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Psoriasis (
/ is a chronic immune-mediated disease that appears on the skin. It occurs when the immune system sends out faulty signals that speed up the growth cycle of skin cells. Psoriasis is not contagious.[]There are five types of psoriasis: plaque, guttate, inverse, pustular and erythrodermic. The most common form, plaque psoriasis, is commonly seen as red and white hues of scaly patches appearing on the top first layer of the epidermis (skin). Some patients, though, have no dermatological symptoms.
In plaque psoriasis, skin rapidly accumulates at these sites, which gives it a silvery-white appearance. Plaques frequently occur on the skin of the elbows and knees, but can affect any area, including the scalp, palms of hands and soles of feet, and genitals. In contrast to eczema, psoriasis is more likely to be found on the outer side of the joint.
The disorder is a chronic recurring condition that varies in severity from minor localized patches to complete body coverage. Fingernails and toenails are frequently affected (psoriatic nail dystrophy) and can be seen as an isolated symptom. Psoriasis can also cause inflammation of the joints, which is known as psoriatic arthritis. Between 10% and 40% of all people with psoriasis have psoriatic arthritis.
The cause of psoriasis is not fully understood, but it is believed to have a genetic component and local psoriatic changes can be triggered by an injury to the skin known as the Koebner phenomenon,[3] see Koebnerisin. Various environmental factors have been suggested as aggravating to psoriasis, including stress, withdrawal of systemiccorticosteroid, as well as other environmental factors, but few have shown statistical significance.[4] There are many treatments available, but because of its chronic recurrent nature, psoriasis is a challenge to treat.
The symptoms of psoriasis can manifest in a variety of forms. Variants include plaque, pustular, guttate and flexural psoriasis. This section describes each type (with ICD-10 code [5]).[6]
Psoriasis is a chronic relapsing disease of the skin that may be classified into nonpustular and pustular types as follows
Nonpustular
Nail psoriasis (L40.86) produces a variety of changes in the appearance of finger and toe nails. These changes include discolouring under the nail plate, pitting of the nails, lines going across the nails, thickening of the skin under the nail, and the loosening (onycholysis) and crumbling of the nail.
Psoriatic arthritis (L40.5) involves joint and connective tissue inflammation. Psoriatic arthritis can affect any joint, but is most common in the joints of the fingers and toes. This can result in a sausage-shaped swelling of the fingers and toes known as dactylitis. Psoriatic arthritis can also affect the hips, knees and spine (spondylitis). About 10–15% of people who have psoriasis also have psoriatic arthritis.
Distribution of severity among people with psoriasisPsoriasis is usually graded as mild (affecting less than 3% of the body), moderate (affecting 3–10% of the body) or severe.[citation needed] Several scales exist for measuring the severity of psoriasis. The degree of severity is generally based on the following factors: the proportion of body surface area affected; disease activity (degree of plaque redness, thickness and scaling); response to previous therapies; and the impact of the disease on the person.
The Psoriasis Area Severity Index (PASI) is the most widely used measurement tool for psoriasis. PASI combines the assessment of the severity of lesions and the area affected into a single score in the range 0 (no disease) to 72 (maximal disease).[16] Nevertheless, the PASI can be too unwieldy to use outside of trials, which has led to attempts to simplify the index for clinical use.[17]
The immune-mediated model of psoriasis has been supported by the observation that immunosuppressant medications can clear psoriasis plaques. However, the role of the immune system is not fully understood, and it has recently been reported that an animal model of psoriasis can be triggered in mice lacking T cells. Animal models, however, reveal only a few aspects resembling human psoriasis.
Compromised skin barrier function has a role in psoriasis susceptibility.
Psoriasis is a fairly idiosyncratic disease. The majority of people's experience of psoriasis is one in which it may worsen or improve for no apparent reason. Studies of the factors associated with psoriasis tend to be based on small (usually hospital based) samples of individuals. These studies tend to suffer from representative issues, and an inability to tease out causal associations in the face of other (possibly unknown) intervening factors. Conflicting findings are often reported. Nevertheless, the first outbreak is sometimes reported following stress (physical and mental), skin injury, and streptococcal infection. Conditions that have been reported as accompanying a worsening of the disease include infections, stress, and changes in season and climate. Certain medicines, including lithium salt, beta blockers and the antimalarial drug chloroquine have been reported to trigger or aggravate the disease. Excessive alcohol consumption, smoking and obesity may exacerbate psoriasis or make the management of the condition difficult or perhaps these comorbidities are effects rather than causes.[ Hairspray, some face creams and hand lotions, can also cause an outbreak of psoriasis. In 1975, Stefania Jablonska and collaborators advanced a new theory that special antibodies tend to break through into the lower layers of the skin and set up a complex series of chemical reactions.
