Wednesday, September 28, 2005
Basic Treatment Protocol For Psoriasis
Treatment of psoriasis is determined by the location, severity and history of psoriasis in each individual. There is no one method of treatment, for each person with psoriasis may respond differently. One main objective of treatment is to slow down the more rapid than usual growth rate of the skin cells. The rapid growth rate of skin cells causes the red, scaly psoriasis patches. The underlying cause of this increased skin growth is not yet known. For patients with minimal psoriasis, therapy is limited to topical medications that are drugs applied to the skin. For patients with moderate to widespread psoriasis, topical treatments are often combined with ultraviolet light therapy. Either sunlight or artificial ultraviolet light therapy can be used. If topical and ultraviolet light therapy are not effective, or are not practical, systemic or oral medications can be used. These may be combined with ultraviolet light therapy, the so-called photo-chemotherapy or PUVA therapy. In severe cases and unresponsive cases of psoriasis, there are oral medications that slow down the growth rate of skin which are helpful. These drugs can have significant side effects and have to be used with the proper safeguard and caution. Even these strong drugs do not cure psoriasis but only help to control the disease.
Sunday, September 25, 2005
Symptoms of Psoriasis
Individuals with psoriasis experience symptoms such as itching, cracking, stinging, burning, or bleeding. Lack of sunlight and low indoor humidity in the winter months can cause the psoriasis symptoms to worsen. The skin is most likely to crack at the joints where the body bends, or in areas where the individual scratches. Scratching should be strictly avoided, because it can cause bleeding and infection. Psoriasis has also been known to cause pits or dents to form in fingernails and toenails. There is also the possibility that the soft tissue inside the mouth and genitalia can be affected. In some cases, psoriasis will cause joint inflammation that produces arthritis symptoms. This condition is called psoriatic arthritis.People with psoriasis may notice that there are times when their skin worsens, then improves. Conditions that may cause flare-ups include changes in climate, infections, stress, and dry skin. Also, certain medicines, most notably beta-blockers, which are used in the treatment of high blood pressure, and lithium or drugs used in the treatment of depression, may cause an outbreak or worsening of the disease.
Saturday, September 24, 2005
General Definition of Psoriasis
Psoriasis is a chronic scaling skin. It may range from just a few spots anywhere on the body to large areas of involvement. It is not contagious or spread able from one part of the body to another or from one person to another. There is no blood test to diagnose psoriasis. The diagnosis is made by observation and examination of the skin. Sometimes microscopic examination of the skin (biopsy) is helpful where the changes are not typical or characteristic. The exact cause of psoriasis is unknown, but hereditary and genetic factors are important. Psoriasis runs in families. This does not mean, however, that every child of a parent with psoriasis will develop psoriasis, but it is common that somewhere down the line psoriasis will appear in families. Psoriasis is not caused by allergies, infections, dietary deficiencies or excesses, or nervous tension.
Thursday, September 22, 2005
The Appearance of Scalp Psoriasis
Scalp psoriasis occurs in at least half of all people with psoriasis. It can range from very mild with fine scaling to very severe with thick, crusted plaques. Scalp psoriasis may appear as lesions that extend from the hairline onto the forehead and the nape of the neck. It is common for the psoriasis to appear behind the ears. Scalp psoriasis usually accompanies plaques in other areas of the body. Scalp psoriasis scales appear powdery with a silvery sheen. Possible causes of scalp psoriasis include: scalp treatments and severe psoriasis can both cause temporary hair loss; itching, picking and scratching lesions can worsen the psoriasis by causing a Koebner phenomenon (psoriasis appearing on the site of skin injuries).
Saturday, September 17, 2005
Treating The Different Types of Psoriasis
There are five different types of psoriasis. The most common form of psoriasis is called "plaque psoriasis," which is characterized by well-defined patches of red, raised skin. About 80 percent of people with psoriasis have this type. Plaque psoriasis can appear on any skin surface, although the knees, elbows, scalp, trunk and nails are the most common locations. The other types of psoriasis are: Guttate described as small, red, individual drops on the skin. Inverse psoriasis is smooth, dry areas of skin, often in folds or creases, that are red and inflamed but do not have scaling Erythrodermic psoriasis is characterized as periodic, widespread, fiery redness of the skin. Pustular psoriasis which involves either generalized, widespread areas of reddened skin, or localized areas, particularly the hands and feet (palmo-plantar pustular psoriasis).Typically, people have only one form of psoriasis at a time. Sometimes two different types can occur together, one type may change to another type, or one type may become more severe. For example, a trigger may convert plaque psoriasis to pustular.
Tuesday, September 13, 2005
Large Plaque and Small Plaque Parapsoriasis
Current terminology of parapsoriasis refers to 2 disease processes that are caused by T-cell–predominant infiltrates in the skin. These disease processes are large plaque parapsoriasis and small plaque parapsoriasis.
