Juliana Chan, PharmD, FCCP, BCACP

• Clinical Associate Professor, Colleges of Pharmacy and Medicine, University of Illinois at Chicago
• Clinical Pharmacist�Gastroenterology/Hepatology, Illinois Department of Corrections Hepatology Telemedicine, Sections of Hepatology, Digestive Diseases and Nutrition, Chicago, Illinois

https://pharmacy.uic.edu/profiles/jchan/

Pathophysiology Predisposing factors the risk of frostbite increases with alcohol use and smoking [1] gastritis diet 500 ditropan 2.5 mg low cost. Investigations Technetium99 bone scintigraphy may be helpful in evaluating outcome in frostbite injury and indicating the level of amputation needed in severe cases [8] gastritis newborn order ditropan online from canada. Magnetic resonance angiography may also be beneficial gastritis and dyspepsia 2.5mg ditropan free shipping, with the ability to visualize directly any vascular occlusion gastritis diet ������ discount ditropan, and simultaneously image the surrounding soft tissues gastritis diet 4 you order ditropan without a prescription. Pathology Freezeinduced damage results largely from the formation of ice in both the intracellular and extracellular compartments [2] gastritis diet zantrex ditropan 5 mg on-line. Fast freezing tends to produce intracellular ice, while slow freezing causes the formation of extracellular ice. Ice crystals not only injure cellular architecture but also disturb the flux of electrolytes and water across cell membranes [3]. Slow rewarming causes the formation of larger, more destructive ice crystals and the development of greater osmotic stresses. As well as the direct effects on Management First line It is important that immediate warming techniques are instituted. Debridement surgery should be delayed until the full extent of the recovery/persisting damage is clear. As the water will cool rapidly, it will need to be topped up to maintain the temperature, and circulated around the limb. Rapid rewarming has been shown to be more effective than slow rewarming and the tissue can be considered completely rewarmed when it takes on a red/purple appearance and is soft and pliable to the touch. The area should be air dried or patted dry to avoid shearing forces damaging tissue [9]. The Wilderness Medicine Society recommends their use at 12 mg/kg body weight twice daily in order to reduce levels of prostaglandins and thromboxanes that may contribute to vasoconstriction, ischaemia and tissue damage. Topical aloe vera gel has been suggested on the basis that it may also reduce inflammatory prostaglandins; however there is a lack of strong clinical evidence or animal studies to confirm efficacy. It is recommended that nonhaemorrhagic blisters should be aspirated as the blister fluid may also contain prostaglandins and thromboxanes. Trench foot h Definition and nomenclature Trench foot describes a combination of stasis, nonfreezing cold injury and wet conditions leading to numbness and skin changes on the distal legs and feet. Trench foot was a common problem suffered by soldiers in the early years of trench warfare in the First World War [1] but is now mostly encountered among the homeless population [2]. A similar entity, tropical immersion foot, is a warm water immersion injury and is less severe. Pathophysiology Predisposing factors Smoking and peripheral vascular disease probably contribute to the severity of the tissue damage. Pathology the pathological changes are those of dependent oedema and lymphovenous stasis. Perivascular inflammation occurs and in severe cases arterial occlusion and ischaemic necrosis. Second line In the hospital setting, other pharmacological interventions can be beneficial. In this study, the incidence of amputation reduced from 41% (untreated) to 10% in those treated within 24 h of injury. Clinical features Affected individuals develop numbness of the feet and distal legs accompanied by skin changes caused by nonfreezing cold injury. This is compounded by wet conditions and aggravated by leg dependency, immobility and constrictive footwear. There is erythema, oedema, tenderness and, in severe cases, areas of superficial gangrene. Differential diagnosis Other causes of limb ulceration should be considered, such as diabetes, arterial and venous insufficiency, autoimmune disease, inflammatory disease such as pyoderma gangrenosum and infections. Third line Surgical removal of gangrenous tissue should be delayed until there is a distinct demarcation between viable and nonviable tissue, a process that usually takes several weeks. Prognosis Initially the ability to sweat is lost but with time there is hyperhidrosis, cold sensitivity and vasomotor instability. Usually there is a clear history of cold water immersions and no specific investigations are required. Conservative excision of necrotic tissue may be necessary and antibiotics should be given if there is evidence of infection. Perniosis o Definition and nomenclature Perniosis describes localized inflammatory lesions on the acral skin, which occur as an abnormal reaction to cold in susceptible individuals [1]. Inflammation occurring in the deeper dermis and subcutis may be explained by the combined effects of external cooling together with insulation from internal warming [7]. Genetics There may be a genetic influence in perniosis since several generations within a family can be affected [1]. Environmental factors Perniosis occurs in susceptible individuals during the autumn or winter in a climate that is both cold and damp. Clinical features Introduction and general description Perniosis lesions are cold induced and affect areas of the skin vulnerable to cold exposure, such as the digits, nose and ears. Perniosis develops symmetrically on the acral skin, in particular the fingers and toes, but other body extremities may also be involved including the heels, lower legs, nose and ears. Erythrocyanotic papules, located on the fingers and toes, develop in cold weather and tend to persist, in some cases becoming ulcerated [9]. Perniosis may also complicate haematological malignancy, typically myelodysplastic syndrome and chronic myelomonocytic leukaemia (see Chapter 148). Cyanotic swelling of acral digital skin, particularly the toes, has been reported in these patients [11]. The onset of perniosis may coincide with a blast crisis, which can be demonstrated on skin biopsy by the presence of large, atypical mononuclear cells in the perivascular infiltrate [12]. Pathophysiology In perniosis there is a persistent coldinduced vasoconstriction of the deep cutaneous arterioles with concomitant dilatation of the smaller, superficial vessels. This is in contrast with normal subjects, in whom cold exposure induces cutaneous vasoconstriction succeeded by vasodilatation, a homeostatic mechanism necessary for the maintenance of reperfusion. Investigation of the cutaneous nerves in patients with perniosis demonstrated no quantitative or qualitative difference in immunoreactivity for substance P, neuropeptide Y, calcitonin generelated peptide or vasoactive intestinal peptide compared with controls [6]. However, in the affected skin of patients with acral perniosis, who also had a past history of very low body weight, immunohistochemistry revealed a great increase in nerve bundles in the papillary dermis, some with an abnormal morphology [6]. This indicates that in uncomplicated perniosis the neuronal supply to the microvasculature is normal and suggests that the pathology involves the microvessels themselves. In papular perniosis, crops of small chilblains develop on the sides of the fingers often on a background of acrocyanosis [13]. Clinically, these lesions are composed of clustered papules or plaques, which may ulcerate. Tightfitting trousers, such as riding breeches, have been implicated aetiologically [9]. In chronic perniosis, especially in the presence of arterial disease or prolonged cold exposure, irreversible changes of fibrosis, lymphoedema and hyperkeratosis may occur, altering the physical signs. Pathology the histopathology of perniosis usually demonstrates dermal oedema with superficial and deep dermal inflammation [7]. The mononuclear cell infiltration, mostly T cells, is primarily perivascular but also occurs in a perieccrine distribution [8]. Most patients will experience good disease control when steps are taken to prevent cold exposure. Investigations Investigations should be guided by the clinical presentation of the patient but may include a full blood count and/or blood film, protein electrophoresis, an autoimmune screen, cryoglobulins and cold agglutinins. Investigations were positive in 11/20 tested patients from a Mayo Clinic series [2]. A doubleblind, placebocontrolled study demonstrated the efficacy of nifedipine in clearing existing chilblains and preventing the development of new lesions [14]. Acrocyanosis y Definition Acrocyanosis is a persistent cyanotic or erythrocyanotic mottled discoloration of the hands and, less commonly, feet and face. Introduction and general description Acrocyanosis may be idiopathic or secondary to a number of systemic disorders, including an underlying