Individuals suffering from the advanced effects of the human immunodeficiency virus, or HIV, often exhibit psoriasis. This presents a paradox to researchers, as traditional therapies that reduce T-cell counts generally cause psoriasis to improve. Yet, as CD4-T-cell counts decrease with the progression of HIV, psoriasis worsens] In addition, HIV is typically characterized by a strong Th2 cytokine profile, whereas psoriasis vulgaris is characterized by a strong Th1 secretion pattern. It is hypothesized that the diminished CD4-T-Cell presence causes an overactivation of CD8-T-cells, which are responsible for the exacerbation of psoriasis in HIV positive patients. It is important to remember that most individuals with psoriasis are otherwise healthy, and the presence of HIV accounts for less than 1% of cases. The prevalence of psoriasis in the HIV positive population ranges from 1 to 6 percent, which is about three times higher than the normal population. Psoriasis in AIDS sufferers is often severe, and untreatable with conventional therapy.
Psoriasis occurs more likely in dry skin than oily or well-moisturized skin, and specifically after an external skin injury such as a scratch or cut (see Koebner phenomenon). This is believed to be caused by an infection, in which the infecting organism thrives under dry skin conditions with minimal skin oil, which otherwise protects skin from infections. The case for psoriasis is opposite to the case of athlete's foot, which occurs because of a fungus infection under wet conditions as opposed to dry in psoriasis. This infection induces inflammation, which causes the symptoms commonly associated with psoriasis, such as itching and rapid skin turnover, and leads to drier skin, as the infecting organism absorbs the moisture that would otherwise go to the skin. To prevent dry skin and reduce psoriasis symptoms, it is advised to not use shower scrubs, as they not only damage skin by leaving tiny scratches, but they also scrape off the naturally occurring skin oil. It is recommended to use talc powder after washing, as that helps absorb excess moisture which would otherwise go to the infecting agent. Additionally, moisturizers can be applied to moisturize the skin, and lotions used to promote skin oil gland functions.[citation needed]
Classic genomewide linkage analysis has identified nine locations (loci) on different chromosomes associated with psoriasis. They are called psoriasis susceptibility 1 through 9 (PSORS1 through PSORS9). Within those loci are genes. Many of those genes are on pathways that lead to inflammation. Certain variations (mutations) of those genes are commonly found in psoriasis.[28]
The major determinant is PSORS1, which probably accounts for 35–50% of its heritability. It controls genes that affect the immune system or encode proteins that are found in the skin in greater amounts in psoriasis. PSORS1 is located on chromosome 6 in the MHC, which controls important immune functions. Three genes in the PSORS1 locus have a strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6, which encodes a MHC class I protein; CCHCR1, variant WWC, which encodes a coiled protein that is overexpressed in psoriatic epidermis; and CDSM, variant allele 5, which encodes corneodesmosin, which is expressed in the granular and cornified layers of the epidermis and upregulated in psoriasis.[28]
Genome-wide association scans have identified other genes which are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.[28]
Two major genes under investigation are IL12B on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor, and is involved in T cell differentiation. T cells are involved in the inflammatory process that leads to psoriasis.[28]
These genes are on the pathway that ends up upregulating tumor necrosis factor-α and nuclear factor κB, two genes that are involved in inflammation.[28]
The immune system consists of an innate immune system, and an adaptive immune system.
In the innate system, immune cells have receptors that have evolved to target specific proteins and other antigens which are commonly found on pathogens. In the adaptive immune system, immune cells respond to proteins and other antigens that they may never have seen before, which are presented to them by other cells. The innate system often passes antigens on to the adaptive system. When the immune system makes a mistake, and identifies a healthy part of the body as a foreign antigen, the immune system attacks that protein, as it does in autoimmunity.