As the nomenclature and description of the disease spectrum under the descriptive term parapsoriasis evolved, the primary focus has been on the distinction of whether the disorder progresses to mycosis fungoides (MF) or cutaneous T-cell lymphoma (CTCL). Small plaque parapsoriasis is a benign disorder that rarely if ever progresses. Large plaque parapsoriasis is more ominous in that approximately 10% of patients progress to CTCL. Controversy exists in the classification of large plaque parapsoriasis because some think it is equivalent to the earliest stage CTCL, the patch stage.
The duration of parapsoriasis can be variable. Small plaque disease lasts several months to years and can spontaneously resolve. Large plaque disease is chronic, and treatment is recommended because it may prevent progression to CTCL.
Pathophysiology: The initiating cause of parapsoriasis is unknown, but the diseases likely represent different stages in a continuum of lymphoproliferative disorders from chronic dermatitis to frank malignancy of CTCL.
Small plaque parapsoriasis likely is a reactive process of predominantly CD4+ T cells. Genotypic pattern observed in small plaque parapsoriasis is similar to that observed in chronic dermatitis, and the pattern of clonality of T cells is consistent with the response of a specific subset of T cells that have been stimulated by an antigen. Multiple dominant clones can be detected by polymerase chain reaction (PCR) of T-cell receptor gene usage, which supports a reactive process. Lymphocytes do not show histologic atypia to suggest malignant transformation. Southern blot analysis of T-cell receptor genes from parapsoriasis does not identify a dominant clone of T cells.
Some physicians believe that small plaque parapsoriasis is an abortive T-cell lymphoma; however, no clear distinguishing evidence, such as genetic changes observed in other malignancies, exists to support this contention. Nevertheless, a hint to the verity of this hypothesis is the recent identification of increased telomerase activity in T cells from CTCL at low-grade stages, high-grade lymphoma, and in parapsoriasis, which is activity not exhibited in normal T cells. A better understanding is likely to develop from further molecular characterization.
Large plaque parapsoriasis is a chronic inflammatory disorder, and the pathophysiology has been speculated to be long-term antigen stimulation. This disorder is associated with a dominant T-cell clone, one that may represent up to 50% of the T-cell infiltrate. If the histologic appearance is benign, without atypical lymphocytes, classification of large plaque parapsoriasis is made. If atypical lymphocytes are present, many would classify such patients as having patch stage CTCL.
As the nomenclature and description of the disease spectrum under the descriptive term parapsoriasis evolved, the primary focus has been on the distinction of whether the disorder progresses to mycosis fungoides (MF) or cutaneous T-cell lymphoma (CTCL). Small plaque parapsoriasis is a benign disorder that rarely if ever progresses. Large plaque parapsoriasis is more ominous in that approximately 10% of patients progress to CTCL. Controversy exists in the classification of large plaque parapsoriasis because some think it is equivalent to the earliest stage CTCL, the patch stage.
The duration of parapsoriasis can be variable. Small plaque disease lasts several months to years and can spontaneously resolve. Large plaque disease is chronic, and treatment is recommended because it may prevent progression to CTCL.
Pathophysiology: The initiating cause of parapsoriasis is unknown, but the diseases likely represent different stages in a continuum of lymphoproliferative disorders from chronic dermatitis to frank malignancy of CTCL.
Small plaque parapsoriasis likely is a reactive process of predominantly CD4+ T cells. Genotypic pattern observed in small plaque parapsoriasis is similar to that observed in chronic dermatitis, and the pattern of clonality of T cells is consistent with the response of a specific subset of T cells that have been stimulated by an antigen. Multiple dominant clones can be detected by polymerase chain reaction (PCR) of T-cell receptor gene usage, which supports a reactive process. Lymphocytes do not show histologic atypia to suggest malignant transformation. Southern blot analysis of T-cell receptor genes from parapsoriasis does not identify a dominant clone of T cells.
Some physicians believe that small plaque parapsoriasis is an abortive T-cell lymphoma; however, no clear distinguishing evidence, such as genetic changes observed in other malignancies, exists to support this contention. Nevertheless, a hint to the verity of this hypothesis is the recent identification of increased telomerase activity in T cells from CTCL at low-grade stages, high-grade lymphoma, and in parapsoriasis, which is activity not exhibited in normal T cells. A better understanding is likely to develop from further molecular characterization.
Large plaque parapsoriasis is a chronic inflammatory disorder, and the pathophysiology has been speculated to be long-term antigen stimulation. This disorder is associated with a dominant T-cell clone, one that may represent up to 50% of the T-cell infiltrate. If the histologic appearance is benign, without atypical lymphocytes, classification of large plaque parapsoriasis is made. If atypical lymphocytes are present, many would classify such patients as having patch stage CTCL.
Thursday, September 08, 2005
Pityriasis Lichenoides
Pityriasis lichenoides variants describe scaly dermatoses with necrotic papules that are clinically and histologically different from parapsoriasis. These diseases generally are benign and undergo spontaneous resolution.
