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Recognition of seborrheic dermatitis is important for the primary care physician, because it may be associated with systemic disease, such as Parkinson's disease and human immunodeficiency virus (HIV) infection. Differential diagnosis includes psoriasis, atopic dermatitis, allergic or irritant contact dermatitis, and dermatophyte (tinea) infections. Treatment includes medicated shampoos containing zinc pyrithione, selenium sulfide, salicylic acid, coal tar, or ketoconazole in combination with topical corticosteroids. Differential diagnosis includes verruca vulgaris (warts), epidermal nevus, melanocytic nevi, and melanoma.
Differential diagnosis includes erythema multiforme, systemic lupus erythematosus (SLE), bullous pemphigoid, mastocytosis. Treatment includes elimination of known causes, antihistamines (H1 and H2 blockers), oral corticosteroids for acute flares, and, in refractory cases, immunosuppresants such as sulfasalazine and cyclosporine.
Differential diagnosis includes urticaria, bullous arthropod reaction, drug eruption, and bullous pemphigoid. Differential diagnosis includes tinea versicolor, pityriasis alba, postinflammatory hypopigmentation, and hypopigmented mycosis fungoides. Treatment includes broad-spectrum sunscreens, potent topical corticosteroids, topical calcineurin inhibitors (tacrolimus or pimecrolimus), narrow band ultraviolet (UV) B phototherapy, psoralen with UVA (PUVA) therapy, or total depigmentation for extensive disease. The most common cause of erythema nodosum in the pediatric population is streptococcal pharyngitis. Treatment includes identifying and eliminating known causes, bed rest and elevation of the extremities, aspirin or nonsteroidal anti-inflammatory medications (NSAIDs), colchicine, and supersaturated potassium iodide.
Pemphigus vulgaris can develop at any age, but it most commonly occurs in the fourth to sixth decades of life, usually in people of Mediterranean or Jewish ancestry.2 Morbidity and mortality are significant, even with treatment. Differential diagnosis includes bullous pemphigoid, Stevens-Johnson syndrome, and epidermolysis bullosa acquisita. Treatment includes good wound care for affected skin, systemic corticosteroids, various steroid-sparing immunosuppressants, rituximab, intravenous immunoglobulin (IVIg), and plasmapheresis. Bullous pemphigoid occurs most commonly in the elderly, with an onset between 65 and 75 years of age.
Differential diagnosis includes bullous SLE, epidermolysis bullosa acquisita, cicatricial pemphigoid, and dermatitis herpetiformis. Treatment includes topical and systemic corticosteroids, steroid-sparing immunosuppressants, and tetracycline in combination with niacinamide.
Treatment includes topical and systemic corticosteroids, steroid-sparing immunosuppressants, colchicine, and plasmapheresis. Differential diagnosis includes pilar or epidermal inclusion cyst, adnexal tumor, neurofibroma, and lipoma.
Differential diagnosis includes allergic or irritant contact dermatitis (especially if bilateral), psoriasis, and dermatophyte (tinea) infection. Acanthosis nigricans can develop following the use of some medications, such as systemic corticosteroids, nicotinic acid, diethylstilbestrol, and isoniazid (INH). Differential diagnosis includes confluent and reticulated papillomatosis of Gougerot and Carteaud and Dowling-Degos disease.
Treatment for type I acanthosis nigricans includes identifying and removing the malignant tumor.
Sweet's syndrome can occur with inflammatory bowel disease, bowel bypass syndrome, and pregnancy. Differential diagnosis includes erythema multiforme, deep fungal infection, pyoderma gangrenosum, and cutaneous metastases. Differential diagnosis includes pemphigus vulgaris, bullous pemphigoid, and erythema multiforme.
Treatment includes treatment of the underlying malignancy, systemic corticosteroids, steroid-sparing immunosuppressants, rituximab, and plasmapheresis. Erythema gyratum repens is a rare but very distinctive skin disease characterized by reddened concentric bands in a whorled or woodgrain pattern. Carney complex encompasses LAMB syndrome (lentigines, atrial myxoma, mucocutaneous myxomas, and blue nevi) and NAME syndrome (nevi, atrial myxoma, myxoid neurofibromas, and ephelides), entities known to pediatricians, cardiologists, and dermatologists. Differential diagnosis includes cutis laxa, Ehlers-Danlos syndrome, and perforating calcific elastosis.
Ehlers-Danlos syndrome is a heterogeneous group of connective tissue disorders characterized by joint hyperextensibility, hypermobility, skin and vessel fragility, and fish-mouth scars. Eleven types of Ehlers-Danlos syndrome have been identified with varying associated features, including mitral valve prolapse, blue sclerae, vascular aneurysm, aortic dissection, hernias, angina, gastrointestinal bleeding (perforation), and peripheral vascular disease. Sarcoidosis is a multisystem, granulomatous disease of the lungs, bones, central nervous system, lymph nodes, eyes, and skin. Differential diagnosis includes rosacea, trichoepitheliomas, granulomatous syphilis, and granuloma annulare. Treatment includes TNF-α inhibitors, metrotrexate, NSAIDs, and steroid-sparing immunosuppressants. Lupus erythematosus is an autoimmune photosensitive dermatosis that can be localized or systemic, often with significant overlap. The cutaneous manifestations of SLE include malar erythema, photosensitivity, oral ulcers, discoid plaques, bullae, purpura, calcinosis cutis, and alopecia.
Differential diagnosis includes diabetic sclerodema, scleromyxedema, and chronic graft-versus-host disease.
Treatment includes vasodilating drugs, phototherapy (UVA1) for limited disease, methotrexate, and cyclophosphamide. Reactive arthritis (Reiter's syndrome with conjunctivitis, urethritis, and diarrhea) (Fig.
Differential diagnosis includes psoriasis, juvenile plantar dermatoses, rheumatoid arthritis, ankylosing spondylitis, and gout. Treatment includes topical corticosteroids, cyclosporine, or acitretin for refractory disease. Erythema chronicum migrans, the hallmark of Lyme disease, reflecting early infection with the tick-borne spirochete Borrelia burgdorferi, develops as a red macule or papule at the site of the tick bite and gradually enlarges to an annular, reddened plaque (Fig. Differential diagnosis includes cellulitis, spider bite, erythema multiforme, and erythema annulare centrifugum.
Diagnostic criteria include the aforementioned changes plus elevated creatine kinase or aldolase level, positive Jo-1 antibody, and electromyographic changes. Treatment includes systemic corticosteroids, methotrexate and other steroid-sparing immunosuppressants, and TNF-α inhibitors. Differential diagnosis includes linear IgA dermatosis, bullous pemphigoid, scabies, contact dermatitis, and bullous lupus erythematosus.
Acrodermatitis enteropathica is an inherited or acquired condition characterized by pustules, bullae, scaling in an acral and periorificial distribution, and concomitant zinc deficiency.
Differential diagnosis includes other nutritional deficiencies, such as niacin or biotin deficiency, and necrolytic migratory erythema.
Necrolytic migratory erythema (glucagonoma syndrome) is a rare disease characterized by erythematous, scaly plaques on acral, intertriginous, and periorificial areas, in association with an islet cell tumor of the pancreas.
Necrolytic acral erythema, characterized by pruritic keratotic plaques on the upper and lower extremities, is a distinctive finding in hepatitis C infection and can resemble a deficiency dermatosis. Gardner's syndrome is an autosomal dominant cancer syndrome characterized by colonic polyposis, osteomas (maxilla, mandible, skull), scoliosis, epidermoid cysts, and soft-tissue tumors (fibromas, desmoids, lipomas). Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) is an autosomal dominant disorder characterized by numerous telangiectases on the skin and oral mucosa (Fig. Treatment includes estrogen therapy or oral contraceptives in postpubertal women, laser cauterization, selective embolization, and supportive care.