In psoriasis, DNA is an inflammatory stimulus. DNA stimulates the receptors on plasmacytoid dendritic cells, which produce interferon-α, an immune stimulatory signal (cytokine). In psoriasis, keratinocytes produce antimicrobial peptides. In response to dendritic cells and T cells, they also produce cytokines, such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signals more inflammatory cells to arrive and produces further inflammation.[28]
Dendritic cells bridge the innate and adaptive immune system. They are increased in psoriatic lesions and induce the proliferation of T cells and type 1 helper T cells. Certain dendritic cells can produce tumor necrosis factor-α, which calls more immune cells and stimulates more inflammation. Targeted immunotherapy, and psoralen and ultraviolet A (PUVA) therapy, reduces the number of dendritic cells.[28]
T cells move from the dermis into the epidermis. They are attracted to the epidermis by alpha-1 beta-1 integrin, a signalling molecule on the collagen in the epidermis. Psoriatic T cells secrete interferon-γ and interleukin-17. Interleukin-17 is also associated with interleukin-22. Interleukin-22 induces keratocytes to proliferate.[28]
One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.[28
Complications of psoriasis
0919 606 00 22 / 226 27 24 / 0933 962 90 49
Psoriasis
from kaingin aguncilio lemery batangas phil
| Psoriasis | |
|---|---|
| Classification and external resources | |
 A person whose back and arms are affected by psoriasis | |
| ICD-10 | L40. |
| ICD-9 | 696 |
| OMIM | 177900 |
| DiseasesDB | 10895 |
| MedlinePlus | 000434 |
| eMedicine | emerg/489Dermatology:derm/365 plaque derm/361 guttate derm/363 nails derm/366 pustular Arthritis derm/918 Radiology radio/578 Physical Medicine pmr/120 |
| MeSH | D011565 |
/ is a chronic immune-mediated disease that appears on the skin. It occurs when the immune system sends out faulty signals that speed up the growth cycle of skin cells. Psoriasis is not contagious.[]There are five types of psoriasis: plaque, guttate, inverse, pustular and erythrodermic. The most common form, plaque psoriasis, is commonly seen as red and white hues of scaly patches appearing on the top first layer of the epidermis (skin). Some patients, though, have no dermatological symptoms.In plaque psoriasis, skin rapidly accumulates at these sites, which gives it a silvery-white appearance. Plaques frequently occur on the skin of the elbows and knees, but can affect any area, including the scalp, palms of hands and soles of feet, and genitals. In contrast to eczema, psoriasis is more likely to be found on the outer side of the joint.
The disorder is a chronic recurring condition that varies in severity from minor localized patches to complete body coverage. Fingernails and toenails are frequently affected (psoriatic nail dystrophy) and can be seen as an isolated symptom. Psoriasis can also cause inflammation of the joints, which is known as psoriatic arthritis. Between 10% and 40% of all people with psoriasis have psoriatic arthritis.
The cause of psoriasis is not fully understood, but it is believed to have a genetic component and local psoriatic changes can be triggered by an injury to the skin known as the Koebner phenomenon,[3] see Koebnerisin. Various environmental factors have been suggested as aggravating to psoriasis, including stress, withdrawal of systemiccorticosteroid, as well as other environmental factors, but few have shown statistical significance.[4] There are many treatments available, but because of its chronic recurrent nature, psoriasis is a challenge to treat.
The symptoms of psoriasis can manifest in a variety of forms. Variants include plaque, pustular, guttate and flexural psoriasis. This section describes each type (with ICD-10 code [5]).[6]
Psoriasis is a chronic relapsing disease of the skin that may be classified into nonpustular and pustular types as follows
Nonpustular
- Psoriasis vulgaris (chronic stationary psoriasis, plaque-like psoriasis)(L40.0) is the most common form of psoriasis. It affects 80 to 90% of people with psoriasis. Plaque psoriasis typically appears as raised areas of inflamed skin covered with silvery white scaly skin. These areas are called plaques.