malignancy (Box 125. Clinical features Idiopathic acrocyanosis usually starts in adolescence and persists into adult life. The changes may be transient after cold exposure but usually persist during the winter and even throughout the summer months. Clinically there is a painless mottled duskiness of both hands in the presence of normal peripheral pulses. Acrocyanosis must be distinguished from the Raynaud phenomenon, which occurs episodically with triphasic colour changes and often involves just a few digits. In cases of acrocyanosis developing for the first time in adult life a secondary cause should be sought (Box 125. Epidemiology Age and sex Presentation is typically in adolescence, with a reported female preponderance [2]. Pathophysiology There is vasospasm of peripheral arterioles, aggravated by cold, and dilatation of the subpapillary venous plexus [3]. The condition is most probably a primary vascular defect since studies have not demonstrated a deficit of neuronal supply to the cutaneous vessels [4]. Differential diagnosis this includes Raynaud phenomenon, arterial occlusion and venous occlusion. However, the usefulness of this technique in distinguishing primary acrocyanosis from connective tissue disease has yet to be firmly established. Prognosis the disorder may persist indefinitely but spontaneous improvement can occur in adolescent patients. Vasodilator therapies, such as the calciumchannel antagonists, do not appear to be beneficial. Treatment of an underlying systemic disorder may improve the appearance in secondary acrocyanosis. Warm clothing, exercise, weight reduction and elastic support hosiery may be helpful. Introduction and general description Erythrocyanosis is a condition that predominately affects the lower legs, distinguishing it from acrocyanosis, which affects peripheral areas such as digits and appendages [1]. Introduction and general description Livedo reticularis is a lacelike pattern on the surface of the skin created by low blood flow within anastomoic areas of the skin. Each cone is supplied by an arteriole, which passes through the dermis perpendicular to the surface. Livedo reticularis may be physiological, idiopathic or secondary to intravascular obstruction or vessel wall disease (Box 125. Age and sex Erythrocyanosis occurs most commonly in adolescent girls and middleaged women. Pathology There is hyperkeratosis, red blood cell aggregates and vessel wall thickening in the deep dermis. If the livedo reticularis is caused by vasculitis, there will be vascular inflammation and arterial obliteration in the deep dermis and the subcutaneous tissue. There is no difference in the histological features between the blanched and erythematous areas [2]. Clinical features Erythrocyanosis is seen on the lower legs of adolescent girls, the thighs and buttocks of overweight boys and the thighs and lower legs of middleaged women. It is characterized by dusky discoloration of the skin and may be accompanied by keratosis pilaris, angiokeratomas and telangiectases. Nodular perniotic lesions occurring after cold exposure may complicate erythrocyanosis. Clinical features Livedo reticularis most commonly occurs on the legs but the arms and trunk may also be affected. Cold usually exacerbates the cyanotic discoloration, while leg elevation tends to decrease the intensity of the colour changes. Diffuse arterial disease or hyperviscosity problems give rise to diffuse livedo reticularis; limited arterial disease leads to patchy mottling. In many cases livedo reticularis forms a complete network, in other cases there is a branching Differential diagnosis Whilst the diagnosis is often clinically apparent, other vascular disorders and livedo reticularis may be considered in the differential. Also known as cutis marmorata, this is a transient cyanotic mottling of the skin that occurs as a physiological response to cold exposure and disappears with warming. It is usually encountered in healthy infants and resolves during the first year of life. Physiological livedo reticularis rarely occurs in adults, but in this situation is often associated with a disorder that causes stasis within blood vessels, for example paralysis. Lesions are usually asymmetrical, typically on a limb, less often involving the torso or head. Usually congenital livedo reticularis occurs in isolation but it may be associated with a variety of other congenital abnormalities. In most cases the condition gradually resolves, with most improvement occurring during the first 2 years of life. Mild degrees are harmless, while more severe cases are associated with ulceration, usually in the winter. Ulceration of the dark areas occurs rarely but, if present, suggests significant largevessel vasculitis or intraluminal thrombosis. The appearance of livedo reticularis is initially reversible if the underlying cause is treated, but with chronic problems permanent telangiectases develop.

In severe cases faecal material may pass through the fistula gastritis on ct order discount ditropan on line, leading to soiling of underwear and skin irritation gastritis symptoms light headed purchase line ditropan. There is often a history of an abscess that failed to heal after surgical drainage or recurred at the same site gastritis diet for ditropan 2.5 mg amex. Complications and comorbidities Squamous cell carcinoma is a rare complication that may arise in chronic complex fistulae gastritis dieta recomendada buy cheap ditropan 2.5mg on-line. Setons maintain the patency of the fistula track gastritis diet 7 up calories ditropan 5 mg fast delivery, acting as a wick and allowing the drainage of pus and healing to occur gastritis diet king buy ditropan 5 mg fast delivery. Second line External sphincter Fibrin glue can be injected into the fistula track and is a sphincter sparing technique. Formation of a colostomy is considered a last resort in nonhealing anal fistula [2]. Defunctioning colostomy is more frequently utilzed in Crohn disease where wound healing is poor following other surgical procedures. B: intersphincteric fistula track between the internal and external sphincters in the intersphincteric space. C: trans sphincteric fistula track crossing both the external and internal anal sphincters. D: suprasphincteric fistula passing outside the internal and external anal sphincters over the top of the puborectalis muscle and penetrating the levator muscle before tracking down to the skin. E: extrasphincteric fistula tracking outside the external anal sphincter and penetrating the levator muscle into the rectum. The consequences may include chronic pain, bleeding, incontinence, cellulitis and systemic sepsis. Definition and nomenclature An anal fissure is a longitudinal ulcer occurring in the squamous epithelium of the anal canal located distal to the dentate line. Introduction and general description Primary anal fissures are idiopathic and usually affect the posterior midline. Secondary anal fissures usually occur in the lateral aspect of the anal canal and are associated with underling diseases such as Crohn disease. The aims of management are to eradicate the fistula and prevent recurrence while maintaining continence. Successful management of an anal fistula requires that all primary and secondary tracks are drained and eradicated [2]. Antibiotics are not usually effective in treating perianal abscess or infection associated with anal fistula, but are recommended in patients who have cellulitis [3]. Epidemiology Incidence and prevalence the exact incidence is unknown and probably underreported as it is likely that many patients do not seek medical advice as the fissure heals without intervention. First line Surgical procedures performed by a colorectal specialist include fistulotomy and seton insertion (see below) [7]. Fistulotomy entails the division of superficial tissue to lay open the fistula track and is an effective way to treat low fistulae. Fistulotomy should be avoided where there is significant anal sphincter involvement to avoid the risk of postoperative faecal incontinence. A seton is a thread (usually a nonabsorbable suture or vascular sling) placed Age Anal fissures are commonly encountered in young adults but may affect extremes of age [2]. Pathophysiology Disease course and prognosis More than 50% of acute fissures heal spontaneously with conservative management [2]. Only 10% of chronic fissures will heal spontaneously and either surgical or medical intervention is required to achieve healing. Trauma causing pressure or necrosis by the passage of hard stools is thought to be an initating factor. Pregancyassociated anal fissures are thought to arise due to shearing forces during labour. Investigations Proctoscopy and histological assessment is mandatory if the aetiology is in doubt. In secondary anal fissures, specific pathology such as anal carcinoma or Crohn disease will be identified. Warm sitz baths (a shallow bath used for cleansing the perineal and perianal skin) can help with symptomatic relief [4]. The aim of management of chronic fissures is to treat the triad of anal pain, spasm and ischaemia. Clinical features History