Muir-Torre syndrome is a disorder characterized by one or more sebaceous tumors (adenoma, epithelioma, carcinoma) and one or more internal neoplasms, usually colorectal or genitourinary, rarely lymphoma.
Peutz-Jeghers syndrome is an autosomal dominant disease characterized by lentigines on the skin (periorbital region, dorsal surfaces of the fingers and toes) and mucosa (lips, buccal mucosa) and hamartomas of the stomach, small intestine, and colon. Differential diagnosis includes LEOPARD syndrome, Carney complex, and Cronkhite-Canada syndrome. Treatment includes regular and routine endoscopy and symptomatic treatment for hypogeusia and diarrhea. Pyoderma gangrenosum is a neutrophilic dermatosis characterized by painful ulcers with boggy, undermined edges and a border of gray or purple pigmentation (Fig. Differential diagnosis includes infection, vasculitis, spider bite, and factitious disorder. Treatment includes treatment of underlying disease if applicable, local wound care, systemic and intralesional corticosteroids, cyclosporine, and infliximab. Nephrogenic systemic fibrosis, also known nephrogenic fibrosing dermopathy, is a recently described disorder that resembles scleroderma. Treatment includes immunosuppressive agents, phototherapy, topical steroids, retinoids, and photopheresis, all with little benefit. Birt-Hogg-Dubé syndrome is a disorder characterized by multiple fibrofolliculomas and trichodiscomas (skin-colored dermal papules on the face and trunk). Porphyrias are inherited or acquired disorders of heme biosynthesis and can be erythropoietic, hepatic, or mixed in nature, each associated with a specific enzyme defect in the heme pathway. Precipitating factors include alcohol ingestion, estrogen administration, certain hepatotoxins (dinitrochlorobenzene, carbon tetrachloride), HIV infection, hemochromatosis, and hepatitis C infection. Differential diagnosis includes bullous SLE, epidermolysis bullosa acquisita, pseudoporphyria, and variegate porphyria. Pseudoporphyria mimics porphyria cutanea tarda without an enzyme defect; plasma and urinary porphyrins are normal. By recognizing cutaneous manifestations of systemic diseases, the internist can often determine the appropriate diagnosis and therapy or the need for referral to a dermatologist. Joly P, Benichou J , Lok C, et al: Prediction of survival for patients with bullous pemphigoid. Kury S, Dreno B , Bezieau S, et al: Identification of SLC39A4, a gene involved in acrodermatitis enteropathica.
High WA, Ayers RA , Chandler J, et al: Gadolinium is detectable within the tissue of patients with nephrogenic systemic fibrosis. Because your feet are so far away from your heart, it takes them much longer to heal than other parts of the body – this is because it takes much longer to circulate blood from your heart to your feet. Swelling of the feet and ankles is normally caused by a serious condition of either the heart, kidneys, of blood vessels. Tom Corson-Knowles Blog by Tom Corson-Knowles is licensed under a Creative Commons Attribution-ShareAlike 3.0 Unported License. The contents of this Site, such as text, graphics, images, and other material contained on the Site ("Content") are for informational purposes only.
Swelling of the eyelids seems to be a symptom which is very common in many individuals and they complain about it a lot.
Eyelid swelling may be caused by nail polish, makeup, hair spray allergies, animals or plant allergies, chemical allergies. Blepharitis is a very exasperating situation which reoccurs and causes inflammation of the eyelids. Styes are sebaceous glands located near the base of the eyelashes which have become inflamed.
If the swollen eyelid comes with itching as well as burning, using a cold compress can offer some reprieve.
If you have been diagnosed as having high blood pressure, limit salt intake from your diet.
These bags contains tannic acid which are enormously helpful in reducing eyelid swelling as well as giving aid to the burning eyes. Take thin slices of potato and place them on your closed eyelids for 15-30 minutes for a comforting effect. This website is for informational purposes only and Is not a substitute for medical advice, diagnosis or treatment. This normal consequence of vaccination is a viral cellulitis at the vaccination site of varying degree that peaks at about 7-10 days following vaccination.
None of these expected variations of normal reactions require any treatment other than symptomatic relief.
Many disorders of the alimentary tract have dermatologic manifestations (see Table 1 below). Kaposi sarcoma (KS) is a neoplasm of vascular endothelial and lymphoreticular cells that can involve the skin and numerous visceral organs. Human herpesvirus type 8 (HHV-8) has been implicated in the pathogenesis of KS in both HIV-infected and non-HIVa€“infected patients.[9, 10, 11, 12] KS may in fact be a hyperplasia caused by infection with HHV-8, rather than a sarcoma. The cutaneous lesions of KS (occurring primarily in the classic and epidemic forms) begin as pink or red macules, which darken and become increasingly papular as they enlarge. Treatment of localized cutaneous disease includes radiotherapy, surgical excision, systemic therapy, or intralesional chemotherapy. GI involvement occurs in 50-80% of patients with cutaneous KS and in almost 100% of those with oral lesions (see the image below). Complications include progressive painless dysphagia, which is described by patients as a choking sensation that worsens with solid foods.
Diagnosis involves laboratory evaluation to confirm the presence of iron deficiency anemia and cineradiography to detect esophageal webs, which occur in the first 2-4 cm of the esophagus. The name epidermolysis bullosa (EB) is given to a diverse group of rare inherited diseases that cause fragile skin.[18] The skin of these patients tends to form blisters at sites of minimal trauma, with symptomatology beginning at birth or early infancy. A retrospective analysis of 223 patients with EB found 58% of patients had GI complications.[19] In EB simplex, constipation and gastroesophageal reflux (GOR) were frequently observed.
Systemic sclerosis (SSc) describes a multisystem disease of unknown etiology that causes fibrotic changes in the skin, blood vessels, lungs, heart, kidneys, and GI tract.[20, 21] The disease affects all races and occurs worldwide, with clinical manifestations appearing most often in the third to fifth decade of life. Esophageal symptoms are the most common and include a feeling of premature fullness, reflux esophagitis, dysphagia, and epigastric pain, all of which stem from an incompetent lower esophageal sphincter. It is reported that stomach involvement occurs in 10-75% of SSc patients.[23] The gastric manifestations of SSc include gastric antral vascular ectasia (GAVE) and gastroparesis.
Colonic involvement has been demonstrated by barium studies to affect between 10-50% of patients with scleroderma.
The small intestine is the second most commonly involved portion of GI tract during SSc, following the esophagus.
Pemphigus vulgaris (PV) is a rare autoimmune blistering disorder primarily affecting the skin and mucosa. Acrokeratosis neoplastica is a psoriasiform (psoriasislike) skin eruption, which most often occurs at the distal extremities, but can also involve the nose and helices of the ears. This relatively common skin finding appears as a brown-to-black, smooth, velvety plaque found in areas of skin folds, most commonly the neck, axillae, and groin (see the image below).
Of note, tripe palms can be diagnosed clinically by its distinctive appearance, and more than 40% of the time it is the first sign of an undiagnosed cancer.[29] Therefore, all patients with a diagnosis of tripe palms should receive a full workup for cancer, particularly lung or stomach cancer.
In patients with acanthosis nigricans, the possibility of an intra-abdominal malignancy should be considered, especially in patients without an obvious predisposing condition.[30] Clinical features such as a large number of plaques, weight loss, rapid progression of lesions, or the discovery of plaques in unusual locations, such as the lips, oral mucosa, hands, and genitalia, should be additional alerting factors. Prognosis is very poor for these patients, with a 1-year mortality rate of greater than 50%.