- Psoriatic erythroderma (erythrodermic psoriasis)(L40.85)involves the widespread inflammation and exfoliation of the skin over most of the body surface. It may be accompanied by severe itching, swelling and pain. It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic treatment. This form of psoriasis can be fatal, as the extreme inflammation and exfoliation disrupt the body's ability to regulate temperature and for the skin to perform barrier functions.[8]
Pustular
Pustular psoriasis (L40.1-3, L40.82) appears as raised bumps that are filled with noninfectious pus (pustules). The skin under and surrounding the pustules is red and tender. Pustular psoriasis can be localised, commonly to the hands and feet (palmoplantar pustulosis), or generalised with widespread patches occurring randomly on any part of the body. Types include:- Generalized pustular psoriasis (pustular psoriasis of von Zumbusch)
- Pustulosis palmaris et plantaris (persistent palmoplantar pustulosis, pustular psoriasis of the Barber type, pustular psoriasis of the extremities)
- Annular pustular psoriasis
- Acrodermatitis continua
- Impetigo herpetiformis
Other
Additional types of psoriasis include[9]:- Inverse psoriasis (flexural psoriasis, inverse psoriasis)(L40.83-4) appears as smooth inflamed patches of skin. It occurs in skin folds, particularly around thegenitals (between the thigh and groin), the armpits, under an overweight abdomen (panniculus), and under the breasts (inframammary fold). It is aggravated byfriction and sweat, and is vulnerable to fungal infections.
Nail psoriasis (L40.86) produces a variety of changes in the appearance of finger and toe nails. These changes include discolouring under the nail plate, pitting of the nails, lines going across the nails, thickening of the skin under the nail, and the loosening (onycholysis) and crumbling of the nail.
Psoriatic arthritis (L40.5) involves joint and connective tissue inflammation. Psoriatic arthritis can affect any joint, but is most common in the joints of the fingers and toes. This can result in a sausage-shaped swelling of the fingers and toes known as dactylitis. Psoriatic arthritis can also affect the hips, knees and spine (spondylitis). About 10–15% of people who have psoriasis also have psoriatic arthritis.
Signs and symptoms
Plaque of psoriasis
Plaque of psoriasis
An arm covered with plaque psoriasis
Psoriasis of a fingernail
Severity
The Psoriasis Area Severity Index (PASI) is the most widely used measurement tool for psoriasis. PASI combines the assessment of the severity of lesions and the area affected into a single score in the range 0 (no disease) to 72 (maximal disease).[16] Nevertheless, the PASI can be too unwieldy to use outside of trials, which has led to attempts to simplify the index for clinical use.[17]
Cause
The cause of psoriasis is not fully understood. There are two main hypotheses about the process that occurs in the development of the disease. The first considers psoriasis as primarily a disorder of excessive growth and reproduction of skin cells. The problem is simply seen as a fault of the epidermis and its keratinocytes. The second hypothesis sees the disease as being an immune-mediated disorder in which the excessive reproduction of skin cells is secondary to factors produced by the immune system. T cells(which normally help protect the body against infection) become active, migrate to the dermis and trigger the release of cytokines (tumor necrosis factor-alphaTNFα, in particular) which cause inflammation and the rapid production of skin cells. It is not known what initiates the activation of the T cells.The immune-mediated model of psoriasis has been supported by the observation that immunosuppressant medications can clear psoriasis plaques. However, the role of the immune system is not fully understood, and it has recently been reported that an animal model of psoriasis can be triggered in mice lacking T cells. Animal models, however, reveal only a few aspects resembling human psoriasis.
Compromised skin barrier function has a role in psoriasis susceptibility.
Psoriasis is a fairly idiosyncratic disease. The majority of people's experience of psoriasis is one in which it may worsen or improve for no apparent reason. Studies of the factors associated with psoriasis tend to be based on small (usually hospital based) samples of individuals. These studies tend to suffer from representative issues, and an inability to tease out causal associations in the face of other (possibly unknown) intervening factors. Conflicting findings are often reported. Nevertheless, the first outbreak is sometimes reported following stress (physical and mental), skin injury, and streptococcal infection. Conditions that have been reported as accompanying a worsening of the disease include infections, stress, and changes in season and climate. Certain medicines, including lithium salt, beta blockers and the antimalarial drug chloroquine have been reported to trigger or aggravate the disease. Excessive alcohol consumption, smoking and obesity may exacerbate psoriasis or make the management of the condition difficult or perhaps these comorbidities are effects rather than causes.[ Hairspray, some face creams and hand lotions, can also cause an outbreak of psoriasis. In 1975, Stefania Jablonska and collaborators advanced a new theory that special antibodies tend to break through into the lower layers of the skin and set up a complex series of chemical reactions.
