MSH). Because patients have a tendency to bruise easily with delicate skin which is easily damaged, and have an increased risk of infection, post-operative problems are increased.
This disorder is much less common than myasthenia gravis. It is characterized by proximal muscle weakness, depressed tendon reflexes, post-tetanic potentiation and autonomic changes, including dry mouth and constipation. Onset can be in adolescence, but is usually after 40 years of age. Other autoimmune diseases may associate, notably thyroid disease and vitiligo, and other autoantibodies occur at increased frequency.
Cutaneous manifestations of Addison's disease include increased brownish pigmentation over exposed body areas such as the face, neck, arms, and dorsum of the hands, and over friction or pressure points such as the elbows, knees, fingers, toes, and nipples. Pigmentation of mucous membranes, darkening of nevi and hair, and longitudinal pigmented bands in the nails may be seen. Vitiligo, mucocutaneous candidiasis, and alopecia may occur with Addison's disease that has an autoimmune cause. Women with Addison's disease may exhibit decreased growth of axillary and pubic hair because of adrenal androgen deficiency. This is not seen in men because of adequate testicular androgen.
PSGs can play an important role in educating patients about ways in which they can become involved in clinical research. The National Eczema Society recognised this and encouraged its members and other dermatology patient groups to volunteer to join the Cochrane Skin Group (see Chapter 4) as consumer representatives. Under the auspices of an umbrella organisation of UK skin support groups called the Skin Care Campaign (formerly a project of the National Eczema Society), a meeting was held to inform consumers about the Cochrane Collaboration and how they as consumers could contribute to its work. Some consumers subsequently contributed by hand-searching journals, commenting on protocols and reviews, translating reviews and co-authoring a review (on vitiligo). From this meeting, a focus group was set up to help identify suitable questions for eczema research.
Other factors which may influence the size of the reaction include age (skin test weals increase from infancy to adulthood and then often decline after the age of 50), race (dark skin pigmentation elicits a greater weal response from histamine), season, pathological conditions, and drugs.
Consumer involvement has been a strong feature of the CSG from the very beginning. This is because skin disease greatly affects the quality of life of the individual and because much of the trial work in skin disease has been dominated by answering questions that are important to the pharmaceutical industry. Consumers help us to redress that imbalance. At present (Autumn 2002) the skin group has 55 groups working on topics, both common and rare, such as acne, alopecia, bullous pemphigoid, eczema, excessive sweating, psoriasis, skin cancer and vitiligo. About 30 active consumers are involved at many levels. Initially they were recruited mainly through the National Eczema Society and the Vitiligo Society, but since we decided to always include a relevant consumer in the peer-review process, more consumers have become involved in this way. Increasingly consumers also take part in writing the review two of the reviews in preparation have a consumer as lead author.
All the above roles are relevant to dermatology, but not special to it. What distinguishes skin disease from other kinds of illnesses is that it is much more visible to the world. This means that its social effects are often far greater than for other illnesses of comparable seriousness, and that the patient's self-image is often harmed. Healthy people, including many health professionals, do not sufficiently understand these aspects, and do not cope adequately with them. Consumers and patients can help them understand and learn what matters to people with various skin conditions. In the case of vitiligo, for example, doctors sometimes base treatment decisions on how they perceive the degree of distress. Many think that white patients suffer less than those with darker skins, but studies as well as anecdotal experience have shown that this may not be true.1 Nor is the extent of the disease always the most important factor in the patient's suffering. Self-esteem, self-image, the site...
In 1965, DiGeorge described a child without a thymus or parathyroid glands due to congenital malformation of the third and fourth pharyngeal pouch. Most patients have microdeletions at chromosome 22qll, or less frequently at 10pl3, where there are probably genes which control the development of the neural crest, from which cells migrate to the pharan-gea) pouches. The disorder is familial in a few cases and the prevalence is about 5 per 100 000 children. A spectrum of severity has been recognized, with some children lacking all thymic and parathyroid tissue, sometimes with additional abnormalities in midline structures such as the lips, palate, heart and major thoracic vessels, while others retain some thymic tissue and have mild symptoms. In the severe type, there is a virtual absence of circulating T lymphocytes, sometimes with a relative expansion of B cells. These patients are capable of making antibodies after immunization, although it is unclear whether the quality or quantity...