FCP can be difficult to distinguish from viral warts, and the diagnosis is most easily clarified by pathological evaluation of a lesion biopsy specimen.
Arteriovenous malformations as seen on CT scan in a patient with Osler-Weber-Rendu syndrome. The dermatologic examination reveals numerous 1- to 3-mm macular or papular, sharply demarcated telangiectases on the face, lips, palate, tongue, ears, chest, or extremities, with occasional presentation under nails.
The most common and often cardinal clinical manifestation of Osler-Weber-Rendu disease is epistaxis, which generally starts in childhood and occurs in up to 80% of patients during their lifetime. The second most common manifestation involves spontaneous hemorrhage from vascular telangiectasia within the GI tract.[45, 46] The GI lesions resemble the skin lesions in form and size and are most often found in the stomach or duodenum. Another GI manifestation is the presence of arteriovenous malformations (AVMs), which can occur in the lungs, brain, and liver. Hemochromatosis is a disorder of iron overload leading to excess deposition in multiple body organs.[47, 48] The hereditary form was first identified in the late 19th century as the classic triad of glycosuria (diabetes), bronze skin pigmentation, and cirrhosis.
Other characteristic skin findings in hemochromatosis include skin atrophy, ichthyosis, partial hair loss (most often in the pubic region), and koilonychia.[49] The characteristic skin changes of hemochromatosis are believed to result from increased melanin.
The most common GI finding in hemochromatosis is hepatomegaly, which is observed in more than 95% of symptomatic patients. Overall, patients with hereditary hemochromatosis have an estimated 5% annual risk for hepatocellular carcinoma after the development of cirrhosis. Porphyria cutanea tarda is the most common porphyria occurring in adults, with a prevalence ranging from 1 case in 5,000 to 1 case in 36,000 people.
The disease can be either sporadic or familial, but, in either case, it is clear that extrinsic factors play an important role in producing a clinical manifestation of the disease. The first step of treatment involves the removal of possible triggers, including iron supplementation, alcohol, and estrogens. Other options include chloroquine and hydroxychloroquine, which form water-soluble complexes with the porphyrins, facilitating their excretion in the urine. The prevalence of hepatitis C in patients with PCT has been measured in series of patients from many countries, with rates of as high as 85% in these patients.[52, 53] Interestingly, multiple studies into the extrahepatic manifestations of patients with hepatitis C have failed to find an increased rate of PCT. The cause of the probable association between hepatitis C and PCT has been debated extensively in the literature. First identified in 1883 by Chiari, the term pancreatic fat necrosis describes the association of skin nodules with pancreatic disease. The presence of these fluctuant lesions on the skin surface has been used to identify underlying pancreatic disease.[55, 56] Often, it is the skin eruption that leads the patient to seek medical care in the first place. The development of subcutaneous nodules in cases of pancreatic disease may derive from the release of pancreatic lipolytic enzymes, a hypothesis confirmed by the biochemical discovery of persistently elevated serum lipase and trypsin levels 100-fold in one case report.
Lichen planus is an idiopathic inflammatory disorder of the skin and mucous membranes known to be associated with a variety of liver diseases. The pathogenesis of lichen planus is not clear, but several authors have postulated an association with both primary biliary cirrhosis (PBC) and chronic hepatitis B and C.[60, 61, 62, 63, 64, 65, 66] The association of PBC is particularly compelling because both diseases involve immunopathologic mechanisms that are not yet fully understood.
This syndrome was first described by Armand Trousseau in 1865, when he observed migratory thrombophlebitis in cancer patients.
Migratory thrombophlebitis presents as inflamed, red-colored, and painful linear lesions, representing a vasculitis caused by clot formation. Necrolytic migratory erythema presents as annular (ring-shaped) patches of erythema that blister, erode, and crust over.
In the literature, up to 70% of necrolytic migratory erythema is associated with glucagonomas, which are glucagon-secreting tumors of the pancreatic alpha cells.
Necrolytic acral erythema (NAE) was first described in 1996 in Egypt by el Darouti and Abu el Ela.[71] NAE manifests as a psoriasiform eruption with well-circumscribed violaceous-to-erythematous plaques with thick adherent scale.
Peutz-Jeghers syndrome (PJS) is an autosomal dominant disorder affecting approximately 1 in 10,000 live births.
GI manifestations of PJS involve the presence of multiple hamartomatous polyps occurring most commonly in the jejunum (see the image below). This small vessel vasculitis manifests clinically as palpable purpura, arthralgias, abdominal symptoms, and glomerulonephritis.[80, 81] Males are affected twice as frequently as females, with an overall incidence of 14 cases per 100,000 population.
The skin abnormalities are present in all patients at some point in their disease process and involve the presence of palpable purpuric lesions found most commonly on the buttocks and legs.
A retrospective study aimed at determining the distribution of GI involvement in seven patients with HSP found the duodenum and small intestine to be the most frequently involved sites. This uncommon blistering disorder is characterized by the development of small vesicular lesions found in a symmetric distribution of both upper and lower extensor surfaces and the scalp. Twenty percent of patients with DH have a clinically overt celiac disorder, while almost 100% of patients with DH have demonstrable pathologic changes of celiac disease on small intestinal biopsy.[87, 88] Both DH and celiac disease have been found to share class II HLA allele sites in immunogenetic studies, a finding confirmed clinically by case reports of monozygotic twins afflicted by both diseases.
The clinical manifestations of the celiac disease (also known as gluten-sensitive enteropathy and celiac sprue) are caused by the inability to absorb gluten from the diet. This rare disorder is characterized by the combination of cutaneous vascular malformations and GI bleeding due to the presence of vascular malformations.[89, 90] A clinical syndrome first described by Bean in 1958, transmission may be sporadic or autosomal dominant.
The GI manifestations of the blue rubber bleb nevus syndrome involve the presence of vascular malformations found most frequently in the small intestine and colon (although lesions have been identified in the mesentery, lung, liver, eye, and CNS.) The malformations project into the gut lumen and resemble the nodular skin lesions in appearance.
The GI manifestation of Gardner syndrome involves the presence of adenomatous polyps, which are believed to occur in 100% of patients at some point in their lifetime.
Muir-Torre Syndrome (MTS) is an autosomal dominant disorder with variable expressivity and is characterized by skin lesions with colonic malignant potential.[93] Described separately by Muir and Torre in 1967, the syndrome associates sebaceous neoplasms with an increased propensity for colorectal carcinoma. Unlike the universal presence of polyps in Gardner syndrome, patients with MTS have colonic polyposis in only approximately half the cases.
Cowden disease is a rare disease of autosomal dominant inheritance that is characterized by hamartomas of various tissues. Colonic polyps occur in up to 95% of patients with Cowden disease.[95] The most common sites of polyposis are the colon and rectum, although polyps have been documented in the esophagus, stomach, gallbladder, and small bowel.
A review of the 67 patients with Cowden disease who have undergone endoscopic evaluation over the past 30 years[96] demonstrates that most polyps discovered are nonadenomatous, although approximately 24% were adenomatous. This is a rare autosomal dominant genodermatosis with the classic triad of macrocephaly, genital lentiginosis, and intestinal polyposis. This tetrad of diffuse macular hyperpigmentation, alopecia, nail atrophy, and GI polyposis initially was described in 2 patients by Cronkhite and Canada in 1952.[97, 98] This extremely rarely identified syndrome has been further defined with the collection of more than 50 cases from the literature. Cronkhite-Canada syndrome is fatal in about one half of patients, usually as a result of malnutrition or persistent diarrhea.

