Pityriasis Rosea Pityriasis rosea is a common skin disease.

It appears as a rash that can last from several weeks to several months. The way the rash looks may differ from person to person. It most often develops in the spring and the fall, and seems to favor adolescents and young adults. Pityriasis rosea is uncommon in those over 60 years old. It may last months longer when it occurs in this age group. Usually there are no permanent marks as a result of this disease, although some darkerskinned persons may develop long-lasting flat brown spots. Pityriasis rosea is an acute, self-limiting skin eruption with a distinctive and constant course, with an initial lesion or grouping of lesions ("herald patch") that is followed after 1 or 2 weeks by a generalized, much more spread, secondary rash with a typical distribution and lasting for about 6 weeks. Pityriasis rosea is a rash that occurs most commonly in people between the ages of 10 and 35, but may occur at any age. The rash can last from several weeks to several months. Usually there are no permanent marks as a result of this condition, although some darker-skinned persons may develop long-lasting flat brown spots that eventually fade. It may occur at anytime of year, but pityriasis rosea is most common in the spring and fall. Signs and Symptoms Pityriasis rosea usually begins with a large, scaly, pink patch on the chest or back, which is called a "herald" or "mother" patch. It is frequently confused with ringworm, but antifungal creams do not help because it is not a fungus.Within a week or two, more pink patches appear on the chest, back, arms, and legs. Patches may also occur on the neck, but rarely on the face. The patches are oval and may form a pattern over the back that resembles the outline of a Christmas tree. Sometimes the disease can produce a very severe and widespread skin eruption. About half the patients will have some itching, especially when they become warm. Physical activities like jogging and running, or bathing in hot water, may cause the rash to temporarily worsen or become more obvious. There may be other symptoms including fatigue and aching. The rash usually fades and disappears within six to eight weeks, but can sometimes last much longer. The skin rash follows a very distinctive pattern. In 3/4 of the cases, a single, isolated oval scaly patch (the "herald patch") appears on the body, particularly on the trunk, upper arms, neck, or thighs. Often, the herald patch is mistaken for ringworm (tinea corporis) or eczema. Within a week or two more pink patches will occur on the body and on the arms and legs. These patches often form a pattern over the back resembling the outline of an evergreen tree with dropping branches. Patches may also appear on the neck and, rarely, on the face. These spots usually are smaller than the "herald" patch. The rash begins to heal after 2-4 weeks and is usually gone by 6-14. Pityriasis rosea does not seem to spread from person to person and it usually occurs only once in a lifetime.Sometimes the disease can cause a more severe skin

reaction. Some patients with this disease will have some itching that can be severe, especially when the patient becomes overheated. Occasionally there may be other symptoms, including tiredness and aching. The rash usually fades and disappears within six weeks but can sometimes last much longer. Physical activity, like jogging or running, or bathing in hot water may cause the rash to temporarily worsen or reappear. In some cases, the patches will reappear up to several weeks after the first episode. This can continue for many months. The cause is unproven. It definitely is not caused by a fungus or bacterial infection. It also is not due to any known type of allergic reaction. This condition is not a sign of any type of internal disease. Since it is neither contagious nor sexually transmitted, there is no reason to avoid close or intimate contact when one has this eruption. There is some evidence that it is a relapse of Human Herpes Virus type 7 (HH7) infection, as this virus has been isolated from blood, skin lesions, and white blood cells (lymphocytes) of pityriasis rosea patients. In other people HH7 is only found in the lymphocytes. This virus infects most of us as children, and we develop immunity to it. This is the reason it is so very uncommon for other members of the same household to come down with pityriasis rosea at the same time. A dermatologist can usually diagnose the condition quickly with an examination, but at times the diagnosis is more difficult. The numbers and sizes of the spots can vary and occasionally the rash can be found in an unusual location, such as the lower body or on the face. When there is no "herald" patch, reactions to medications, infection with fungus or syphilis (a type of VD), or other skin diseases may resemble this rash. The dermatologist may order blood tests, skin scrapings or even may take a sample from one of the spots to examine under a microscope to reach a diagnosis. Treatment may include external and internal medications for itching. Aveeno oatmeal baths, anti-itch medicated lotions and steroid creams may be prescribed to combat the rash. Lukewarm, rather than hot, baths may be suggested. Strenuous activity, which could aggravate the rash, should be discouraged. Ultraviolet light treatments given under the supervision of a dermatologist may be helpful. Recently, both the antiviral drug Famvir and the antibiotic erythromycin have been claimed to produce healing in one to two weeks. For severe cases a few days of oral anti-inflammatory medications such as prednisone may be necessary to promote healing. For mild cases, no treatment is required as this disease is not a dangerous skin condition. Soothing medicated lotions and lubricants may be prescribed. Lukewarm rather than hot baths may be suggested. Ultraviolet light treatments given under the supervision of a dermatologist may be helpful. Remember that pityriasis rosea is a common skin disorder and is usually mild. Most cases usually do not need treatment and fortunately, even the most severe cases eventually go away. What is Dermatomyositis? Dermatomyositis (DM) is a connective-tissue disease related to polymyositis (PM) that is characterized by inflammation of the muscles and the skin.

Dermatomyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Dermatomyositis cardinal symptom is a skin rash that precedes or accompanies progressive muscle weakness. The rash looks patchy, with bluish-purple or red discolorations, and characteristically develops on the eyelids and on muscles used to extend or straighten joints, including knuckles, elbows, heels, and toes. Red rashes may also occur on the face, neck, shoulders, upper chest, back, and other locations, and there may be swelling in the affected areas. The rash sometimes occurs without obvious muscle involvement. Adults with dermatomyositis may experience weight loss or a low-grade fever, have inflamed lungs, and be sensitive to light. Children and adults with dermatomyositis may develop calcium deposits, which appear as hard bumps under the skin or in the muscle (called calcinosis). Calcinosis most often occurs 1-3 years after the disease begins. These deposits are seen more often in children with dermatomyositis than in adults. In some cases of dermatomyositis, distal muscles (muscles located away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Dermatomyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus. The cause is unknown, but it may result from either a viral infection or an autoimmune reaction. Some cases of dermatomyositis actually "overlap" (are combined with) another autoimmune disease such as lupus, scleroderma, or vasculitis. Because of the link between DM and autoimmune disease, doctors and patients suspecting DM may find it helpful to run an ANA - antinuclear antibody test. Diagnosis Doctors use the following criteria to make the diagnosis of polymyositis or dermatomyositis:

Muscle weakness at the shoulders or hips A characteristic rash Increased blood levels of certain muscle enzymes (especially creatine kinase) in the blood, indicating muscle damage Abnormalities in muscle electrical activity as measured by electromyography (see Diagnosis of Brain, Spinal Cord, and Nerve Disorders: Electromyography and Nerve Conduction Studies), or on appearance on a magnetic resonance imaging (MRI) scan Characteristic changes in muscle tissue obtained by biopsy and observed under a microscope (the most conclusive evidence) X-ray findings sometimes include dystrophic calcifications in the muscles, and patients may or may not notice small calcium deposits under the skin. Many do not have any calcium deposits of any kind. The rash also may come and go, and may not be dependent on the severity of the muscle involvement at the time. "Gottron's papules", pink patches on the knuckles, and priapism. There is no cure for dermatomyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for dermatomyositis is a

corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with dermatomyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion. Many individuals with dermatomyositis may need a topical ointment, such as topical corticosteroids, for their skin disorder. They should wear a high-protection sunscreen and protective clothing. Surgery may be required to remove calcium deposits that cause nerve pain and recurrent infections. What is the prognosis? Most cases of dermatomyositis respond to therapy. The disease is usually more severe and resistant to therapy in individuals with cardiac or pulmonary problems. Scleroderma is a chronic autoimmune disease characterized by fibrosis (or hardening), vascular alterations, and autoantibodies. There are two major forms: Limited cutaneous scleroderma (or morphea)[1] mainly affects the hands, arms and face, although pulmonary hypertension is frequent. Diffuse cutaneous scleroderma (or systemic sclerosis)[2] is rapidly progressing and affects a large area of the skin and one or more internal organs, frequently the kidneys, esophagus, heart and lungs, and can be fatal. There are no treatments for scleroderma itself, but individual organ system complications are treated. Prognosis is good for limited cutaneous scleroderma, except for <10% of those who develop pulmonary arterial hypertension 10 to 20 years. 5-year survival is 90%, 10-year survival 75%. Prognosis is worse for diffuse cutaneous disease, particularly in older age, and for males. Death occurs most often from pulmonary, heart and kidney complications. 5-year survival is 70%, 10-year survival 55%. The cause is unknown. Scleroderma runs in families, but the genes have not been identified. It affects the small blood vessels known as arterioles, in all organs. First, the cells on the inner lining, or endothelium, of the arteriole die off, along with smooth muscle cells, by a process of apoptosis. They are replaced by collagen and other fibrous material. Inflammatory cells, particularly CD4+ helper T cells, infiltrate the arteriole, and cause further damage. Many of the inflammatory and destructive protein signals have been identified, and they are potential targets for drugs that could interrupt the process Scleroderma is characterized by the appearance of circumscribed or diffuse, hard, smooth, ivory-colored areas that are immobile, and which give the appearance of hidebound skin, a disease occurring in both localized and systemic forms. This disease is found among all races worldwide, but women are four times more likely to develop scleroderma than men. Diagnosis Typical scleroderma is classically defined as symmetrical skin thickening, with about 90% of cases also presenting with Raynaud's phenomenon, nail-fold capillary changes, and anti-nuclear antibodies. Patients may or may not experience systemic organ involvement. Atypical scleroderma may show any variation of these changes without skin changes or with finger