Individuals suffering from the advanced effects of the human immunodeficiency virus, or HIV, often exhibit psoriasis. This presents a paradox to researchers, as traditional therapies that reduce T-cell counts generally cause psoriasis to improve. Yet, as CD4-T-cell counts decrease with the progression of HIV, psoriasis worsens] In addition, HIV is typically characterized by a strong Th2 cytokine profile, whereas psoriasis vulgaris is characterized by a strong Th1 secretion pattern. It is hypothesized that the diminished CD4-T-Cell presence causes an overactivation of CD8-T-cells, which are responsible for the exacerbation of psoriasis in HIV positive patients. It is important to remember that most individuals with psoriasis are otherwise healthy, and the presence of HIV accounts for less than 1% of cases. The prevalence of psoriasis in the HIV positive population ranges from 1 to 6 percent, which is about three times higher than the normal population. Psoriasis in AIDS sufferers is often severe, and untreatable with conventional therapy.
Psoriasis occurs more likely in dry skin than oily or well-moisturized skin, and specifically after an external skin injury such as a scratch or cut (see Koebner phenomenon). This is believed to be caused by an infection, in which the infecting organism thrives under dry skin conditions with minimal skin oil, which otherwise protects skin from infections. The case for psoriasis is opposite to the case of athlete's foot, which occurs because of a fungus infection under wet conditions as opposed to dry in psoriasis. This infection induces inflammation, which causes the symptoms commonly associated with psoriasis, such as itching and rapid skin turnover, and leads to drier skin, as the infecting organism absorbs the moisture that would otherwise go to the skin. To prevent dry skin and reduce psoriasis symptoms, it is advised to not use shower scrubs, as they not only damage skin by leaving tiny scratches, but they also scrape off the naturally occurring skin oil. It is recommended to use talc powder after washing, as that helps absorb excess moisture which would otherwise go to the infecting agent. Additionally, moisturizers can be applied to moisturize the skin, and lotions used to promote skin oil gland functions.[citation needed]
Genetics
Psoriasis has a large hereditary component, and many genes are associated with it, but it is not clear how those genes work together. Most of them involve the immune system, particularly the major histocompatibility complex (MHC) and T cells. The main value of genetic studies is they identify molecular mechanisms and pathways. for further study and potential drug targets.[28]Classic genomewide linkage analysis has identified nine locations (loci) on different chromosomes associated with psoriasis. They are called psoriasis susceptibility 1 through 9 (PSORS1 through PSORS9). Within those loci are genes. Many of those genes are on pathways that lead to inflammation. Certain variations (mutations) of those genes are commonly found in psoriasis.[28]
The major determinant is PSORS1, which probably accounts for 35–50% of its heritability. It controls genes that affect the immune system or encode proteins that are found in the skin in greater amounts in psoriasis. PSORS1 is located on chromosome 6 in the MHC, which controls important immune functions. Three genes in the PSORS1 locus have a strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6, which encodes a MHC class I protein; CCHCR1, variant WWC, which encodes a coiled protein that is overexpressed in psoriatic epidermis; and CDSM, variant allele 5, which encodes corneodesmosin, which is expressed in the granular and cornified layers of the epidermis and upregulated in psoriasis.[28]
Genome-wide association scans have identified other genes which are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.[28]
Two major genes under investigation are IL12B on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor, and is involved in T cell differentiation. T cells are involved in the inflammatory process that leads to psoriasis.[28]
These genes are on the pathway that ends up upregulating tumor necrosis factor-α and nuclear factor κB, two genes that are involved in inflammation.[28]
Immunology
In psoriasis, immune cells move from the dermis to the epidermis, where they stimulate skin cells (keratinocytes) to proliferate. Psoriasis does not seem to be a true autoimmune disease.[28] In an autoimmune disease, the immune system confuses an outside antigen with a normal body component, and attacks them both. But in psoriasis, the inflammation does not seem to be caused by outside antigens (although DNA does have an immunostimulatory effect). Researchers have identified many of the immune cells involved in psoriasis, and the chemical signals they send to each other to coordinate inflammation. At the end of this process, immune cells, such as dendritic cells and T cells, move from the dermis to the epidermis, secreting chemical signals, such as tumor necrosis factor-α, interleukin-1β, and interleukin-6, which cause inflammation, and interleukin-22, which causes keratinocytes to proliferate.[28]The immune system consists of an innate immune system, and an adaptive immune system.
