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#1
16.04.2009, 18:40
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Зуд: возможные анализы для установления причин
Здравствуйте!
Уже очень долгое время мучает зуд в районе между большими и малыми половыми губами. По ощущениям начался после того, как я сменила мыло для интимной гигиены, сразу прекратила, но зуд не прошёл. Очень конкретно локализирован, сверху по линии роста волос и затем только по одной стороне. Внешне ничего не заметно, по крайней мере врачи так говорят. Я указала врачу, что в некоторых местах чувствую подкожные шарики, небольшие, мне сказали, что это особенности кожи, то есть нормально. Не так давно заметила на поверхности между половыми губами (обычно безволосой) несколько волосков, что мне кажется очень странным. Несколько раз была у врача, по результатам анализов и мазка никаких инфекций не выявлено. Разные врачи рекомендовали последовательно: Gyno-Daktarin, затем betnelam-v, так как подозревал, что возможно это экзематозное, другой - ещё раз лекарство от грибка (одна таблетка мне и мужу, хотя признаков грибка не было), затем просто специальное успокаивающий крем от раздражения и зуда Saforelle. Совершенно ничего не помогло. Просыпаюсь по ночам от зуда (днём почти не беспокоит). Зависимости между стрессовыми и спокойными периодами не наблюдаю и думаю, что должна быть объективная причина. Бельё ношу только хлопковое, никакими средствами для интимной гигиены уже давно не пользуюсь, других возможных раздражителей нет. Я хотела бы узнать какие можно количественно-качественные анализы ещё сделать, чтобы установить возможную причину. Допытывалась у врача, говорит, что уже всё проверили и что следующий шаг - только биопсия кожи, но довольно серьёзное вмешательство. Заранее благодарна за советы. Ольга 
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#2
17.04.2009, 16:40
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- как одна из причин возможного зуда железодефицит-необходимо сдать железо сыворотки, ОЖСС, ферритин
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#3
24.04.2009, 17:07
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Спасибо большое за реакцию. А желозодефицит может как-то ощущаться? Я сдавала железо, но давновато, сказал врач - не критично, в норме, но ближе к нижней границе. Я не вегетарианка.
Я постараюсь, в ближайшее время сдать ещё раз. Проблема с зудом меня мучает уже очень давно - года два, была за это время раз 5 у врачей (у трёх разных). Лекарства предлагают и пожимают плечами. Я уже думаю, что зуд может быть причиной чего-то серьёзного, намекала на рак врачу, он странно посмотрел, но сказал, что было бы заметно снаружи и заговорил, что возможно сделать биопсию.. Хм.. Всё равно спасибо за совет.
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#5
26.04.2009, 15:44
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Цитата:
Цитата:
- это только звучит грозно. на самом деле, у вас с применением местного обезболивания возьмут маленький кусок кожи (скорее всего, не более 3-4 мм в диаметре) и посмотрят его под микроскопом. никаких последствий после нее быть не должно. рубец будет настолько маленьким, что вы его не будете видеть без лупы.
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#6
26.04.2009, 15:45
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Dermatitis of the vulva
INTRODUCTION — Vulvar dermatitis (also called vulvar eczema) is the most common vulvar dermatosis in women. One-third to one-half of women's vulvar complaints stem from this problem [1-3]. It can develop in isolation or may occur as part of dermatitis in other areas of the body. Women with vulvar dermatitis experience chronic irritation and/or pruritus, which causes them to persistently rub and scratch the vulva. These activities lead to histological changes in the dermis, termed squamous hyperplasia or lichen simplex chronicus. ENDOGENOUS VERSUS EXOGENOUS DERMATITIS — The two types of vulvar dermatitis are endogenous and exogenous. Endogenous vulvar dermatitis is the term used to describe atopic dermatitis of the vulva. Atopic dermatitis has a familial predisposition, often begins in childhood, and is characterized by pruritus. Although some experts feel that vulvar involvement is unusual, even when there is severe and widespread atopic dermatitis elsewhere (show picture 1), others believe it is more prevalent than previously acknowledged [4,5]. In women with atopic dermatitis at nongenital periorificial sites, the occurrence of erythema in the labial folds, the perianal region, and in the skin between the buttocks probably represents endogenous vulvar dermatitis. (See "Epidemiology, clinical manifestations, and diagnosis of atopic dermatitis (eczema)"). Exogenous vulvar dermatitis results from external factors, and is also called contact dermatitis (show picture 2 and show picture 3). In allergic contact dermatitis (20 percent of cases), the trigger (allergen) induces an immune response, while in irritant contact dermatitis (80 percent of cases), the trigger (irritant) itself directly damages the skin. Although exposure to irritants may have been the initial cause of the dermatitis, secondary sensitization to allergens can also occur. The