The two main diseases under the umbrella of inflammatory bowel disease (IBD) are Crohn disease (CD) and ulcerative colitis (UC). CD is characterized clinically by symptoms of fever, abdominal pain, fatigability, and diarrhea that may or may not be bloody.
Cutaneous manifestations of inflammatory bowel disease are quite common, with various studies suggesting skin involvement in 9-19% of patients with UC and 9-40% in patients with CD.
Although an infrequent phenomena in patients with UC, fissures of the skin in patients with CD are common and often quite uncomfortable. Mouth findings of patients with CD include findings such as angular cheilitis, aphthous ulceration, or mucosal cobblestoning. Pyoderma gangrenosum (PG) is classically an ulcerative disease, but it can present in several forms, including ulcerative, bullous, pustular, and superficial. PG is most commonly associated with UC; therefore, an evaluation of the colon should be considered in all patients presenting with PG.
This relatively common dermatologic finding presents as tender, nonulcerative, red nodules found most frequently on the lower legs.
Immunosuppressive medications used to treat IBD can lead to an increase in the risk of skin cancers, particularly in patients on thiopurines and anti-TNF therapy.[103] Regular skin cancer screening in this patient population may be warranted.
1) is a common chronic, superficial inflammatory disease of the scalp, face (especially the eyebrows and nasolabial folds), ears, and central chest, affecting 2% to 5% of the population. Patients who have had a cerebrovascular accident (CVA) can develop seborrheic dermatitis on the scalp in a unilateral distribution, corresponding to the affected hemisphere. Alternatively, fluconazole 400 mg (one dose) may be effective in combination with a mild topical corticosteroid. 2), the most common benign cutaneous neoplasms, are warty, age-related hyperkeratotic papules and plaques that appear anywhere on the body, most commonly the trunk. 3), or hives, is most often caused by medication (commonly penicillin or other antibiotics, sulfa drugs, aspirin) or food (shellfish, nuts, chocolate), and less often by infection. Wheals in a fixed location for more than 24 hours suggest the possibility of urticarial vasculitis and warrant a skin biopsy. 4), a cutaneous hypersensitivity reaction, is usually caused by infection (herpes simplex virus or Mycoplasma pneumoniae) and less commonly by drug sensitivity (sulfonamides, barbiturates, antibiotics). 5) is characterized by a focal or generalized distribution of depigmented macules and patches. 6), the most common type of panniculitis, is characterized by painful, erythematous nodules on the shins and occasionally elsewhere.
Other infectious causes include tuberculosis, gastrointestinal (GI) infections with Yersinia, Salmonella, or Shigella, and systemic fungal infections.
7) is an uncommon chronic and debilitating blistering disease characterized by painful mucosal erosions and flaccid blisters that become erosive. 8) is the most common bullous disease and is characterized by large, tense subepidermal blisters, which are often pruritic.
Prognosis is influenced by age and general condition of the patient, not by extent of disease activity.3 Treatment of older patients in poor health requires caution. 9) is an uncommon bullous disease characterized by skin fragility, milia (small cysts), scarring alopecia, and nail dystrophy. 11) is an uncommon condition characterized by unilateral eczematous plaque of the nipple and areola.
Extramammary Paget's disease affects older adults and is often associated with an underlying adnexal (apocrine) carcinoma or an underlying cancer of the genitourinary tract or distal gastrointestinal tract. Occasionally, acanthosis nigricans is a marker of an underlying adenocarcinoma, especially of the gastrointestinal tract (60% gastric).
Treatment for types II and III includes weight loss and treatment of the underlying endocrine disorder, if applicable. 13), or acute febrile neutrophilic dermatosis, has a strong association with acute myelocytic or myelomonocytic leukemia. Affected patients have papules on the eyelids and extremities that become purpuric and ecchymotic due to increased blood vessel fragility secondary to amyloid infiltration of the vessels.
15), characterized by intractable stomatitis and blisters on the trunk and extremities, has features of pemphigus and erythema multiforme.
16), an acronym for lentigines, electrocardiographic changes, ocular telorism, pulmonary stenosis, abnormal genitalia, retarded growth, and deafness. Recognition of these syndromes is critical because identification and removal of the associated atrial myxomas may be lifesaving. 17) is characterized by yellow papules over redundant skin folds on the neck, abdomen, and groin, giving the skin the appearance of plucked chicken skin. Ehlers-Danlos syndrome is characterized by abnormalities in collagen biosynthesis, which can affect many organ systems.
Genetic testing for specific mutations has demonstrated redundancy and has reduced Ehlers-Danlos syndrome from eleven to seven types. Asymmetric fusiform swelling of the distal interphalangeal joints (sausage digits), in association with oligoarthritis and tenosynovitis can be seen in up to 70% of PsA patients.
20) is characterized by annular pink to red plaques in a sun-exposed, shawl-like distribution on the chest, back, and arms. The localized form, known as morphea, begins as erythematous patches that evolve into dusky, hypopigmented, indurated plaques with violaceous borders, usually on the trunk. In adults, dermatomyositis has a strong association with neoplasm, usually an adenocarcinoma of the breast, gastrointestinal tract, or lung.
25) is a chronic, intensely pruritic blistering disease characterized by symmetric grouped vesicles, papules, and wheals on the elbows, knees, scalp, and buttocks. When inherited, acrodermatitis enteropathica results from a mutation in SLC39A, which encodes an intestinal zinc transporter.8 In infants, deficiency can follow breast-feeding, when maternal breast milk contains low levels of zinc. 26) associated with circulating type II cryoglobulins, usually yields palpable purpura on the lower extremities. 27) is characterized by violaceous, flat, polygonal papules, often on the flexor aspects of the wrists, trunk, medial thighs, genitalia, and oral mucosa. This syndrome results from an inactivating germline mutation of the DNA mismatch repair genes, most often MSH-2. The polyps are usually benign with low malignant potential, but patients have a 10 to 18 times greater lifetime risk of cancer, especially GI malignancies. Nephrogenic systemic fibrosis occurs in patients who have end-stage renal disease and are on dialysis and occasionally in patients with acute renal failure or after kidney transplantation. Patients have a significantly increased risk of renal oncocytoma and chromophobe renal carcinoma. Porphyria cutanea tarda, the most common porphyria, is a hepatic porphyria with acquired and sporadic forms (Fig. Manifestations of porphyria cutanea tarda include photosensitivity, skin fragility, bullae and erosions on sun-exposed skin (especially dorsal hands), and hypertrichosis. Medications (NSAIDs [especially naproxen], furosemide, and tetracycline) are the most common cause of pseudoporphyria.
Box 1 outlines the most common cutaneous manifestations of diabetes, arranged by frequency of occurrence (most to least frequent).
From acute febrile neutrophilic dermatosis to neutrophilic disease: Forty years of clinical research.
This normally occurs in the ankles, feet, and legs but it can also affect any area of your body.
With diabetes and metabolic syndrome growing at skyrocketing rates, it’s now very common to suffer from swollen legs, feet and ankles due to poor circulation and cardiovascular problems, as well as common injuries. Lecithin Seeds – This is an effective treatment for chronic or long term foot swelling. Mustard Oil – It has shown that massaging your foot with warm mustard oil will help to relieve swelling and pain in the feet and ankles. Apple Cider Vinegar – Applying this to the affected area will help to reduce the excess of fluid in your foot or ankle and relieve swelling and pain in the affected body part. Exercise – This will help by taking pressure off the leg and reducing any swelling you may have. Molasses and Saunf Drink – Boil one or two glasses of water with a half teaspoon of molasses and a tablespoon of saunf.