Painful defecation occurs, often described as a tearing sensation. Anal fissures result in significant morbidity and reduction of quality of life [3]. Acute fissures are usually superficial with welldelineated mucosal edges and granulation tissue at the base. Chronic fissures may have a fibrotic rolled edge, sentinel tag at the anal pole of the fissure and visible transverse fibres of the internal anal sphincter. Fissures occurring in patients older than 65 are usually secondary and appropriate investigations are required to exclude underlying disease. Second line Surgery is the mainstay of treatment for chronic anal fissures unresponsive to first line measures. Lateral internal sphincterotomy results in cure rates of up to 98% but may compromise anal continence in up to 30% [2]. The relatively high risk of anal incontinence following surgical intervention has led to the search for medical therapy to reduce anal pressure. Options that may be tried prior to surgery include oral calcium channel blockers. Clinical variants Although not true anal fissures, erosions and fissures may occur in the sulcus beneath odematous haemorrhoids or in any area of perianal skin disease including the natal cleft. These fissures, which are secondary to inflammatory skin disease such as psoriasis or lichen simplex, or to trauma, are sometimes referred to as anal rhagades. The presence of even a small fissure in an area of cutaneous inflammation maintains the pruritus and may predispose to infection. Haemorrhoids Definition and nomenclature Haemorrhoids are dilatations in the venous system draining the anus. The anal column blood vessels are largest at the left lateral, right posterior and right anterior quadrants of the anal canal where the subepithelial tissues expand to form three anal cushions. The cushions help to seal the anal canal to maintain continence to faeces and flatus, and are also important in the pathogenesis of internal haemorrhoids. Other predisposing factors include portal hypertension due to liver cirrhosis and malignancy causing compression of the superior rectal vein. Haemorrhoids are often familial and there may be a family history of leg varicose veins. Age-related loss of anal canal muscle support may explain the increase in prevalence with age [2]. Internal haemorrhoids are proximal to the dentate line and have visceral innervation with an absence of pain fibres. External haemorrhoids are varicosities of tributaries of the inferior rectal vein and are Clinical features History Symptoms are bleeding, mucous or faecal discharge, pruritus ani and the sensation or awareness of prolapse. Haemorrhoidal bleeding consists of bright red blood on the stool or toilet paper or dripping into the toilet. The symptoms of haemorrhoidal disease do not correlate with the size of the haemorrhoids. External thrombosed haemorrhoids can be differentiated as they are covered by squamous epithelium. A perianal dermatitis may occur secondary to skin irritation resulting from faecal leakage, or a contact dermatitis (irritant or allergic) secondary to overwashing or medicaments. Examination should include digital rectal examination to exclude the presence of a mass and proctocopy to evaluate if there is any other anorectal pathology. In contrast to external haemorrhoids, perianal skin tags do not swell with blood when the patient strains or reduce with pressure. Severity First degree Second degree Third degree Fourth degree Definition Contained within the anal canal 113. Perianal haematoma (perianal thrombosis) is caused by the rupture of tributaries of the inferior rectal vein as a result of coughing or straining, with the appearance of a haematoma affecting perianal skin (incorrectly called a thrombosed haemorrhoid). A blueblack nodule that can be multilocular can be seen on inspection of the anal margin region. If the overlying skin perforates, a clot of blood is extruded leading to pain relief. Differential diagnosis the differential diagnosis includes anorectal malignancy, Crohn disease, perianal metastases and Kaposi sarcoma. The aims of management include addressing any predisposing factors such as constipation or diarrhoea. Symptomatic relief for perianal symptoms can be achieved with topical agents including lubricants and mild topical steroids. First line options include injection sclerotherapy, rubber band ligation, infrared coagulation and cryotherapy. These techniques result in tissue destruction, subsequent fibrosis and resultant resolution of the haemorrhoid. Surgical procedures include excisional haemorrhoidectomy, stapled haemorrhoidopexy and Dopplerguided transanal haemorrhoid devascularization [3]. Trauma and artefact Definition Trauma includes accidental, or self-induced, or iatrogenic injury, as well as sexual abuse. Introduction and general description Anal, perianal and perineal trauma is not uncommon. Clinical features Clinical variants Pressure sores (synonym decubitus sores) in the sacral area are common. The perineal body is absent and there is minimal tissue separating the anus from the vagina. Degree of trauma First degree Second degree Third degree Definition Laceration of vaginal mucosa or perineal skin only Involvement of perineal muscles but not anal sphincter Disruption of anal sphincter muscles: 3a: <50% of external anal sphincter torn 3b: >50% of external anal sphincter torn 3c: internal anal sphincter also torn Fourth degree Third degree tear with disruption of anal epithelium or bedridden patients, a persistent patch of nonblanchable erythema on the sacral or ischial region is a sign of impending ulceration. Progression to ulceration can be prevented if this early stage is identified promptly [2]. Clinical signs of perianal and anal trauma following sexual abuse in children include gaping of the anus and anal fissures [3]. Perianal skin diseases can be mistaken for sexual abuse including lichen sclerosus and perianal Streptococcus infection. Prospective studies using endoanal ultrasound scanning have identified that occult anal sphincter injury is common [4]. Perineal and perianal pain Functional anorectal pain occurs in the absence of any underyling discernable organic disease. Functional disorders of the perineum causing pain include proctalgia fugax, levator ani syndrome and idiopathic coccygodynia [1]. Proctalgia fugax is characterized by severe, selflimiting, fleeting, episodic anorectal pain. The pathogenesis is unknown but may be due to spasm of the internal anal sphincter or compression of the pudendal nerve. Chronic proctalgia (chronic idiopathic anal pain) can be defined as chronic or recurrent episodes of anorectal pain lasting more than 20 min in the absence of organic cause. Levator ani syndrome causes recurrent or persistent pain, pressure or discomfort in the perineal region and is commoner in females [4]. Digital rectal examination distinguishes between levator ani syndrome and unspecified functional anorectal pain. Tenderness occurs on palpation of the puborectalis muscle in levator ani syndrome but not in patients with unspecified functional anorectal pain. It is usually precipitated by prolonged sitting and rising from the seated position. Secondary causes of coccygodynia include trauma, arthritis or rare tumours such as chordoma, intradural schwannoma, perineural cyst or intraosseous lipoma [5]. Descending perineum syndrome is commoner in females and is associated with multiparity. Clinical features include poorly localized deep perineal discomfort, faecal incontinence, constipation, rectal prolapse and perineal descent [6]. Precipitating factors of pain in chronic pain syndromes include sitting, defecation and psychological stress. Treatment options for chronic pain include analgesia, biofeedback, sitz baths, tricyclic antidepressants, botulinum toxin injections and sacral nerve stimulation. Other diseases and infections Sexually transmitted diseases 1 Singhrao T, Higham E, French P. Lymphogranuloma venereum presenting as perianal ulceration: an emerging clinical presentation Perianal manifestations of human immunodeficiency virus infection: experience with 260 patients. Hidradenitis suppurativa: a retrospective study of 846 Dutch patients to identify factors associated with disease severity. This typically involves a collection device worn on the skin, usually held in place by an adhesive material. Skin problems are the commonest longer term complications and figures from several studies suggest that between onethird and twothirds will experience a skin problem around their stoma at some time that will interfere with normal appliance use [1]. In theory, most dermatoses could affect peristomal skin but in practice the majority fall into one or more of a few groups that are predictable because of the occluded nature of the peristomal skin, prolonged contact with the appliance and any medicaments or cleansers, leakage of urine or faeces onto the skin and the underlying abdominal disease itself. The common cutaneous complications are: irritant reactions (including dermatoses exacerbated by trauma), allergic reactions, infections, common generalized inflammatory dermatoses.