swelling only.[8][9] Additional symptoms of scleroderma typically present themselves within two years of Raynaud's phenomenon.[7] Laboratory testing can show anti-topoisomerase antibodies (causing a diffuse systemic form), or anti-centromere antibodies (causing a limited systemic form, and the CREST syndrome). Other autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase. Treatment There is no direct cure for scleroderma. Because the exact cause is unknown, any treatment is patient-specific and aimed at ameliorating symptoms of the disease. For example, patients who experience Raynaud's phenomenon may be treated with agents to increase blood flow to the fingers, including nifedipine, amlodipine, diltiazem, felodipine, or nicardipine. Fibrosis of the skin has been treated with varying degrees of success with agents such as dpenicillamine, colchicine, PUVA, Relaxin, and cyclosporine. Because scleroderma is an autoimmune disease, one of the major pillars of treatment involves the use of immunosuppressive agents. These drugs include methotrexate, cyclophosphamide, azathioprine, and mycophenolate. Patients with lung involvement benefit from Oxygen therapy, which increases oxygen saturation in tissues damaged by the progression of scleroderma. The additional oxygen in the blood reduces the effort of the heart, decreasing shortness of breath. PRECANCER; Actinic keratosis can be the first step leading to squamous cell carcinoma and is therefore known as a precancer. Although the vast majority of actinic keratoses remain benign, some studies report that up to ten percent may advance to squamous cell carcinoma. This percentage does not sound very large, but it has a large impact. When it comes to squamous cell carcinomas, 40-60 percent begin as untreated actinic keratoses and may advance to invade the surrounding tissues. About 2 to 10 percent of these squamous cell carcinomas spread to the internal organs and are life threatening. Another form of actinic keratosis, actinic cheilitis, develops on the lips and may evolve into squamous cell carcinoma. The more keratoses you have, the greater the chance that one or more mayturn into skin cancer. In fact, some scientists interpret actinic keratosis as the earliest form of squamous cell carcinoma.

What Is Actinic Keratosis? An actinic keratosis, also known as a solar keratosis, is a scaly or crusty growth (lesion). It most often appears on the bald scalp, face, ears, lips, backs of the hands and forearms, shoulders, neck or any other areas of thebody frequently exposed to the sun. Youll most often see the plural, keratoses, because there is seldom just one. In the beginning, actinic keratoses are frequently so small that they are recognized by touch rather than sight. It feels as if you were running a finger over sandpaper. There are many times the number of invisible (subclinical) lesions as visible ones on the skin surface. Most often, actinic keratoses develop slowly and reach a size from an eighth to a quarter of an inch. Early on, they may disappear only to reappear later. Most become red, but some will be light or dark tan, pink, red, a combination of these, or the same color as your skin. Occasionally they itch or produce a pricking or tender sensation. They can also become inflamed and surrounded by redness. In rare instances, actinic keratoses can even bleed. If you have actinic keratoses, it indicates that you have sustained sun damage and could develop any kind of skin cancer not just squamous cell carcinoma. Premalignant, preneoplasia Any of a broad group of conditions with a malignant predisposition; epithelial precancers may be 1. Glandulareg, adenomatous hyperplasiaendometrium and adenomatous polypscolon, stomach, which evolve towards adenocarcinoma of their respective organs or 2. Squamouseg, dysplasia of the uterine cervix or other urogenital mucosae; premalignant lesions of mesenchymal origin include prelymphoma and 'presarcoma'an ad hoc coinage, the latter of which may be due to predisposing factorseg, osteosarcoma may arise in Paget's disease of bone, radiation, hereditary multiple exostoses, polyostotic fibrous dysplasia, enchondroma, Maffucci's enchondromatosis; osteosarcomas may be induced experimentally by various traumachemicaleg, turpentine, mechanical eg, local pressure, indwelling foreign bodies, ischemiaeg, vessel clamping. Cf Preneoplastic state. See Fragile X syndrome, Hereditary neoplasms, Premalignancy. Precancer Chromosome breakage syndromes Bloom syndrome, Fanconi syndrome Genodermatoses Albinism, dyskeratosis congenita,epidermodysplasia verruciformis, polydysplastic epidermolysis bullosa, Werner syndrome, xeroderma pigmentosa Hamartomatous syndromes Multiple exostoses, neurofibromatosis, Peutz-Jegher syndrome, tuberous sclerosis, von Hippel-Lindau syndrome Immunodeficiency syndromes Ataxia-telangiectasia, Wiskott-Aldrich syndrome, Xlinked agammaglobulinemia