In addition to making antibodies, most people will also demonstrate delayed hypersensitivity to Candida antigens when subjected to skin testing with extracts of this organism. As described above, patients with defects in cell-mediated immunity are at higher risk for superficial Candida infections. This finding is especially apparent in conditions such as AIDS and in the condition known as chronic mucocutaneous candidiasis. AIDS patients are commonly afflicted with recurrent oral Candida infections. Patients with chronic mucocutaneous candidiasis have long-lasting and often disfiguring superficial candidiasis without obvious predisposing causes. Endocrinopathies, thymomas, vitiligo, alopecia, and a tendency to develop other types of infections are found in some of these patients. A variety of immunologic abnormalities have been described in this condition, but of these, defective cell-mediated immunity to Candida antigens, as manifested by negative delayed hypersensitivity skin tests...
Racial variation in reaction to physical stigma a study of degree of disturbance by vitiligo among black and white patients. J Health Soc Behav 1991 32 192-204. 3. Papadopoulos L, Bor R, Legg C. Coping with the disfiguring effects of vitiligo a preliminary investigation into the effects of cognitive-behavioural therapy. Br J Med Psychol 1999 72 385-96. 4. Picardi A, Abeni D. Can cognitive behavioral therapy help patients with vitiligo Arch Dermatol 2001 137 786-8. 5. Lesage M. Vitiligo understanding the loss of skin colour. London The Vitiligo Society, 2002.
This is a rare multisystem disorder due to infection by an organism called Tropheryma whippelii that invariably affects the small bowel and may also be associated with skin pigmentation, arthralgias, endocarditis, and other heart problems and central nervous system abnormalities. In the small bowel, it causes malabsorption with diarrhea, steatorrhea, abdominal pain, distension, and weight loss. It is diagnosed by the presence of periodic acid-Schiff-positive granules in macrophages.
When both alleles for a particular trait are identical, the organism is said to be homozygous for that trait. When the alleles differ, the organism is heterozygous. The presence of two different alleles raises the question of whether one or the other, or both, will determine the phenotype of the organism. For his experiments on peas, Mendel chose traits for which one allele of each pair had a decisive effect, completely determining the phenotype even in the presence of the other allele. He called the determining allele dominant and the other allele recessive. Only when the organism is homozygous for the recessive allele does the phenotype show the recessive trait. For instance, the albino skin pigmentation allele is recessive to other pigmentation alternatives.
Vitamin D is a potent steroid hormone with a wide distribution of receptors suggesting diverse physiological roles.1'2 Despite its name, relatively little vitamin D comes from dietary sources (apart from fortified foods or supplements). In healthy people of normal mobility under most climatic conditions, the majority of their vitamin D requirements are produced through the sunlight-mediated (via ultraviolet, UV B) photochemical conversion of 7-dehy-drocholesterol in the skin to cholecalciferol (vitamin D3).3 The rate of this conversion is reduced by increased skin pigmentation, by covering up when outdoors or by staying indoors.3 5 Cholecalciferol is hydroxylated in the liver to 25-hydroxycholecalciferol (25(OH)D3) by the enzyme 25-hydroxylase. In turn, 25(OH)D3 is hydroxylated (principally though not exclusively in the kidney) to many metabolites (Fig. 1). The main ones are the biologically active metabolite 1,25-dihydroxyvitamin D (l,25(OH)2D3), via the enzyme 1-a-hydroxylase, and...
It is important to be aware that these autoimmune endocrinopathies have a long prodromal phase and may remain subclinical throughout a patient's life the presence of appropriate antibodies in such patients may be a marker for future endocrine dysfunction and for the presence of a more extensive autoimmune process than can be appreciated clinically. In particular, occult pernicious anemia atrophic gastritis may be more frequent than generally appreciated, as revealed by biopsy or achlorhydria after pentagastrin stimulation. Patients with pernicious anemia are especially prone to develop vitiligo.
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