At this concentration gastritis symptoms child order ditropan 5 mg, weak irritant reactions are quite common gastritis diet brat buy ditropan 5 mg low price, especially in atopics gastritis diet queen buy ditropan 2.5 mg low price, but lower concentrations will miss relevant positives [51] gastritis diagnosis code buy ditropan amex. Dilutions can be tested to assist in distinguishing allergic from irritant reactions gastritis fatigue buy discount ditropan 2.5 mg on line. The clinical relevance of a positive palladium chloride patch test reaction is questionable in many instances chronic gastritis stomach generic ditropan 5mg with visa, and may just be a reflection of nickel allergy. Stomatitis and lichen planus have nevertheless been related to palladium in dental materials [9,10]. The removal of prostheses or dental alloys containing palladium may need to be considered in these instances. A granulomatous reaction after ear piercing has also been seen with palladium allergy [11]. Gold salts, such as gold trichloride and potassium dicyanoaurate, are recognized as sensitizing as well as irritant. Gold salts are used in the plating, electronics, photographic, glass and porcelain industries [1]. Metallic gold has, until recently, been regarded as safe and very unlikely to sensitize. However, when gold sodium thiosulphate was added to the standard patch test series, positive reactions were obtained in 8. There is a female predominance, and where relevance has been found it has usually been in the context of jewellery or gold dental work [3]. However, the allergic mechanism behind the positive patch tests, and their relevance, have been questioned [3,4]. There is a relationship between the amount of dental gold and frequency of allergy [5]. There is also evidence of an increased rate of allergy to gold after the use of goldplated cardiac stents (see the section on cutaneous reactions to implanted metals later in this chapter) [6]. In our experience a relevance for a gold sodium thiosulphate positive patch test is found infrequently, and generally these patients can wear jewellery and have gold dental fillings without problems [2,3]. Nevertheless, analysis of the involved anatomical sites has been undertaken by others who have found that involvement of fingers, ear lobes and eyes by dermatitis predominates [3]. A seborrhoeic eczema pattern has been described [7], as have persistent papules and nodules on the ear lobes, with lymphomatoid or granulomatous histology [8,9]. Nearly always there is concomitant sensitivity to nickel, and guinea pig and clinical studies have suggested this may be a true crossreaction [4,5]. Acral dermatitis has been described from allergy to gold salts in the gilding industry [15]. Many gold salts have been used for patch testing, but most centres now use gold sodium thiosulphate 0. Late reactions are common and an additional 7day or even 2 or 3week reading has been advised [16]. The controversy over the debatable relevance has led many to advise against routine standardseries screening for gold allergy [4]. The metal is used in instruments and amalgam (alloy of silver or copper and mercury) for filling teeth. Mercury and inorganic mercurials may be used in disinfectants, fungicides, herbicides, insecticides, detonators, emulsion paints and jewellery, as well as in the production of caustic soda and chlorine. Organic mercurials may be found in topical and parenteral medicaments (see the section on organic mercurial later in this chapter). Orofacial granulomatosis has also been seen in association with mercury allergy and has resolved after removal of amalgam fillings [6,12]. Generalized exanthems and erythema multiforme have been reported from mercury exposure, including inhalation, dental fillings, following the breakage of thermometers in the mouth and also the use of an antiparasitic powder for the treatment of crab lice [13,14]. In our view, malaise and general ill health are not related to allergy to mercury in amalgams. Red mercuric sulphide (cinnabar) in a tattoo may induce granulomatous reactions in allergic subjects [17]. We have seen several granulomatous and lichenoid reactions confined to the red parts of tattoos but none of our patients has been allergic to mercurials. However, mercury compounds can be irritant, and aqueous solutions of mercury salts may react with aluminium in Finn chambers to cause false positive reactions [2]. Patch testing with both mercury and ammoniated mercury is suggested if allergy is suspected [2]. Patch testing to amalgam is also possible and is available commercially at 5% pet. Most reported cases are from aluminium adsorbed vaccines and parenteral solutions used for hyposensitization, with granulomatous reactions at the injection site [1,2]. It is found in antiperspirants, and axillary dermatitis (usually irritant) may occur. Allergy in a child with chronic otitis externa treated with aluminium acetate ear drops has been seen [3]. As Finn chambers are aluminium, a positive patch test, often annular in configuration, may develop under every single test site in sensitized persons. Patch testing is best undertaken with plastic chambers if this diagnosis is suspected. Pure aluminium metal or salts, for example aluminium acetate 10% aqueous or aluminium chloride 2% aqueous, can be used for testing. Hypertrophic amalgam dermatitis simulating carcinoma of the tongue has been described in one patient [3]. There are many reports of oral lichen planus in association with amalgam fillings [4,5] but the relationship is not consistent [6,7]. Patch tests to mercury are frequently positive when lichen planus is adjacent to amalgam fillings, but less so when there is not a close anatomical relationship [5]. In many sensitized subjects, the condition will improve or settle when the amalgam is removed [5,9]. The relationship between oral inflammation, burning mouth syndrome and mercury allergy is contentious [6,10,11], but some individuals with mercury allergy have responded to amalgam Other metals Copper is a ubiquitous metal found especially in coinage, jewellery, pipes, electrical equipment and wiring. Its salts are used in insecticides, fungicides, wood preservatives, food processing, fertilizers and fur dyes. Dermatitis has been reported from copper intrauterine contraceptive devices and proven by patch testing and resolution of the dermatitis after removal [1,2]. Commercially available perfumes are mixtures of essential oils from these sources and synthetic compounds, with usually at least 10, and up to several