most common agents that cause irritant or allergic contact dermatitis of the vulva are listed in the table (show table 1). Active and inert constituents of topical medications are a very common etiology of allergic dermatitis of the vulva in women with persistent vulvar symptoms [6]. Sensitivity to latex or proteins in seminal plasma are infrequent etiologies [7]. (See "Overview of dermatitis", section on Contact dermatitis). PATHOPHYSIOLOGY — Vulvar tissue is more permeable than exposed skin due to differences in structure, occlusion, hydration, and susceptibility to friction [8]. The vulvar skin is particularly vulnerable to irritants. Compared with other body regions, the stratum corneum overlying the vulva appears to function less efficiently as a barrier, thereby permitting increased susceptibility to irritants [9]. As an example, benzalkonium chloride and maleic acid induce a greater response after application to normal vulvar skin than when applied to the skin of the forearm [10]. The vulvar skin is also sensitive to allergens. New exposure to an allergen is most likely to induce a reaction, although patients may also react to products that they have used for months or years. In contrast to the immediate response to irritants, an allergic reaction takes from 12 to 72 hours to develop, is usually pruritic, and often lasts for several weeks. In acute cases, an exposure occurring up to two weeks prior to the dermatitis can often be identified. In chronic cases, the dermatitis may have been present for months or years; identifying the offending trigger in these patients can be difficult. Self-medication and persistent rubbing and scratching because of pruritus, and excessive washing of the vulva by women fearful of a lack of cleanliness often aggravate the dermatitis. CLINICAL MANIFESTATIONS AND DIAGNOSIS — The most common symptom of vulvar dermatitis is pruritus, which can be intense and nocturnal. Other symptoms include burning, rawness, or stinging. The diagnosis is clinical, based upon a history of chronic vulvar irritation and/or pruritus causing persistent rubbing and scratching. History — Women with vulvar complaints should be questioned regarding a personal or family history of atopy, asthma, rhinitis, conjunctivitis, or hives. The presence of symptoms indicating skin involvement elsewhere on the body or chronic pruritus should be ascertained. Specific areas to address in the history include: What are her major complaints? Pruritus can vary from mild to intolerable, sometimes interfering with sleep or other activities. When the dermatitis involves mucosal areas, burning, rawness, and stinging are more common than pruritus and the symptoms are often exacerbated during menstruation and with coitus. What are her hygienic practices (eg, daily use of panty liners, feminine products, baby wipes)? Women often erroneously regard their personal practices as safe since they have engaged in them for a long time. Does she wear occlusive clothing, such as tight lycra garments, or confining undergarments, such as non-cotton underwear or thongs? These types of garments trap sweat, promote Candidiasis, and chafe the skin. Does she apply any medications (antifungal drugs) or other agents (eg, contraceptives, perfumed or deodorant soaps) to the vulva? Women seldom reveal this information unless asked directly. Patients with vulvar dermatitis have often been treated with multiple antifungal agents without success. A report that these creams never helped their symptoms is significant information, indicating that Candida is probably not the source of the complaints. The answers to these questions help to differentiate an endogenous process (eg, atopy) from that induced by an exogenous agent. Conscientious analysis of the woman's personal practices is the best way to detect potential irritants and allergens in her environment, as well as habits unhealthy for the vulvar skin. In a study of 530 women attending a specialty clinic for vulvar diseases, over 60 percent of patients described adverse personal hygiene and/or self-treatment practices when specifically questioned [11]. Physical examination Acute vulvar dermatitis — In acute cases, the skin displays mild to severe erythema of varying extent with some scaling in dry areas. Fissures may be present along the labial folds. Excoriations from scratching are common and can be complicated by secondary infection with yeast or bacteria (eg, Staphylococcus aureus, Streptococcus pyogenes, or Escherichia coli). Although crusts and scales are commonly observed with dermatitis elsewhere on the body, these signs are often not present in the moist areas of the vulva. Chronic vulvar dermatitis — In chronic cases, the vulvar mucosa is erythematous and may display papillae, a sign of chronic inflammation. Papillomatosis is not a cause of vulvar pain. The origin of vulvar papillomatosis is uncertain; the papillae can be normal anatomical variants of the vestibular mucosa or a postinflammatory change (show picture 4) [12,13]. In response to the epithelial disruption and persistent irritation, the patient chronically rubs her skin, which thickens in a way that enhances the appearance of the normal crosshatch