Pityriasis lichenoides is a rare cutaneous disorder of unknown etiology. Pityriasis lichenoides encompasses a spectrum of clinical presentations ranging from acute papular lesions that rapidly evolve into pseudovesicles and central necrosis (pityriasis lichenoides et varioliformis acuta or PLEVA) to small, scaling, benign-appearing papules (pityriasis lichenoides chronica or PLC). Although historically, the term Mucha-Habermann disease has referred only to PLEVA, the term applies broadly to the entire spectrum of disease including PLC. A rare febrile ulceronecrotic variant has been reported, which is a severe form of PLEVA with high fever and marked constitutional symptoms. Lesions may self-involute and resolve completely over weeks, or new lesions occasionally may appear in crops, waxing and waning spontaneously for months to years thereafter.
Mucha-Habermann disease is not a vasculitic process despite reports of immunoglobulin and complement deposition in vessels. Fibrin is not present in the walls of vessels, and thrombi are not found in the lumen. A cell-mediated mechanism has been proposed based on a T-lymphocytic infiltrate with a cytotoxic/suppressor phenotype, diminished epidermal Langerhans cells, and a reduction of the CD4/CD8 ratio. Mucha-Habermann disease is not a lymphoproliferative disorder. CD30 (Ki-1) cells, which are associated with large cell lymphoma, have been identified in the infiltrate of both lymphomatoid papulosis and Mucha-Habermann disease, leading some authors to view this as a self-limited self-healing lymphoproliferative disease.
Pityriasis lichenoides is a rare cutaneous disorder of unknown etiology. Pityriasis lichenoides encompasses a spectrum of clinical presentations ranging from acute papular lesions that rapidly evolve into pseudovesicles and central necrosis (pityriasis lichenoides et varioliformis acuta or PLEVA) to small, scaling, benign-appearing papules (pityriasis lichenoides chronica or PLC). Although historically, the term Mucha-Habermann disease has referred only to PLEVA, the term applies broadly to the entire spectrum of disease including PLC. A rare febrile ulceronecrotic variant has been reported, which is a severe form of PLEVA with high fever and marked constitutional symptoms. Lesions may self-involute and resolve completely over weeks, or new lesions occasionally may appear in crops, waxing and waning spontaneously for months to years thereafter.
Mucha-Habermann disease is not a vasculitic process despite reports of immunoglobulin and complement deposition in vessels. Fibrin is not present in the walls of vessels, and thrombi are not found in the lumen. A cell-mediated mechanism has been proposed based on a T-lymphocytic infiltrate with a cytotoxic/suppressor phenotype, diminished epidermal Langerhans cells, and a reduction of the CD4/CD8 ratio. Mucha-Habermann disease is not a lymphoproliferative disorder. CD30 (Ki-1) cells, which are associated with large cell lymphoma, have been identified in the infiltrate of both lymphomatoid papulosis and Mucha-Habermann disease, leading some authors to view this as a self-limited self-healing lymphoproliferative disease.
Monday, September 05, 2005
What is Parapsoriasis?
Parapsoriasis describes a group of cutaneous diseases that can be characterized by scaly patches or slightly elevated plaques that have a resemblance to psoriasis, hence the nomenclature. However, this description includes several inflammatory cutaneous diseases that are unrelated with respect to pathogenesis, histopathology, and response to treatment. Because of the variation in clinical presentation and a lack of a specific diagnostic finding on histopathology, a uniformly accepted definition of parapsoriasis remains lacking.
In 1902, Brocq initially described 3 major entities that fit the description:
Pityriasis lichenoides (acuta and chronica)
Small plaque parapsoriasis
Large plaque parapsoriasis (parapsoriasis en plaque)
In 1902, Brocq initially described 3 major entities that fit the description:
Pityriasis lichenoides (acuta and chronica)
Small plaque parapsoriasis
Large plaque parapsoriasis (parapsoriasis en plaque)
Friday, September 02, 2005
Alternative Treatments For Psoriasis
The success rates of alternative treatment for psoriasis are difficult to measure, as conclusive test results are not available. Psoriasis has traditionally been one of the skin conditions that has stumped researchers and has proven very difficult to cure. Unfortunately, many alternative treatment types available may not actually work, and many “cures” play on the need of the patient and as merely a means to make money. There is not one treatment out there that is a miracle cure. If that was the case, the cure would widely be known and not be a secret, hidden cure.
However, there is no doubt that some alternative treatment types do work, and some treatments may benefit one person and not another. Many natural treatments include Acupuncture, Ayurveda, Dermatitis-Ltd, Manipulation, Osteopathy, Climate, Diet, Dietary Supplements, Homeopathy, Water Therapy, Chinese Medicine, Meditation and Relaxation, Herbal therapies, Topical Moisturizing Products, and Magnets. Seeking consultation from a doctor is very important before trying any self-treatments.
However, there is no doubt that some alternative treatment types do work, and some treatments may benefit one person and not another. Many natural treatments include Acupuncture, Ayurveda, Dermatitis-Ltd, Manipulation, Osteopathy, Climate, Diet, Dietary Supplements, Homeopathy, Water Therapy, Chinese Medicine, Meditation and Relaxation, Herbal therapies, Topical Moisturizing Products, and Magnets. Seeking consultation from a doctor is very important before trying any self-treatments.
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