hundred, ingredients [3]. It comes from a tree, Myroxylon pereirae, that grows in Central America (not Peru! The balsam was given its name because it was packed in, and shipped from, Peru to Europe [5]. It was widely used earlier this century for treating wounds, and also for scabies [4]. Its composition is still not completely known, but the balsam does contain benzyl benzoate, benzyl cinnamate, cinnamic acid alcohol and aldehyde, benzoic acid, vanillin, farnesol and nerolidol [6]. It may crosssensitize with resorcinol monobenzoate used in cellulose ester plastics [7]. Other related balsams include balsam of Tolu, balsam of spruce, gum benzoin and storax. Examples of natural flavours include citrus fruit peel, peppermint oil, spearmint and vanilla. In the modern food industry a large number of synthetic flavouring agents are used. Of these, 54 are single chemicals and 28 are natural extracts, which in turn include all the ones that are required to be listed on consumer products. In addition 12 of the chemicals and eight of the natural extracts were found to pose a high risk of sensitization to the consumer, when considering the high number of reports with at least 100 such cases. In general, as measured by the frequency of allergic reactions in routinely patchtested patients, fragrances are the second most common allergen (after nickel). Studies have indicated that fragrance allergy affects in the region of 1% of the adult population [8], whereas children and adolescents have shown rates of 1. In those clinics investigating allergic contact dermatitis, the rates have varied between 5. Sex incidence has generally only shown a slight preponderance of females, and in some instances it has been equal [10]. There is evidence from some centres that perfume allergy is increasing quite significantly [1]. This is thought to reflect a decreasing concentration of these materials in cosmetics in the last 17 years. Routine patch testing with balsam of Peru as a marker of allergy to perfume and certain flavours has shown a positive rate of allergy of around 4% [11]. It was thought to be a decreasingly relevant marker of perfume allergy but a recent study from Finland has revealed a sharp rise in the frequency of allergy, perhaps in parallel with increased exposure to relevant components [12]. One or more of 26 named fragrance allergens will be found on the ingredient label if present at 10 ppm or more in leaveon products and 100 ppm or more in rinseoff products. This should improve evaluation and surveillance of fragrance allergy within the population in the future. Perfumes, cosmetics, moisturizers, deodorants, aftershaves, soaps, bath additives, aromatherapy oils and toilet tissues and wipes are typical sources. In the domestic environment cleansers, fabric conditioners, candles, pot pourri, air fresheners and polishes may all be perfumed. Autooxidation of terpenes may make a significant contribution to the allergenicity of perfumes [15]. There is evidence that allergy to more than one perfume component may result in a synergistic effect [1]. Furthermore, those who are aware of their allergy may continue to suffer dermatitis by failing to take appropriate avoidance measures, for example by unwittingly applying perfumed medicaments and cosmetics to their skin. Aromatherapists and their clients are liable to sensitization in sites where there is contact with the essential oils [19,20]. Peeling of citrus fruit in the domestic environment may also induce allergic hand dermatitis. Cheilitis may be a reflection of allergy to flavouring agents in toothpastes [22,23], lipsalves [24] and food and drink [25]. Gingivitis has occurred from allergy to eugenol in dental cement [26], and cinnamon has induced oral blisters, erosions and lichen planus [27,28]. Balsam of Peru is still used as a medicament, particularly in haemorrhoid preparations, and allergy is therefore relevant to perianal problems. Sensitizing balsams are used in medicaments and balms for wounds, sprains and joint pains, particularly in the Far East [29]. Tincture of benzoin is used in a similar way, and may also be used under orthopaedic plaster casts [30]. Vesicular hand dermatitis has been related to dietary intake of flavours related to balsam of Peru [31]. Musk ambrette is a synthetic perfume component responsible for photoallergy, and although its use has been stopped in the western world it may still be present in perfumed materials from other parts of the world. Fragranceallergic subjects appear to be at an increased risk of more frequent and more severe eye and respiratory symptoms than would be expected by chance [32]. Perfumes are marketed as concentrated liquids and in more diluted forms such as eau de toilette, or as sprays, and all should be avoided. The application of perfume to clothing may still cause problems in allergic subjects, who often believe they will only react if perfume is applied directly to the skin. Occasionally, affected subjects are able to use a specific perfume without any problem. Other perfumed skin products to be avoided include deodorants, aftershaves, talcum powders, soaps and bath additives. Surprisingly, some prescribable moisturizers, emollients, bath additives and corticosteroids, as well as overthecounter medicaments, contain perfume. Menthol, lavender oil and peppermint oil are the top allergens in patients reacting to a cream [33]. Fragrance allergic patients with ongoing problems should also be counselled carefully about avoidance of these sources in medicaments. In the domestic situation, perfumecontaining sprays such as air fresheners, insect repellents and hairsprays should be avoided, as should skin contact with perfumed household cleansing products and polishes. The levels of perfume residues from washing powders and fabric conditioners for clothes are probably too low to cause clinical problems [34], but in those with a clothing pattern of eczema, extra rinsing and avoidance of fabric conditioners can be considered. Peeling citrus fruit with the bare hands should be avoided by those with hand eczema and an allergy to balsam of Peru. In the occupational environment many cleansers, conditioning creams and barrier creams are perfumed, and similar avoidance measures are needed. Some work materials, including cutting oils and paints, may contain masking perfume and enquiries may be necessary to establish their components. Dietary measures may be helpful not only for oral and perioral allergy from flavours but also in those with vesicular palmar eczema associated with balsam of Peru allergy.