markings [14,15]. Ultimately, the vulva become hypopigmented or hyperpigmented, and may show hyperkeratosis (hypertrophy of the epidermis). Labial skin folds appear greatly exaggerated, often edematous, and pubic hair can be broken or sparse [6,14]. The resulting appearance is typical of lichenification and is called lichen simplex chronicus (squamous cell hyperplasia), the end-stage reactive process occurring in response to chronic irritation and scratching from any cause (show picture 5) [16]. Lichen simplex chronicus is diagnosed when anatomic and clinical findings have excluded specific causes of hyperplastic epithelial changes, such as lichen sclerosus and lichen planus (show picture 6 and show picture 7), psoriasis, seborrheic dermatosis, human papillomavirus infection, and Candida infection. The histology of lichen simplex chronicus (squamous cell hyperplasia) consists of elongation, widening of the rete ridges and irregular thickening of the Malpighian layer of rete ridges (acanthosis), hyperkeratosis, and parakeratosis with a mid-dermal inflammatory infiltrate [17]. Vaginal discharge is usually unremarkable in women with vulvar dermatitis. Patch test — Patch testing may be required to distinguish between atopic and contact dermatitis; biopsy is not helpful. Patch testing is also useful to determine the cause of contact dermatitis. The recommended patch test series are the standard series, a panel of common medications, the patient's own topical medications, popular remedies, and other suspected products [18]. Positive patch tests for relevant substances occur in 25 to 60 percent of women with vulvar pruritus [6,19-22]. Skin prick tests are an alternative. (See "Overview of dermatitis"). Biopsy — A biopsy should be performed when the diagnosis cannot be determined after visual inspection and culture. Lichen sclerosus, lichen planus, psoriasis, and most primary diseases of the vulva (eg, vulvar intraepithelial neoplasia) display distinct histologic features that establish these diagnoses. Differential diagnosis — Dermatoses, infection, and primary diseases of the vulva are all sources of vulvar complaints (show table 2). Vulvar lesions are discussed in detail separately. (See "Diagnostic evaluation of vulvar lesions" and see "Differential diagnosis of vulvar lesions").
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#7
26.04.2009, 15:47
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Dermatoses
Seborrheic dermatitis results from chronic inflammation in areas of the body that are rich in sebaceous glands (show picture 8), such as the scalp, face, axilla, groin, and upper trunk; involvement of the vulva is uncommon. The etiology is not known. The lesions are pink-orange, have scales, are poorly defined, and can be secondarily infected. (See "Overview of dermatitis", section on Seborrheic dermatitis). Psoriasis appears as bright red, sharply demarcated lesions that are raised above the surrounding normal skin (show picture 9 and show picture 9A). Silver scales, commonly observed in psoriasis, may be seen on the mons, but are not found elsewhere on the vulva. (See "Epidemiology, clinical manifestations, and diagnosis of psoriasis"). Lichen planus — The classical papulosquamous form of lichen planus appears as shiny, purple papules, often in multiple sites on the body, especially flexor surfaces (show picture 7). White striae sometimes occur on the inner aspects of the vulva and typical papules are seen on keratinized anogenital skin. (See "Vulvar lichen planus"). Mucosal lichen planus may appear white, inflamed, or erosive. Erosive lesions are the most common type occurring in the inner aspects of the vulva and vagina. (See "Drug eruptions", section on Drug-induced lichen planus). Vulvo-vaginal-gingival syndrome is a variant of this disease that can affect the vagina, vulva, and oral cavity either concurrently or individually [23]. Vulvar lesions are painful, glassy erosions, while those in the vagina are erythematous and friable. Synechiae can develop in the vagina, which may become obliterated with severe disease. (See "Vulvar lichen planus", section on Vulvo-vaginal-gingival syndrome). Lichen sclerosus — Lichen sclerosus is a chronic inflammatory mucocutaneous disease of the vulva that occurs in women of all ages. Intense pruritus is the predominant symptom, although women can be totally asymptomatic even in the presence of active disease. Lichen sclerosus is characterized by "parchment-like" or "cigarette paper" skin, although thickened, hyperplastic or lichenified areas are not uncommon. Untreated disease leads to loss of the normal architecture of the external genitalia and constriction of the vaginal orifice (show picture 10). Fissures and telangiectasia are common. The clinical diagnosis can be confirmed by histological examination of biopsy specimens. (See "Vulvar lichen sclerosus"). Infection — Candida vulvovaginitis causes irritation and pruritus of the vulva, and should be excluded. (See "Candida vulvovaginitis"). Testing for herpes simplex virus is recommended when recurrent ulcerations are noted, as these may be a sign of genital herpes. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection"). If there is a malodorous vulvar exudate, bacterial cultures of the vulva should be performed to aid in diagnosis of secondary bacterial infection. However, bacterial cultures of the vagina are not recommended, as the results are usually nonspecific. Vulvodynia — Vulvodynia refers to vulvar discomfort usually described as burning pain; pruritus is uncommon. Nevertheless, persistent pruritus and erythema with a negative yeast culture, nonspecific vulvar biopsy, and failure to respond to standard treatment raises the possibility of vulvodynia. Vulvodynia is a diagnosis of exclusion after specific, relevant infectious, inflammatory, neoplastic, and neurologic disorder have been ruled out. (See "Clinical manifestations and diagnosis of generalized vulvodynia"). MANAGEMENT — The treatment of vulvar dermatitis requires a two-pronged approach: behavioral modification and medication. An explanation of the condition, emphasizing the need for long-term treatment with maintenance regimens, and vigilance to prevent and diagnose recurrent yeast infections are important factors for success. Therapy that fails to interrupt the itch-scratch cycle will not lead to consistent, prolonged clinical improvement. In the absence of data from large, randomized trials, we suggest the following regimen based on our clinical experience and results from small and observational studies: Diagnosis and treatment of coexistent infection — Diagnosis of coexistent infections is essential. Candidiasis should be excluded in all patients by yeast culture on Sabaraud's medium, if the organism is not present on wet mount with 10 percent potassium hydroxide (which is only 50 percent sensitive). (See "Candida vulvovaginitis", section on Diagnosis). Candidiasis may be present without the usual vaginal symptoms when the yeast infects the skin, and may be the cause of recurrent vulvar fissures. Candidiasis should be treated with fluconazole; oral therapy is recommended because women with infection superimposed on vulvar dermatitis are at increased risk for worsening dermatitis from the irritant effects of topical drugs [24]. If the candida is not felt to be part of an ongoing chronic infection, fluconazole 150 mg can be given as a one time dose and then repeated in three to seven days. However, recurrent or more complicated involvement with candida may require long-term suppression. Nonalbicans yeast will not usually respond to fluconazole, and will require alternative treatment. (See "Candida vulvovaginitis", section on Complicated infections). If a vulvar exudate is present, a vulvar bacterial culture is obtained. Heavy growth of Staphylococcus or Streptococcus should be treated [25]. We use cephalexin (500 mg orally three times per day) or cefadroxil (500 mg orally twice daily) for five to seven days, if appropriate by sensitivity testing. For women allergic to penicillin, we prescribe azithromycin (250 mg as a single oral dose daily for six days). Vaginal bacterial cultures are not generally useful because many types of bacteria normally colonize the vagina. If herpes simplex virus is detected, appropriate suppressive therapy can be considered. (See "Treatment of genital herpes simplex virus infection"). Attention to personal habits and hygiene If the patient has clothing and/or hygiene habits that facilitate dermatitis, these habits must be modified. Elements of healthy vulvar hygiene are listed in the table (show table 3). Known or suspected allergens and irritants in the environment should be eliminated. Therapy General measures — Soaking in warm water, without additives, relieves vulvar discomfort and pruritus by restoring a more physiologic environment to the sensory nerve endings [15]. Immersion for 10 minutes in the morning and at night prior to applying a topical corticosteroid hydrates the skin and allows better absorption of the medication (see below). A sedating antihistamine such as hydroxyzine given in low dosages (10 to 30 mg at 7:00 pm) helps to control nighttime itching and scratching. Nonsedating antihistamines are of little benefit for vulvar pruritus. Mild symptoms — Mild symptoms usually respond to low to medium potency topical corticosteroid ointments (eg, hydrocortisone 1 or 2.5 percent or triamcinolone 0.1 percent daily for two to four weeks, then twice per week). Topical corticosteroid can be used one or more times daily, although a clear benefit has not been demonstrated with more than once daily application [26-28]. Therapy is continued indefinitely, at the minimum frequency necessary to control pruritus. Moderate to severe symptoms — For moderate to severe symptoms, a higher potency corticosteroid ointment is often required (show table 3A-3B). We use clobetasol propionate or betamethasone dipropionate ointment (0.05 percent at night daily for 30 days), and then reevaluate. Another acceptable regimen is to give one of these steroids twice daily for two weeks, then daily for two weeks, then Monday and Wednesday and Friday for two weeks, and then reevaluate. If there is a partial response, we either continue corticosteroids for another two weeks or else switch to intralesional injections or calcineurin inhibitors. Potent topical steroids have been used