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Whatever you do, do not neglect the early signs because early detection can help in proper treatment of the conditions. The common conditions associated with diabetes are atherosclerosis, acanthosis nigricans, diabetic stiff skin, diabetic dermopathy and diabetic bullae or blisters. The symptom of this condition, which is caused by thickening of the arteries, is that the skin turns hairless and shiny. This is a common condition of the skin where brown or tan, raised spots appear in some places.
Diabetic stiff skin or diabetic cheiroarthropathy is the condition where the patient finds difficulty in moving his or her hand joints. Diabetic dermopathy is generally noticed in elder patients who have been suffering from diabetes for a long time.
You will be able to identify these lesions by the round or oval shape of reddish brown color.
Diabetic blisters, diabetic bullae or bullosis diabeticorum the same thing with various names. 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.
The condition of gangrene is a serious one, primarily marked by loss of adequate supply of blood to the tissues of the body, ultimately resulting in its necrosis or death.


Injury to the tissues, infection (mostly of bacterial origin) and presence of any underlying health ailment that inflicts damage to the blood carrying vessel structure form the three key underlying mechanisms that are responsible for initiation and development of irreversible tissue damage and life threatening condition of gangrene.
As already explained, one of the causes of gangrene in the toes and fingers is linked with damaged blood vessels. High level of blood glucose associated with diabetes mellitus also damages the nerves (known as peripheral neuropathy), especially the nerves in the lower extremities. The dullness or lack of sensation puts diabetic individuals at an increased risk of injuring the skin of their fingers or feet without having any realization (it mostly goes unnoticed in the feet region). The sore or foot ulcer formed takes an extended time to heal because of both, poor circulation of blood through the injured area as well as lesser number of defence cells.
Bacterial infection also forms another causative factor that makes the diabetic individual more prone to developing gangrene. Such type of infection is marked by noticeable skin discolouration and dryness along with the formation of skin blisters. The weakened immune system (seen in diabetes) further raises the risk of incurring serious infection, which later develops, into gangrene. Ocular (eye) herpes is usually caused by the herpes simplex type 1 virus (HSV-1), the same virus that causes cold sores on the lips and mouth.
More rarely, ocular herpes can be a complication of shingles, which is a reactivation of the Varicella zoster virus (the virus that causes chicken pox, which is also a member of the herpes family). In most people, eye herpes will only affect the topmost layer of the cornea, called the epithelium. The viral infection affects the retina (the light-sensitive tissue that lines the back of the eye), causing acute retinal necrosis. If the infection is in the stroma, steroid drops may be used to decrease inflammation and promote healing. If the cornea has become scarred beyond repair, a corneal transplant may be necessary to restore vision. If you believe you may have ocular herpes, you should see your eye doctor as soon as possible to begin treatment and prevent scaring and vision problems. However, if your child has developed a rash and seems unwell, or if you're worried, you should see your GP to find out the cause and for any necessary treatment.
Eczema is a long-term condition that causes the skin to become itchy, red, dry and cracked. Impetigo is a highly contagious bacterial infection of the surface layers of the skin that causes sores and blisters.
If you think your child has impetigo, see your GP for a prescription of antibiotic cream, which should clear the infection within seven to 10 days. A heat rash (prickly heat) may flare up if your child starts to sweat, for example because they are dressed in too many clothes or the environment is hot and humid. Keratosis pilaris is a common and harmless condition where the skin becomes rough and bumpy, as if covered in permanent goose pimples. It commonly affects young children aged one to five years, who tend to catch it after close physical contact with another infected child. Children tend to catch it after close physical contact with another infected adult or child – for example, during play fighting or hugging.
Hives (also known as urticaria) is a raised, red, itchy rash that appears on the skin.
Most children won't need treatment as slapped cheek syndrome is usually a mild condition that passes in a few days. Psoriasis is a skin condition that causes red, flaky, crusty patches of skin covered with silvery scales. There is no cure for psoriasis, but a range of treatments can improve symptoms and the appearance of the affected skin patches. Cellulitis is a bacterial infection of the deeper layers of the skin and the underlying tissue. It causes a red-brown spotty rash, which tends to start behind the ears and spread to the head, neck, legs and rest of the body. Most childhood rashes are not measles, but you should see your GP if you notice the above signs.