She loves to write about natural health solutions, women health, nutrition, diet and green living. The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment.
Supporting evidence includes lack of clonality, multifocality, symmetry, absence of metastasis, and spontaneous regression with immune reconstitution.
Although the classic KS lesions tend to occur on the legs and feet, the epidemic KS lesions are more common on the face and trunk. In patients with widespread disease, careful consideration must be given to potential adverse effects.[14] Amongst the agents that attain a 30% response rate are interferons, antiviral agents (eg, zidovudine), cytotoxic agents (eg, vinblastine, etoposide), and combination therapy. The GI tract may be involved at any level, although the most frequently afflicted sites (in order) are the small intestine, stomach, and esophagus.
Although the earlier diagnosis of iron deficiency and the ready availability of iron replacement have made this disease less common, the diagnosis of Plummer-Vinson syndrome nonetheless should be considered in patients presenting with long-standing intermittent dysphagia.
In 5-10% of patients with a postcricoid web, esophageal carcinoma eventually may develop (see the image below).
Note the 2 small openings within the web at the 2- and 6-o'clock positions, representing a significantly compromised proximal esophageal lumen.
Treatment involves iron supplementation, which often leads to rapid resolution of the dysphagia. The disease is divided clinically into the following three forms depending on the layer in which blister formation occurs: dystrophic (beneath lamina densa), junctional (within the lamina lucida), and simplex (intraepidermal).
In junctional EB, failure to thrive and protein-losing enteropathy (PLE) were the prominent findings. The lesions can be seen most prominently at the 2-o'clock position proximally and the 3-o'clock position distally. As many as 90% of patients with SSc demonstrate GI manifestations.[22] As in other organ systems, GI disease in SSc results from the excess collagen production, enhanced immunologic activity, and flawed cellular immune response. As with other forms of reflux esophagitis, Barrett esophagus may develop, with the accompanying potential to transform to adenocarcinoma. Changes within the large intestine may result in chronic constipation, fecal impaction, and bowel obstruction. Colon hypomotility is the most common complication, resulting in constipation and evacuation difficulty. It is characterized by loss of cell-to-cell adhesion in the epithelial suprabasal layer, leading to superficial, easily ruptured blisters. A thorough workup of the patient should also be done, with at least a chest radiograph, CBC count, and liver panel, but also other imaging directed by the patienta€™s symptoms.
Tumor products may have their effect on skin through activation of insulinlike growth factors or their receptors in the skin. More than 90% of patients with tripe palms have an underlying malignancy, mostly commonly of gastric or pulmonary etiology.[29] The malignancies associated with acanthosis nigricans include adenocarcinoma (85% of cases), of which gastric carcinoma is present in 60%. In patients with successful tumor resection, the skin lesions often disappear spontaneously over time. As such, this finding may be more useful in younger patients, when there is a rapid increase in the size and number of lesions or when other suspicious findings such as acanthosis nigricans, florid cutaneous papillomatosis, weight loss, dysphagia, or changes in bowel movements are present. Mayo in 1928, and the Sister's name was not attached to the lesion until the 11th edition of Hamilton Bailey's Physical Signs in Clinical Surgery. The patches of hyperdensity within the liver are the result of previous embolization procedures. The age of onset for the telangiectases is most often the third decade of life, although earlier presentations may occur during adolescence.
The epistaxis results from spontaneous bleeding from telangiectases of the nasal mucosa and is generally recurrent.
A ring of less vascularized tissue surrounding the GI lesions is a characteristic finding on endoscopy.
The actual presence of iron seen in dermal sweat glands and the basal layer of the epidermis lead to the pigmentation seen in the late stages.
Despite clinical findings of functional liver impairment (eg, hair loss, gynecomastia, testicular shrinkage), laboratory findings are generally unimpressive.
Primary treatment involves phlebotomy and chelating agents, with conventional management of hepatic failure should this condition arise. Porphyria cutanea tarda results from the decreased activity of the enzyme uroporphyrinogen decarboxylase (UROD), the fifth enzyme in the heme biosynthetic pathway. Endogenous and exogenous factors (eg, alcohol, iron, estrogen, porphyrins, chronic hepatitis C virus infection, polychlorinated biphenyls, polychlorinated cyclic hydrocarbons) produce oxidative stress on the liver, leading to inhibition or decreased production of UROD.
If symptoms persist, repeated phlebotomy decreases the total iron load and leads to significant clinical improvement. Antimalarial therapy can be quite dangerous in patients with porphyria; it may precipitate massive hepatic injury. This disparity may be explained by the fact that the background rate of PCT is relatively low in the populations in these latter studies and that finding an association would require study of larger populations of patients. Some contend that hepatitis C serves to trigger attacks of PCT in predisposed patients, but this theory remains to be conclusively proven.
The dermatologic lesions can be painless or painful and tend to appear first on the legs followed by the buttocks and trunk.[54] Initial presentation may include pruritus of lower extremities with associated splotchy erythema.
Pancreatic fat necrosis occurs in up to 65% of patients with pancreatic cancer and in up to 22% of patients with pancreatitis.
However, not all authors have agreed that these associations occur at any more than the expected random frequency. Two years later, he diagnosed the syndrome on himself and eventually succumbed to gastric cancer. When observing a patient, all stages of the lesions, from patches, to vesicles, to crusts, may be seen synchronously. However, necrolytic migratory erythema can also be associated with liver disease and intestinal malabsorption.[70] The pathogenesis of this condition is unknown. However, owing to the poor prognosis of glucagonomas, the outcome of this condition is also poor.
The lesions are associated with burning or pruritus and are limited to an acral distribution.
PJS is characterized by the presence of mucocutaneous hyperpigmentation together with GI polyposis.
Patients with a clinical diagnosis of PJS should have ongoing surveillance of all these organ systems. The diagnosis usually is made in early childhood, but it also can present in infancy or adulthood.[82] The disease is believed to be due to the deposition of immunoglobulin A (IgA)a€“mediated immune complexes throughout the body. The use of corticosteroids has been reported to be helpful in reducing the GI symptoms.[85] The natural course of the disease is complete resolution over weeks to months. First described in 1884 by Louis Duhring, MD, the usual age of onset of dermatitis herpetiformis (DH) is in the third decade of life. The clinical manifestations most often present in birth or early childhood, although some cases may not be identified until adulthood. Clinically, these malformations usually cause occult bleeding, although frank melena, hematochezia, or even intussusception may occur. The polyps are first noted at an average age of 22 years and tend to occur in large numbers (>100) in any part of the colon. The defect has been attributed to a DNA mismatch repair gene mutation, a discovery that now allows physicians to screen relatives of affected patients.
However, visceral malignancies develop in a large proportion of patients, most frequently in the colon (51% of all primary tumors). Dermatologic findings include trichilemmomas (ie, skin colored papules around facial orifices), acral keratoses, and oral papillomas. Of particular concern are the 12 patients (18%) who had adenomatous colonic and rectal polyps, an established risk factor for colorectal cancer. Given overlap with Cowden syndrome with phenotypic expression and similar allelic syndromes (both with PTEN mutations), both diseases are collectively referred to as PTEN hamartoma-tumor syndrome. Prominent hamartomatous polyposis occurs in 35-45% of cases of Bannayan-Riley-Ruvalcaba syndrome but is not associated with an increased risk of malignancy.