for up to twelve weeks on the vulva without adverse effects [29,30]. Recalcitrant cases — An intralesional injection of triamcinolone acetonide 3.3 to 10 mg/mL may be tried in resistant cases; a total of 1 to 2 mL is given by injecting small amounts to include the entire lesion or plaque; this can be repeated monthly up to three times. Prior application of a small amount of a topical anesthetic, such as EMLA, facilitates injection. Recalcitrant cases have also been treated with the calcineurin inhibitors tacrolimus 0.03 percent ointment or pimecrolimus 1 percent cream, which suppress cellular immunity (inhibit T-lymphocyte activation) [31,32]. The ointment or cream is applied sparingly twice daily for 14 to 30 days, followed by maintenance therapy twice per week. Intermittent prolonged treatment may be necessary because the dermatitis recurs upon discontinuation in 35 to 54 percent of patients. Some patients cannot tolerate tacrolimus because of burning or stinging. These side effects may be minimized by applying a film of petroleum jelly before applying the ointment. The US Food and Drug Administration (FDA) has issued a public health advisory regarding a potential cancer risk (lymphoma, skin cancer) from use of topical calcineurin inhibitors [33]. This concern was based on information from animal studies, case reports in a small number of patients, and knowledge of how drugs in this class work. Given the uncertainty, the FDA advises that these drugs be used only as labeled, and for patients in whom other prescription treatments have failed to work or cannot be tolerated.
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#8
26.04.2009, 15:48
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Another option for severe cases is the use of intramuscular triamcinolone since direct application of a topical glucocorticoid might cause burning or irritation: 1 mg/kg can be given intramuscularly monthly for three months. Petroleum gel can be applied daily for two weeks after the first injection, and then a superpotent topical glucocorticoid can be started. We have found this to cause fewer side effects than a short course of oral prednisone to treat a flare. This should not be used in women with diabetes, and with caution in patients with severe mental health concerns.
SUMMARY AND RECOMMENDATIONS Endogenous vulvar dermatitis is an atopic disorder. Exogenous vulvar dermatitis is a type of contact dermatitis caused by an irritant or allergen. (See "Endogenous versus exogenous dermatitis" above). The most common symptom of vulvar dermatitis is pruritus, which can be intense and nocturnal. Other symptoms include burning, rawness, or stinging. Physical signs depend upon the chronicity of disease and include erythema, papillae, and lichenification. (See "Clinical manifestations and diagnosis" above). Self-medication and persistent rubbing and scratching because of irritation/pruritus, and excessive washing of the vulva by women fearful of a lack of cleanliness often aggravate the dermatitis. (See "Pathophysiology" above). The diagnosis can usually be made clinically, based upon characteristic symptoms and a family history of atopy or personal history of vulvar exposure to medications, perfumes, or other chemicals. Infection should be excluded by vulvar cultures for candidiasis, herpes simplex virus (if fissures or ulcers are noted), and potential bacteria pathogens (if there is a vulvar exudate). In uncertain cases and those not responding to treatment (see below), patch testing and/or biopsy may be necessary to identify the allergen/irritant or an underlying dermatoses. (See "Clinical manifestations and diagnosis" above).
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#9
27.04.2009, 13:45
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Цитата:
- да при локальном зуде это справедливо Цитата:
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#10
27.04.2009, 14:50
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Спасибо большое за ответы. Я бегло просмотрела информацию на английском, прочитаю всё подробно.
Описание абсолютно точное: "The most common symptom of vulvar dermatitis is pruritus, which can be intense and nocturnal. Other symptoms include burning, rawness, or stinging. Self-medication and persistent rubbing and scratching because of irritation/pruritus, and excessive washing of the vulva by women fearful of a lack of cleanliness often aggravate the dermatitis". Я вообще-то склонна к экземам, ставили диагнозы как нейро дермит и экзэма, но сейчас никаких признаков нет. Крем betnelan-v (глюкокортироидный) мне раньше очень быстро помог, когда были экзэмные проявления на руках. Рецидивов уже давно не было. В этом же случае никаких положительных результатов не было, я применяла крем около 2х недель. Правильно ли я поняла, что можно лекарство от дерматита применять внутримышечно и в таком случае эффект лучше? Постараюсь узнать у врача. Спасибо также, что про биопсию пояснили, думаю, нужно делать её. Посмотрим, что покажет.
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#11
28.04.2009, 18:44
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Цитата:
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Линейный вид