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Following absorption gastritis diet india order ditropan australia, a higher state of energy (excited state) is induced in the molecule (photoactivation) chronic gastritis with focal intestinal metaplasia generic 5 mg ditropan visa. Alternatively gastritis diet peanut butter order ditropan with visa, there may be phosphorescence lymphocytic gastritis definition ditropan 2.5 mg otc, heat or other energy transfer to another molecule chronic gastritis with h pylori order ditropan without prescription, or photochemical alteration of the molecule [5] gastritis medical definition purchase generic ditropan pills. When it occurs in vivo the activation may have a phototoxic (nonimmunological) or photoallergic (immunological) action. The photoactivated molecules may be transformed into new substances capable of acting as irritants or haptens. The reaction to a photoallergen is based on the same immunological mechanism as contact allergic reactions. Newly formed haptens may, by virtue of the excited state and freeradical formation, be able to combine chemically with other substances, for example protein, to produce a complete antigen. The photoallergen tribromosalicylanilide has been shown to change into dibromosalicylanilide and monobromosalicylanilide [8], and with sulphonamides it has been suggested that an oxidation product is formed [9]. The duration of the response to light irradiation after stopping the application of a known photoallergen is variable and depends on the photoallergen. Several photoallergic substances simultaneously produce phototoxic reactions when applied in high concentrations and with a sufficient amount and type of radiation. Thus, in an individual case, the two reactions may be clinically indistinguishable. The other main group of photosensitizers are topical nonsteroidal antiinflammatory agents, especially ketoprofen. Nevertheless, other photocontact allergens have been identified with varying degrees of confirmatory evidence, and these are summarized below. Fentichlor (bis(2hydroxy5chlorphenyl)sulphide and bromosalicylchloranilide) is used as a topical antifungal agent in Australia and is used domestically in Sweden. Crossreactions between chemically related substances have been frequently reported. Clinical features Environmental factors Photoallergic contact dermatitis will only occur in the event of exposure to potential photoallergens in the environment. Their presence in cosmetics may be to History the first significant recognized problems from photoallergy were related to the use of chlorinated salicylanilides in germicidal soaps in the early 1960s, with many thousands being affected. Regulatory elimination of these photoallergens resulted in the disappearance of the allergy, but some affected individuals became persistent light reactors [15]. By the mid1980s the most important photoallergen was the fragrance musk ambrette whose use is now Photoallergic contact dermatitis 128. Presentation Photoallergic reactions can resemble sunburn, but usually show the same spectrum of features seen with allergic contact dermatitis. The photoallergen may be transferred from one body site to another, for example, to the contralateral areas, or may be due to a crossleg effect or to transfer by the hands. The intensity of the response to photoallergens depends upon a number of factors: 1 the nature and concentration of the substance applied. The phenomenon has been reported with many different substances, including chlorpromazine [20], halogenated salicylanilides, musk ambrette, promethazine hydrochloride, ketoprofen [21], quindoxin [22] and olaquindox. This chronic photosensitive dermatitis presents as chronic eczematous changes on lightexposed areas with or without spread elsewhere. Patients with established photosensitivity who have a flare of their dermatitis may have reacted to an increase in light levels or reexposure to their primary allergen or a crossreacting allergen by airborne contact. Alternatively, they may have developed a secondary allergic or photoallergic contact sensitivity to their sunscreen or to one of their other medicaments. The disorder of chronic actinic dermatitis (see Chapter 127) may be associated with contact allergy, particularly to Compositae. Phototesting reveals abnormal results but photopatch tests to Compositae and other allergens are generally normal. Nevertheless, persistent light reactivity following photoallergy may progress to chronic actinic dermatitis. Disease course and prognosis Typically, with avoidance of the cause the dermatitis will resolve; rarely, complications supervene. The main clinical indications for photopatch tests include the investigation of patients with eczematous rashes predominantly affecting lightexposed sites and a history of worsening following sun exposure. Grounds may be extended to testing anyone with an exposedsite distribution of dermatitis. Some patients have coexisting photosensitive disorders, causing practical problems in performing and interpreting the investigation. In photobiology centres, the more sophisticated irradiation monochromator may be used as an alternative. The energy source must be monitored regularly, as the tubes deteriorate with time. However, Differential diagnosis Photoallergy may simulate other photosensitive dermatoses and airborne contact allergy, and vice versa. It is also important to recognize that photoallergy may sometimes fail to follow the typical pattern of sparing of lightprotected sites, and airborne contact allergy may paradoxically induce the classic photosensitivity distribution. A similar pattern of dermatitis may also be seen in patients sensitive to colophonium, pine and spruce. It is therefore important to identify every potential component of these clinical presentations by screening for contact allergy using patch tests (especially to plants), for photoallergy with photopatch tests, and also for photosensitivity using phototesting. Day Protocol Protocol 1 Protocol 2 Protocol 3 0 Phototest Apply allergens Apply allergens Apply allergens Phototest 1 Read phototest results Remove patches and irradiate allergens Remove patches, read results and irradiate allergens Read phototest results Remove patches, read results and irradiate allergens From British Photodermatology Group [23]. Read results Read results Read results 2 3 4 the higher doses have the disadvantage of being more likely to induce false positive phototoxic responses without an increased detection of photoallergic subjects, and therefore a dose of 5 J/cm2 is recommended. Usually, the two sets of tests are applied on either side of the vertebral column at the same level. Steps must be taken to avoid any incidental irradiation by natural light of both the irradiated and the control set of allergens. The control site and the rest of the skin must be covered with opaque material during irradiation of the photopatch test site. The European Multicentre Photopatch Test Study Taskforce has recommended such a series based on a recent European study (Table 128. There are occasional difficulties distinguishing a false positive phototoxic reaction from photoallergy, but this is less likely with a dose of 5 J/cm2. Readings are scored identically to conventional patch tests, but the positive symbol is preceded by the prefix Ph, for example Ph++ is a strong positive photoallergic reaction. If the same allergen provokes an equally strong reaction on both sides, it is an indication of contact allergy alone; if it is significantly stronger on the irradiated side, then combined allergy and photocontact allergy may be occurring. Doubtful and slight amplification of photoallergic reactions may be the result of phototoxicity. Photopatch testing: recommendations for a European photopatch test baseline series. However, owing to the relatively short time for which they have been present in the marketplace, further useful information on their photoallergenic potential will be gained by their inclusion in this European baseline photopatch test series 10% pet. Also used in other European countries Widely used in several southern European countries as a topical antihistamine Allergic contact urticaria Definition and nomenclature the term was introduced by Fisher in 1973 [1] and defined as a weal and flare reaction following contact with an external substance, usually appearing within 30 min and completely clearing within hours, without residual signs [2]. Immune contact urticaria is commoner in, but not exclusive to , atopic individuals. It belongs to a heterogenous group of immediate contact inflammatory responses that appear within minutes following contact with eliciting substances. Contact uticaria, in association with protein contact dermatitis, comprises the contact urticaria syndrome. The heterogeneity of this syndrome includes both mechanistic and clinical presentations that can present either locally or generally, and involve organs other than the skin including the respiratory, gastrointestinal and vascular systems, leading to anaphylaxis. Incidence and prevalence In Finland, contact urticaria has been classified as a distinct occupational skin disease since 1989. The most common causes (in decreasing order of frequency) were cow dander, natural rubber latex and flour/grains/feed. These causal agents accounted for 79% of all cases and the most affected occupations (per 100 000 workers), in decreasing order of frequency, were bakers, preparers of processed food and dental assistants [3]. A retrospective Australian study carried out in a tertiarylevel occupational dermatology clinic identified a prevalence of 