The information on this page has been adapted by NHS Wales from original content supplied by NHS Choices. The signs may be directly related to diabetes or can be the result of conditions that occur due to diabetes.
Generally, the early signs of diabetic dermopathy start with lesions appearing on the shins.
They are usually scaly in the beginning and then dissipate and then make an indent on the skin. 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. Death of cell and tissue may target any part of the body, however, it has been typically observed in the extremities, such as the toes, fingers and hands. In both, type 1 and type 2 diabetes, the raised level of sugar is capable of causing damage to the blood vessels and reducing blood supply. Owing to the nerve damage, the transmission of sensation, particularly those of pain to the brain gets impaired.
A notorious bacterial organism, Clostridium perfringes is often linked with gas gangrene; after it attacks the site of injury or sometimes, surgical wound. However, steroids can suppress the body's immune response, and in some people may aggravate the condition, leading to future flare-ups.
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The most common form is atopic eczema, which mainly affects children but can continue into adulthood. The rash can appear almost anywhere on the body, with the scalp, feet and groin being common areas. It causes a non-itchy rash on the palms of the hands and soles of the feet, and can sometimes cause mouth ulcers and a general feeling of being unwell. However, most adults are resistant to the virus, meaning they are unlikely to develop the condition if they come into contact with it.
They leave small red blotches and silver lines on the skin, which may be found on the palms of the hands or soles of the feet.
It happens when a trigger (see below) causes a protein called histamine to be released in the skin. It is estimated that about one-third of all the diabetics suffer from any of the many skin disorders. 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.
In the absence of a continuous supply of nutrient and oxygen rich blood, the cells within the body begin to fail in carrying out their normal function and finally give up.
As a result of restricted blood circulation to the extremities, such as the feet, the area becomes deprived of those cells (white blood cells) which aid in fighting off any infection.
If multiple lesions are found on the shins and the person is yet to be diagnosed with diabetes, then the time has come to go for a check up as he or she may have already reached an advanced stage of diabetes.
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. Swelling and inflammation resulting from the infection causes the local temperature of the area involved to be slightly elevated, and also leads to pain. 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. Erythema nodosum, an acute, painful panniculitis that usually affects the shins, is the most common nonspecific cutaneous manifestation of sarcoidosis.
There are two types of blisters – one is filled with clear, sterile liquid while the other is filled with blood. Type 1 virus is the usual cause of cold sores around the mouth, and herpes simplex infection in the eye.
It is commonly passed on by close contact such as kisses from a family member who has a cold sore.) In many people the primary infection does not cause any symptoms, although in some cases symptoms do occur.
A minor and temporary inflammation of the conjunctiva (conjunctivitis) or eyelids (blepharitis) may occur with active infection, often at the same time as the cornea is infected. Often people who get active eye infection will have had previous cold sores during their lifetime. They may also put some stain on the front of your eye to show up any irregular areas on the cornea.
If your doctor suspects a herpes eye infection you will usually be referred urgently to an eye specialist. This is to confirm the diagnosis and to determine whether the infection is in the top layer of the cornea (epithelial keratitis), or if the deeper layers are involved (stromal keratitis).
These do not kill the virus but stop it from multiplying further until the infection clears. You are likely to be kept under review, until the infection clears, to check that the cornea does not become infected. Note: if you have herpes simplex eye infection, you should stop wearing any contact lens until 24 hours after your symptoms and the infection have completely gone away. As mentioned above, these occur if the virus reactivates from time to time - similar to cold sores. A recurrent infection may occur any time between a few weeks and many years after the first active infection. At least half of people who have one episode of active infection will have a recurrence within 10 years of the first.
If recurrences are frequent or severe, then your eye specialist may advise that you take antiviral tablets each day to prevent episodes of active infection. Studies have shown that, on average, the number of recurrences is roughly halved in people who take regular antiviral tablets.
Some people say that episodes of active herpes infection may be triggered by strong sunlight. It is also possible that active infection may be triggered if you are run down or unwell for another reason. Some women find that they get recurrences around the time of their period but again there is limited evidence to support this. However, severe and recurrent herpes simplex eye infections may lead to serious scarring, impaired vision and even blindness in some cases.




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