The presence of hamartomatous polyps is quite common, with transformation to malignancy occurring in some cases. Therapy involves nutritional support and careful observation for metabolic derangements over the course of the illness.[100] One case report noted a temporal association with the initiation of ranitidine therapy and resolution of clinical symptoms in one patient, although the mechanism of response to therapy in this patient is unclear.
The disease most often is diagnosed in patients aged 15-35 years, although it has been described in people of all ages. Metastatic CD lesions present as linear ulcerations that appear like a knife-cut both on the skin and the mucosa. The most common form of PG is the ulcerative type, but notable is that when the pustular variant is seen, it is most commonly found in patients with IBD. Note the rolled-up, edematous, and undermined border with the surrounding halo of bright-red erythema. Erythema nodosum lesions usually parallel the intestinal disease, which provides helpful information on the overall disease. Clinically, the disease is characterized by thin erythematous plaques, often with a fine, greasy scale. Rarely, seborrheic keratoses indicate an underlying adenocarcinoma of the gastrointestinal tract if they appear suddenly in great numbers (sign of Leser-Trélat).
Chronic idiopathic urticaria for which no trigger can be identified often requires further testing such as serum radioallergosorbent testing (RAST) or skin prick-patch testing. Erythema nodosum occurs most commonly in young women, with a peak incidence between 20 and 40 years.1 In addition to the cutaneous findings, patients can have fever, malaise, arthralgias, or arthritis. Less common causes include drug sensitivity (sulfonamides, salicylates, iodides, oral contraceptives or hormone replacement therapy), and a variety of systemic diseases, most often inflammatory bowel disease (Crohn's disease more than ulcerative colitis) and sarcoidosis. Skin disease typically follows trauma and occurs primarily on the hands, feet, elbows, and knees.
Malignant acanthosis nigricans has a sudden onset and more extensive distribution, including the face, palms, and trunk.
Topical treatments including tretinoin, calcipotriol, urea, and salicylic acid may be helpful.
Affected patients, usually middle-aged women, have painful erythematous to violaceous plaques on the face, extremities, and trunk.
Direct immunofluorescence reveals deposition of IgG intercellularly and at the dermal-epidermal junction. Erythema gyratum repens has a strong association with lung cancer; the association with breast, cervical, and gastrointestinal cancers is less strong.
Pseudoxanthoma elasticum represents a defect in elastic fibers, which become brittle and calcified.
Patients with vascular (type IV) Ehlers-Danlos syndrome are prone to arterial rupture and have the highest mortality.
Skin disease, affecting 25% to 35% of patients, includes red to purple indurated plaques of the nose (lupus pernio) (Fig.
Other presentations include symmetric polyarticular arthritis (15%), distal interphalangeal joint disease with nail damage (16%), arthritis mutilans with erosion of the phalanges (5%), and ankylosing spondylitis (5%). 19), usually localized to the head or neck, is characterized by atrophic, scarring plaques on sun-exposed areas. The systemic or generalized forms are subdivided into CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) and progressive systemic sclerosis. Implicated organisms include Campylobacter, Shigella, Salmonella, Ureaplasma, and Yersinia species. Affected patients can have fever, arthralgia, and myalgia, and, occasionally, Bell's palsy. Biopsy reveals a characteristic neutrophilic infiltrate, and direct immunofluorescence demonstrates deposition of IgA at the dermal-epidermal junction. Lichen planus also occurs with primary biliary cirrhosis and hepatitis B virus immunization. Recurrent epistaxis is the most common presenting manifestation of the syndrome, affecting approximately 85% to 90% of patients. The ulcers often follow trauma (pathergy) and begin as pustules or nodules that ulcerate and extend centrifugally.9 All body areas may be involved, but the legs are the most common site. Nephrogenic systemic fibrosis is characterized by thick, indurated plaques on the extremities and the trunk.
It can be very painful and if not treated right away, can cause permanent damage to your lower limbs. Put your leg up in front of you so it is elevated and apply an ice pack to the swollen area, or a bag of ice wrapped in a clean towel.
Get a slice of cucumber and place it on your foot, wrapping it with a cotton cloth or a bandage. Place your foot in a pan of warm water and pour in ? a cup of salt to jumpstart the swelling reduction process.

It is recommended to rotate your ankle 10 times every 30 minutes to encourage blood flow in the affected area. This will help to remove any salt that is in your urine and in turn will help to reduce swelling in your foot or ankle. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Originally described by Kaposi in 1872, the prevalence of the epidemic form of KS has risen dramatically in the United States over the past 20 years with the spread of AIDS.
For HIV-related KS with a low CD4 count or high viral load, antiretroviral therapy is the first-line therapy[15] ; other modalities include topical alitretinoin gel, daunorubicin, doxorubicin, paclitaxel, and interferon alfa-2b. Oral lesions are most likely to affect the hard palate, followed in order of frequency by the gingiva and the tongue. Reprinted with permission from Gastrointestinal Endoscopy, Second edition, Gower Medical Publishing, New York, 1991. In patients who continue to complain of dysphagia, therapy involves rupture of the esophageal web either by endoscopy or bougienage.
Mutations in genes encoding structural proteins at the dermoepidermal junction and basement membrane have been implicated in different forms of EB. The most commonly affected areas are the esophagus, the mid duodenum, jejunum, and large intestine.
Small intestine hypomotility is the primary abnormality, which can cause nausea, vomiting, bloating, distension, anorexia, and abdominal pain.
Colonic telangiectasias are common and may cause overt bleeding, which can result in anemia. Mucosal sites are commonly are involved, including the oral mucosa (often the presenting site), anus, cervix, and conjunctivae.
The first stage presents with poorly defined psoriasiform plaques involving the ears, nose, nails, fingers, and toes. Alpha-transforming growth factors produced by tumor cells may have a role in malignant acanthosis nigricans through epidermal growth factor receptors found in the skin.
Other reported sites of malignancy include the lung, bladder, endometrium, adrenal, bile duct, kidneys, thyroid, breast, liver, larynx, cervix, ovaries, prostate, and testicles. The cutaneous finding is a firm, nontender nodule of red or purple hue that represents a metastasis from the primary tumor.
Although the distribution of lesions and associated bleeding diathesis are clinically suggestive of hereditary hemorrhagic telangiectasia, it may occasionally be difficult to distinguish from similar cutaneous findings seen in generalized essential telangiectasia. In about one half of patients, the frequency and seriousness of the epistaxis increases as the patient ages, leading to blood transfusions in as many as 30% of patients. Bleeding from these telangiectases tends to begin in the fifth or sixth decade of life and often can be severe. Although the prevalence of these lesions is unknown, they have been blamed for portal hypertension with esophageal varices in some cases. This discoloration has a characteristic metallic gray or bronze-brown color that is generally diffuse, but it may be increased in areas of scars or on the face, neck, extensor surfaces of the arms, and genitalia. Treatment of these patients with phlebotomy or chelating agents results in a decrease in skin pigmentation over time. Because hemochromatosis is not an inflammatory disease, liver enzyme (ie, aspartate aminotransferase, alanine aminotransferase) levels can be normal, even in advanced disease.
Cutaneous findings are characterized by skin photosensitivity with increased skin fragility, facial hypertrichosis, blisters, scarring with milia formation, and skin hyperpigmentation on the hands and other sun-exposed areas. The pathogenesis of iron in porphyria cutanea tarda also provides the link to hereditary hemochromatosis. Phlebotomy may induce clinical remission, reduce urinary porphyrins, and improve the sclerodermalike skin changes, but it is not proven to improve liver histology. Therefore, doses should be initiated at low doses (125 mg, 2-3 times per wk) to reduce the likelihood of acute hepatic injury and retinopathy.