8. Atopy was a significant risk factor for natural rubber latex allergy and contact urticaria induced by foodstuffs or ammonium persulphate. In this study, the three most common occupations were healthcare workers, food handlers and hairdressers [4]. This in turn may present the protein allergens to Thelper 2 cells, inducing a delayedtype hypersensitivity reaction resulting in eczematous lesions. This does not occur in atopic individuals with normal IgE levels or nonatopic controls and may explain why patients with atopic eczema have delayed hypersensitivity on patch testing to aeroallergens and develop a vesicular response to handling food proteins (protein contact dermatitis) [6,7]. Pathology the histology of contact urticaria is identical to that of urticaria from other causes and is not further discussed here. Genetics There is a strong association of allergic contact urticaria with inherited atopic disease of all forms. There is also a reported association between the development of immediatetype hypersensitivity reactions, specifically to peanut, with filaggrin mutations in these individuals [8]. Environmental factors Contact sensitization develops following exposure, and changes in the exposure to an allergen in the environment will influence the development of the allergy. This has been demonstrated by the control of latex allergy by environmental measures and the use of lowproteinpowderfree gloves [9]. Nonimmunological contact urticaria is the more common form of the condition and is secondary to the release of vasogenic mediators without the involvement of immunological processes. The clinical reaction is often erythema without oedema rather than a true weal and flare response. Substances capable of producing nonimmunological contact urticaria are usually lowmolecular weight chemicals that easily cross the barrier of the skin, such as plants, animals or chemical substances. Many of these chemicals are used as flavourings, fragrances and preservatives in the cosmetic, pharmaceutical and food industries [5]. The pathogenesis of immunological (allergic) contact urticaria involves the classic type 1 hypersensitivity reaction mediated by specific immunoglobulin E in a presensitized individual. IgE binding on mast cells, its subsequent degranulation and release of histamine and other vasoactive mediators is described in Chapter 8. Clinical features Presentation the symptoms usually occur within 1 h and fade by 3 h. Local symptoms include itching and burning, and the development of erythema and the characteristic weal and flare reaction. Early symptoms are commonly missed by physicians although well recognized by patients. Exposure to allergens in those who are highly sensitized, topically or via the oral or respiratory route, may result in widespread urticaria and swelling of the mucous membranes, resulting in conjunctivitis, rhinitis, oropharyngeal swelling, bronchoconstriction and rarely anaphylaxis. The commonest causes of contact urticaria are foodstuffs, which can provoke oropharyngeal symptoms (the oral allergy syndrome) following ingestion, or cutaneous hand symptoms in food handlers. Symptoms are usually confined to the localized mucosal surfaces with irritation or tingling. Clinical signs are usually confined to localized mucosal swelling, although anaphylaxis is rarely reported. In the birchrich areas of northern and central Europe almost all birch pollenallergic patients are sensitized to Bet v1, the major allergen component of pollen from Betula verucosa. It has been reported that in patients with atopic eczema and raised IgE levels, the IgE may attach to the highaffinity IgE receptors on the surface of Langerhans cells or other antigenpresenting cells. In Scandinavia, the commonest cause of occupational contact urticaria is from cow dander in farmers [14]. Of those workers exposed to contact allergic urticants, bakers, butchers and agricultural workers appear to be most at risk of becoming sensitized, more so than health care workers. The allergens are present in the watersoluble protein moiety of the sap collected from the rubberbearing tree Hevea braziliensis, harvested mainly in Malayasia and SouthEast Asia. These items are vulcanized at a lower temperature than solid rubber products such as tyres, seals and gaskets. During the production process, the natural rubber latex was not left to stand in holding tanks as long, the process was shortened by lower vulcanization temperatures, and there was less thorough washing of the final product [16]. All these measures led to an increase in the protein content of the gloves and this, coupled with their increasing use, resulted in an increase in the incidence of allergy to natural rubber latex. Anaphylaxis can occur in any sensitized patient, and seems to be particularly prevalent when challenge is via the mucosal surfaces, as in dental and vaginal examinations, intraperitoneal operations, catheter changing (especially in spina bifida patients who have frequent surgery and catheter changes) and barium enemas. Many of the allergenic peptides in natural rubber latex crossreact with those found in other plants [17], such as banana, lychees, chestnuts and avocado, and patients allergic to latex may exhibit sensitivity to such foods. Due to several interventional measures including an increased use of powderfree latex gloves, and nonlatex gloves and medical equipment, the frequency of natural rubber latex allergy in health care workers seems to have peaked [9]. Hjorth and RoedPeterson (1976) defined this as an immediate dermatitis induced by contact with proteins. Application of the relevant food to the affected skin resulted in either urticaria or eczema [18].

Prevalence of skin complaints as a proportion of the total exposed; estimate of prevalence of occupational dermatoses gastritis raw food diet ditropan 2.5mg on-line. Opinions of others gastritis video buy ditropan 5mg cheap, with attribution as to source and estimate of reliability; own opinion gastritis diet ������������� ditropan 2.5mg low cost, with grounds for it (may be inconclusive) gastritis diet 100 purchase discount ditropan online. Summary of findings; recommendations for future investigation gastritis eating before bed purchase discount ditropan line, management and review; followup gastritis type a and b generic 2.5 mg ditropan with amex. Factory (or other workplace) visits can provide many major benefits [64] as follows. A secondbest alternative that can still provide useful information if a factory visit is impossible is to communicate with medical, nursing, employer or employee representatives by letter or telephone. Changes in the process, when practicable, are always likely to be more successful than personal protection [73]. Some preventative measures that are desirable from a dermatological point of view may be unsafe or impractical in an industrial environment. Materials selected for protective clothing may in practice allow many contactants to penetrate. There are now multilayered materials that show much greater resistance to allergens such as methyl methacrylate [80] and irritants such as organic solvents [75]. Even when protective clothing is practicable and competent to protect, the way in which it is taken off and put on again may lead to contamination of inside surfaces. Because occlusion increases penetration, wearing a glove that has been contaminated on the inside can be more harmful than wearing no glove at all [72]. Personal protective equipment is only effective when selected carefully, removed safely and replaced/maintained regularly [25]. Extreme care must be taken to ensure as far as possible that the replacement is genuinely safer in all respects. Topical binding agents may have a role in the prevention of nickel dermatitis [88]. The basic principle of prevention of occupational contact dermatitis continues to be that of reduction of contact, or preferably avoidance. If chemicals remain on the skin for 24 h instead of 8 h, sensitization and irritation occur more readily [72]. Evidencebased skincare recommendations have been published [89] (summarized in Box 130. If improvements are made to the working conditions by intensified preventative measures, then this is likely to lead to a reduction in cases of occupational contact dermatitis [90,91]. A change of job may be considered in firstyear apprentices, in those with uncomplicated allergic contact dermatitis from readily avoidable substances or in atopics who have unavoidable contact with irritants. These methods assess potential; they do not in themselves predict the incidence of dermatitis. Actual risk depends not only on dermatitic potential but also on other factors, the most important of which concern the conditions of exposure. Standardization of test procedures greatly reduces inter and intralaboratory variation in results - but, as this is never likely to cease to be a problem to some degree [114], the development of new tests that may offer greater ease of standardization (and economy) continues [115]. The use of mouse models for the prediction of sensitizing potential is now well established [116,117]. It is eczematous in character and may be provoked by exposure to the allergen in the home/recreational environment as well as at least partly at work. Better history taking [3], more extensive patch testing, workplace visiting and greater use of chemical investigations [3] significantly increase the proportion of patients found to have contact sensitization relevant to their occupation. Allergic contact dermatitis also frequently complicates irritant contact dermatitis in occupational cases. A prime example of occupational