Alternatively, others have hypothesized that patients with PCT are somehow more susceptible to hepatitis C infection. A characteristic finding on close (through a lens) examination is the presence of white or gray linear markings known as Wickham striae. Clinical diagnosis requires histologic identification of intestinal hamartomatous polyps in conjunction with 2 of 3 additional clinical criteria that include small bowel polyposis, mucocutaneous melanotic pigmentation, and a family history of PJS. Symptoms may include abdominal pain, bleeding, rectal prolapse, or obstruction due to intussusception.
A variety of triggers for this process have been proposed, including insect bites, seasonal allergens, upper respiratory tract infections, various medications, and foods.
Definitive diagnosis can be obtained through direct immunofluorescence of early lesions (aged <24 h), revealing a perivascular deposition of IgA.
However, the presentation of HSP differs significantly with age; older patients exhibit much more severe renal and extrarenal manifestations than younger patients.
Most patients experience severe pruritus as a result of the skin lesions, although some are almost completely asymptomatic. Chronic problems with malabsorption eventually may lead to iron or folate-deficient anemia states. These lesions, which also can be found in the duodenum around the ampulla of Vater, eventually progress to carcinoma in almost all patients if left untreated.
Other sites of carcinoma include the larynx, duodenum, ileum, stomach, uterus, ovary, ureter, kidney, and bladder. The disease is associated with a variety of malignancies, including breast, thyroid, endometrial, cervical, and colon cancer.
Although the precise risk of colon cancer in patients with Cowden disease has not been firmly established, all patients should receive a thorough initial GI workup with follow-up care as appropriate.
Mucocutaneous findings include vascular malformations, lipomatosis, speckled lentigines of the penis and vulva, facial acanthosis nigricansa€’like lesions, and multiple acrochordons. Polyps can be located anywhere along the GI tract, with a preference for colonic or rectal localization. The hyperpigmented macules and plaques (85% of patients) most often occur on the upper extremities but may be diffusely distributed. Since there is large overlap between the skin findings in CD and UC, the diseases are considered together in this discussion.
Histologically, the inflammatory lesions of CD extend through all layers of the gut lining and may extend into the mesentery or local lymphatics. The groups have disease-specific cutaneous manifestations, reactive cutaneous manifestations, associated cutaneous disorders, and secondary cutaneous manifestations due to complications of IBD or IBD therapy (see Table 2 below).
The National Cooperative Crohn's Disease study demonstrated that patients with colonic involvement are significantly more likely to have perianal fissures than those with CD affecting other areas of bowel (40% compared to 25%). Importantly, PG does necessarily parallel the intestinal disease; therefore, patients may need further therapy to treat the PG Some patients require systemic treatment with oral corticosteroids, cyclosporine, mycophenolate mofetil, antitumor necrosis factor (TNF) therapy, and other immunosuppressive agents. Studies have shown up to 3.5% of patients on anti-TNF therapy for IBD may develop psoriasis. Vitiligo commonly occurs in periorificial areas (mouth, orbits, vagina, anus) or at sites of trauma (hands, elbows, knees). Biopsy reveals characteristic suprabasilar acantholysis and intraepidermal bullae formation. Immunofluorescence is similar to bullous pemphigoid, with IgG deposition at the dermal-epidermal junction. Skin biopsy reveals swollen, fragmented elastic fibers, and fundoscopic examination reveals angioid streaks in Bruch's membrane. 18), midfacial papules, annular plaques, and plaques or nodules on the trunk and extremities. Presence of anticentromere antibodies correlates with CREST syndrome; SCL-70 antibodies correlate with progressive systemic sclerosis.
Affected patients, usually men, often have vesicles and crusted plaques on the penis (circinate balanitis) and erythematous pustules and papules on the palms and soles (keratoderma blennorrhagicum) that can mimic pustular psoriasis. Most patients have an asymptomatic gluten-sensitive enteropathy or, less commonly, thyroid disease.
Oral erosive lichen planus is the most common expression of lichen planus in hepatitis C patients. Telangiectases can involve the lungs, liver, brain, eyes, and gastrointestinal tract; hemorrhage can occur at any site. Fifty percent of patients have underlying rheumatoid arthritis or inflammatory bowel disease or, less often, a paraproteinemia, usually an IgA gammopathy. It is caused by a deficiency in uroporphyrinogen decarboxylase, leading to the accumulation of uroporphyrin in the urine and serum.
Direct immunofluorescence reveals IgG and C3 at the dermal-epidermal junction and in vessel walls. Never disregard professional medical advice or delay in seeking it because of something you have read on this site! In patients with non-HIVa€“associated KS, both the skin and GI lesions tend to have a relatively indolent course. GOR and dysphagia affected most of the patients with recessive dystrophic EB, with two thirds also having significant esophageal strictures. Clinical manifestations of SSc are heterogeneous and vary as a result of type of disease (limited or diffuse) and organ involvement. Although these particular lesions appear flat, some GI telangiectasias may be slightly elevated. Finally, overt or occult bleeding may develop as a result of trauma to telangiectasias, which may appear anywhere throughout the bowel.
Anorectal involvement can also occur, leading to chronic diarrhea, fecal incontinence, and rectal prolapse. Nail involvement is common in early disease stages, and the patient may report abnormal nails with painful nail folds. After a long period of stability, the AN became much more severe and involved other parts of his skin, including the eyelids and scalp, prompting the search for malignancy. One other hypothesis is that lytic factors produced by tumor cells may weaken the extracellular matrix of the skin, predisposing to acanthosis nigricans.
It presents with the rapid onset of numerous verrucous papules and nodules, which are very similar in appearance to viral warts.[37] Typically, these lesions first appear on the dorsal surface of the hands and wrists, and later spread to other body regions.
The nodule most often results from contiguous extension of the tumor from the peritoneum, although lymphatic and venous pathways likely contribute in some cases. Diagnosis involves the presence of elevated gamma-glutamyltransferase (GGT) or alkaline phosphatase levels, with confirmation by CT scan or color Doppler ultrasound. Approximately 20% of patients also have pigmentation of the buccal mucosa or the conjunctiva.
In patients with long-standing untreated hemochromatosis, cirrhosis may develop, leading to hepatocellular carcinoma in as many as 30% of patients. All patients with porphyria cutanea tarda should undergo screening for hepatitis virus infection and hemochromatosis.[50, 51] Diagnosis of porphyria cutanea tarda involves the discovery of increased porphyrins in the blood, liver, stool, and urine. Such therapy should be attempted only when other therapy has failed and with a clear understanding of the risks involved.
In either case, the probable linkage between these 2 diseases suggests that patients with PCT should be tested for hepatitis C and that their treatment may be augmented by considering concomitant therapy for hepatitis C. The nodules have been described to spontaneously drain white creamy exudate, after which the lesion heals with hyperpigmentation and local scar formation.
They may be found anywhere on the skin, although certain sites, such as the wrists, ankles, shins, lower back, and genitalia, are most commonly affected. Precipitating factors for oral lesions include mechanical trauma from dental procedures and dental prostheses, heat and irritation from tobacco products, and oral habits to include lip and cheek chewing.
The skin findings first appear in infancy or early childhood and involve blue-brown macular lesions of 1-10 mm. Renal findings in patients with this disease include glomerulonephritis with the presence of proteinuria, microscopic hematuria, and often red cell casts. Pruritus can lead to significant excoriation and secondary changes, leading to misdiagnosis of atopic dermatitis.
Therapy involves the adoption of a gluten-free diet, with avoidance of foods such as wheat, barley, and rye.
For patients with mild blood losses over time, therapeutic intervention can involve monitoring, iron replacement, and blood transfusions when needed. Osteomas, located most frequently in the mandible or maxilla, occur in at least 75% of patients with Gardner syndrome. The malignancies associated with MTS tend to be less aggressive than those unassociated with the syndrome, leading to a better prognosis than one might otherwise suppose given the malignancy.
Presentation of polyposis may not manifest until middle age, requiring routine follow-up visits with a yearly hemoglobin test and fecal occult blood test.
Nail dystrophy (affecting 90% of patients) is seen in all fingers and toes and is characterized by onycholysis and a unique pattern of normal nail in the shape of an inverted triangle that borders up against dystrophic nail.
The disease may appear in all areas of the GI tract from the mouth[101] to the anus and often is characterized by skip lesions, areas of the bowel that are completely free of inflammation.
As with other patients with perianal fissures, treatment with topical nitroglycerin or injected botulinum toxin can be quite effective.
Classic ulcerative PG presents as a painful, ulcerative lesion with a well-defined, rolled, dusky-appearing border (see the image below).
Erythema nodosum is associated with a variety of conditions, including medications, malignancy, and infections. The disorder is often associated with autoimmune thyroid disease, insulin-dependent diabetes mellitus, pernicious anemia, or Addison's disease.
Direct immunofluorescence reveals a chicken-wire pattern of deposition of immunoglobulin (Ig) G within the epidermis.
Direct immunofluorescence reveals a linear deposition of IgG at the dermal-epidermal junction.
Associated signs of pseudoxanthoma elasticum include hypertension, peripheral vascular and coronary artery disease, retinal and gastrointestinal hemorrhage, and stroke. More than 50% of patients have sacroiliitis, correlating with the presence of HLA-B27 antigen, but few patients have the classic triad of urethritis, conjunctivitis, and arthritis. Primary endemic areas in the United States are New England, the upper Midwest, and the Pacific Northwest. Approximately 70% of patients have circulating IgA antibodies against the smooth muscle cell endomysium (antiendomysial antibodies), which are somewhat peculiar to dermatitis herpetiformis.
Treatment includes topical and intralesional corticosteroids, topical immunomodulators, and phototherapy.
Autopsies have demonstrated that disease is not limited to the skin; visceral organ and muscle fibrosis has been noted.
Dab the area until the towel dries and then repeat this process for twenty minutes, twice a day. Never put ice straight on the eyes as this can cause ice burn as well as damage to the tissue. In contrast, HIV-associated Kaposi lesions of the GI tract can have an aggressive clinical course, leading to extensive hemorrhage or partial small bowel obstruction. In lcSSc (formerly called CREST [calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias] syndrome), skin tightening is confined to the fingers, hands, and forearms distal to the elbows, with or without tightening of skin of the feet and of the legs distal to the knees. Rarely, pneumatosis cystoides intestinalis (PCI), which is characterized by intramural gas in the GI tract, may occur.
Symptoms of esophageal involvement include persistent sore throat, dysphagia, and odynophagia.
The second stage has more proximal involvement and a violaceous keratoderma with central clearing.
Independent of the malignant variant, other identified associations include obesity, familial trait, diabetes mellitus, other endocrine disorders, or drugs (eg, corticosteroids, estrogens, nicotinic acid). The skin lesions of malignant acanthosis nigricans often are discovered prior to the cancer diagnosis.
Approximately 90% of these malignancies are adenocarcinoma, with gastric or ovarian being the most commonly discovered primary malignancy.
Treatment has tended to be conservative, with limited data on chemoembolization and surgical ligation suggesting that both may be effective when therapeutic intervention is deemed necessary. Cirrhosis or its complications account for approximately 89% of hemochromatosis related deaths. The pathologic correlate includes the presence of subcutaneous fat necrosis together with ghostlike calcified fat cells containing thick shadowy walls and no nucleus. Both cutaneous and oral lesions exhibit KA¶bner phenomenon, occurring at sites of previous trauma.
The lesions most commonly are found on the lips (95% of patients)[76] and buccal mucosa (83%). Musculoskeletal pain can be diffuse and severe in some cases, although less than 20% of patients initially present with this symptom.
The characteristic direct immunofluorescence finding is granular deposition of IgA within the dermal papillae on direct immunofluorescence.
The initiation of therapy with dapsone or sulfapyridine results in a dramatic improvement in both GI and dermatologic symptoms; a prompt improvement following therapy can confirm the diagnosis. In severe cases, treatment may require endoscopic therapy with bipolar electrocautery or YAG laser, or even surgical resection of affected areas. Other associated findings include desmoid tumors (visceral and nonvisceral types), pilomatricomal cysts, dental abnormalities, and pigmented ocular fundal lesions termed congenital hypertrophy of the retinal epithelium.
Treatment of patients with MTS involves regular screening for GI and genitourinary cancers.
During childhood, symptoms include massive watery diarrhea, abdominal pain, painless rectal bleeding, and chronic anemia.
Although UC affects patients in similar age groups, this disease is more likely to result in bloody diarrhea and abdominal distension.
The lesions start as small pustules, which subsequently expand to form the larger noninfectious ulcer.
In one large series of patients, 7% of patients with UC had erythema nodosum, with a less frequent association in CD. Erythema nodosum, an acute, painful panniculitis that usually affects the shins, is the most common nonspecific cutaneous manifestation of sarcoidosis. In dcSSc, more rapid progression of skin fibrosis occurs, with proximal extremities and trunk involvement.
Because the patient may require many years of therapy, careful consideration for the adverse effects of various promotility or antimotility agents should be undertaken. Liver and biliary involvement in SSc is relatively rare; however, primary biliary cirrhosis (PBC) is the most common hepatobiliary manifestation in SSc patients. Other frequently affected sites include the palms of the hands, fingers, nose, gingiva, eyelids, and hard palate.
Adults, in comparison to children, seem to more commonly present with symmetric arthralgias and arthritis of knees and ankles.
The pathologic appearance of this disease demonstrates continuous colonic involvement from the rectum to the junction with the terminal ileum, with the inflammation confined to the mucosal layer. PG can occur as a solitary entity, but up to 50% of patients with PG have an underlying systemic disorder such as IBD.
On endoscopy, the lesions can appear as bullae or irregular erosions covered in white exudate and an erythematous border.
The nodule is easy to biopsy and may save the patient from having to undergo diagnostic surgery. Treatment for both the skin and mucous membrane lesions involves the use of local or systemic steroids, specially formulated oral preparations of topical immunomodulators, and systemic medications, many of which are immunosuppressives, for treatment-resistant cases.. Diagnosis of both diseases generally is made easily with a combination of sigmoidoscopy and barium-assisted radiologic studies. Raynaud phenomenon is present in most patients with SSc and is often the earliest manifestation of disease. Sloughing of the entire esophageal lining (esophagitis dissecans superficialis) may also occur.
Of note, the biopsy aids in successfully diagnosing the primary malignancy site in only approximately half the cases. Diarrhea affected a small proportion of children with recessive dystrophic EB with changes of colitis in the majority of patients. Skin changes usually begin with an early phase of skin edema, which presents as swollen fingers and hands, also known as the a€?puffy hand signa€?. Treatment for esophageal PV involves the administration of steroids or other immunosuppressive agents such as azathioprine, mycophenolate mofetil, methotrexate, or rituximab. In patients with severe EB of any type, nutritional deficiency, anemia, and growth retardation may develop over time, principally from the presence of oral and GI complications.

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