allergic contact dermatitis is that from chromium [6,7] (see Chapter 128). Alkali tests the usefulness of alkali resistance and alkali neutralization tests as predictors of susceptibility to irritants remains controversial. Neither test is sufficiently simple and reliable to achieve widespread clinical use [118,119,120], and their diagnostic value has been overestimated. Susceptibility to one irritant, however, does not necessarily imply susceptibility to another irritant in the same individual [118,121]. Skin irritation thresholds have been correlated with the development of dermatitis in hairdressers [122]. Epidemiology Incidence and prevalence the annual population incidence of occupational contact dermatitis has been estimated to be in the range of 5. The most common allergens are cobalt, chromium, cosmetics, fragrances, epoxy resin, nickel, plants, preservatives, resins and acrylics [8]. Pathophysiology Measurement of skin contamination Methods of quantifying the degree of skin contamination by substances include skin wiping [124], skin rinsing [125], exposure pads [126,127] and the use of natural fluorescence (oils and tars) [128] or fluorescent tracers [129]. Atopy appears to be an independent risk factor for the development of occupational allergic contact dermatitis [8]. The role of filaggrin mutations has not yet been conclusively elucidated in occupational allergic contact dermatitis. Great care must be taken in the accurate distinction between contact dermatitis and endogenous eczema, and between irritant and allergic contact dermatitis (although there can be considerable overlap). Skill is needed, not only in dermatology, but also in taking an occupational history [10,11], and in obtaining as detailed a picture as possible of what the patient actually does at work [12]. The clinical distinction on the hands, forearms or face between endogenous eczema, irritant contact dermatitis and allergic contact dermatitis is beset with pitfalls. Differences in the distribution and morphology are useful guides, but this can be misleading. There is a tendency for vesicular eczema of the palms and sides of the fingers to be endogenous. Gross eyelid swelling usually indicates allergic contact dermatitis, but degrees of eyelid swelling can occur in both irritant contact dermatitis and endogenous eczema. It is difficult to overemphasize the importance of a sound working knowledge of occupational irritants, as well as allergens, and of patch testing, in overcoming these difficulties in clinical differentiation. In identifying the primary and/or major cause of a contact dermatitis, antecedent and aggravating causes should not be neglected. Diagnosis of secondary bacterial infection in occupational contact dermatitis, for example, may allow significant improvement to be obtained with antibiotic therapy. Guidelines on the management of contact dermatitis have been formulated by the British Association of Dermatologists [13]. Disease course and prognosis As seen in occupational irritant contact dermatitis, reactions can persist for months or years despite allergen avoidance. Up to 50% of patients experience significant adverse effects of quality of life, daytoday activities and home relationships [8]. Although testing for immediate hypersensitivity is not always a part of the assessment of contact dermatitis, it can be important, Occupational allergic contact dermatitis 130. The two tests in common use are the skin prick test and the estimation of specific immunoglobulin E (IgE) in the blood. The glove usage or challenge test requires a highly allergenic brand of glove and is potentially dangerous - emergency treatment facilities for the management of anaphylaxis are needed [15]. Skin prick testing involves an intradermal puncture through a drop of allergen or glove. A positive reaction consists of an urticarial weal, which is usually apparent after 15 min, although it may take as long as 45 min to develop. A positive control test of histamine should also be performed to exclude a false negative reaction due to oral antihistamine ingestion. A negative control prick test with for example saline should also be performed to check if the patient is dermographic. Skin prick tests and use tests (where test substances are applied to the skin in ways close to real-life use/exposure and observed) are also useful when investigating protein contact dermatitis in occupations at risk, such as chefs or veterinarians [17]. This is particularly so when the allergens concerned are known to have a multiplicity of industrial uses, such as chromium, cobalt and colophonium. A factory visit can be invaluable in the detection of previously unsuspected sources of allergens [24,25,26]. When clinical assessment points strongly towards an occupational allergic contact dermatitis, the occurrence of negative patch test results should always raise the possibility of the responsible allergen having been inadvertently omitted from testing [22,23]. Routine preemployment testing with potential sensitizers to be used in the future job should not be carried out [21], mainly because of a risk of sensitizing employees. For chemical testing and the principles of a site visit, see occupational irritant contact dermatitis. Artificial fertilizers, disinfectants and cleansers for milking utensils, petrol, diesel oil. Rubber (boots, gloves, milking machines), cement, local remedies for veterinary use, wood preservatives, plants, pesticides, antibiotics in animal feeds, penicillin for mastitis, nickel and cobalt in fertilizers, cobalt and vitamin K3 in animal feeds, ethoxyquin (preservative) in feed, quinoxaline and derivatives (growth factor), dinitolmide (anticoccidiosis), phenothiazine sedatives, soil disinfectants. Four general problems of patch testing are particularly relevant when testing in suspected occupational dermatitis. False positive reactions are commonly obtained if industrial chemicals are applied as patch tests undiluted [20]. Such reactions can be shown to be false positive irritant reactions if testing in control subjects also demonstrates positive reactions; applying serial dilutions of the chemical to the original patient will often demonstrate an abrupt loss of the reaction. The uncritical use of undiluted chemical samples as patch tests also increases the risk of active sensitization and other complications of patch testing (see Chapter 128). When testing an unknown substance, extreme caution is required and where the test is unavoidable, a preliminary open test is advisable [21]. This problem also arises when allergens are found in irritant products such as cutting fluids, solvents and soaps. Dilution of these to avoid a false positive reaction from the irritancy of the sample may overdilute an allergen initially present in only low concentration (see Chapter 128). Unexplained positive reactions found on standard patch testing in suspected occupational cases should always be pursued for Artists [42,43] Irritants. Solvents, oils, cutting oils, paints, glass fibre, carbon fibre, hand cleansers, low humidity, kerosene. Chromate (primers, anticorrosives, oils and cutting oils), nickel, beryllium, cobalt, rubber, epoxy and acrylic resins, dipentene in thinners. Citrus fruits, flour improvers, thiamine, spices (cinnamon, cardamom), essential oils, azo dyes, fat preservatives (lauryl gallate), sodium carboxymethyl cellulose. Fruit and vegetables (onions, garlic, lemons, lettuce, artichokes), hardwood knife handles, spices, formaldehyde, rubber gloves. Cement, chalk, fly ash, hydrochloric and hydrofluoric acids, glass wool, wood preservatives (also phototoxic), organic tin compounds. Cement and fly ash (chromate, cobalt), rubber and leather gloves, additives in shale oils, glues (phenol or urea formaldehyde resins), wood preservatives, teak, glass wool impregnated with phenolformaldehyde resin, epoxy resin, polyurethanes, rubber strip seals, jointing materials. Soldering flux, insulating tape (rubber, colophonium, tar), rubber, nickel, bitumen, epoxy resins, glues (phenolformaldehyde), polyurethanes. Asparagus, carrots, preservatives (hexamethylenetetramine in fish canning), rubber gloves. French polish, solvents, glues, cleansers, wood preservatives (also phototoxic), glass fibre. Soldering flux, organic solvents, hydrofluoric acid, fibreglass, antistatic agents. Soldering flux, chromate, cobalt, nickel, epoxy resins, anaerobic acrylic sealants. Stone dust, coal dust, oil, grease, hydraulic fluid, wood preservatives, cement, powdered limestone and anhydrous calcium sulphate. Wet work, friction, oils, petrol, red feed from mackerel, fish juice (polypeptides). Tars, organic dyes in nets, rubber boots, rubber gloves, marine organisms (Dogger Bank itch) and plants. Chromate (cement), epoxy resin, glues (phenol and ureaformaldehyde), exotic woods, acrylates, varnish (urea formaldehyde), polyurethanes. Plants (Primula obconica, chrysanthemum, Asteraceae (Compositae), weeds, tulips, narcissus, daffodils, Alstroemeria), formaldehyde, pesticides, lichens. Phenol and ureaformaldehyde resins, furan and epoxy resins, chromate (cement, gloves, bricks). Nickel, chromate (antirust agents and dyes, welding fumes), cobalt, colophonium (tall oil), antibacterial agents and antioxidants in cutting oils, and chromate, cobalt and nickel in used cutting oils. Rubber (erasing rubber, mats, cords, finger stalls), nickel (clips, scissors, typewriters), copying papers, glue, felt tip pen dyes. Hair dyes, rubber, nickel, perfumes, lanolin, thioglycolates, cocamidopropyl betaine, methylisothiazolinone. Solvents, turpentine, thinner, emulsion paints, wallpaper adhesive, organic tin compounds.