In the innate system, immune cells have receptors that have evolved to target specific proteins and other antigens which are commonly found on pathogens. In the adaptive immune system, immune cells respond to proteins and other antigens that they may never have seen before, which are presented to them by other cells. The innate system often passes antigens on to the adaptive system. When the immune system makes a mistake, and identifies a healthy part of the body as a foreign antigen, the immune system attacks that protein, as it does in autoimmunity.
In psoriasis, DNA is an inflammatory stimulus. DNA stimulates the receptors on plasmacytoid dendritic cells, which produce interferon-α, an immune stimulatory signal (cytokine). In psoriasis, keratinocytes produce antimicrobial peptides. In response to dendritic cells and T cells, they also produce cytokines, such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signals more inflammatory cells to arrive and produces further inflammation.[28]
Dendritic cells bridge the innate and adaptive immune system. They are increased in psoriatic lesions and induce the proliferation of T cells and type 1 helper T cells. Certain dendritic cells can produce tumor necrosis factor-α, which calls more immune cells and stimulates more inflammation. Targeted immunotherapy, and psoralen and ultraviolet A (PUVA) therapy, reduces the number of dendritic cells.[28]
T cells move from the dermis into the epidermis. They are attracted to the epidermis by alpha-1 beta-1 integrin, a signalling molecule on the collagen in the epidermis. Psoriatic T cells secrete interferon-γ and interleukin-17. Interleukin-17 is also associated with interleukin-22. Interleukin-22 induces keratocytes to proliferate.[28]
One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.[28
Complications of psoriasis
Psoriatic arthritis
Between 10% and 20% of people with psoriasis develop psoriatic arthritis, which causes tenderness, pain and swelling in the joints and connective tissue with associated stiffness. It commonly affects the ends of the fingers and toes. In some people it affects the lower back, neck and knees. About 80% of those affected develop psoriatic arthritis after the onset of psoriasis, but in about 20% the arthritis occurs before the onset of psoriasis.
There is no single test for psoriatic arthritis. It is normally diagnosed using a combination of methods - looking at your medical history, physical examinations, blood tests, X-rays and MRI scans.
Psoriatic arthritis can be treated with anti-inflammatory or anti-rheumatic medicines.
Psychological complications
Due to the unpleasant effects psoriasis can have on physical appearance, feelings of low self-esteem and anxiety are common among people living with this condition. These feelings can then trigger depression, especially if the psoriasis worsens.
Your GP or dermatologist will understand that psoriasis has a psychological and emotional impact, so don't be afraid to discuss any concerns or anxieties you may have.
Many people living with psoriasis have found getting involved in support groups may help. Support groups can help increase your self-confidence and reduce any feelings of isolation, while offering practical advice about living with the condition.
How can jesoga70therapy treat or cure psoriasis.
By using the 14 vitality abdominal impulses functioning system all these white scale on your body easily revome until you see healthy body. Psoriasis isn't a hidden problem. and for sure, on one is sure what causes psoriasis. Doctors knows that it doen't spread from person to person., though it does run in the family. Contact Details (private): 09296143292 that's mr Salva mother who suffer long time ago when psoriasis flares up to her , with red scaly sores from her elbows , knees , scalp , chest , and back , legs itching like crazy and defying all attempts she make them to go away but failed even her attending doctor . But because of the power of jesoga70therapy using the electro chemical neuron on her kidney ignited brain manages to stimulate the impulses of uterus/prostate , ovary/testicle , pancreas and pituitary and thryroid these chain fashion rebalance the che or key of all body fluid(oinic) which immidiately stop the intensive flaking of the skin and itches and cure them seventime faster than normal. These condition notice by the patient during therapy medication. her skin sensation became normal seems no resembling fish scale. There's no known cure for these disease ask you good doctor? if i'm saying wrong information to all of you out dear viewers, and any one from you , knows what has god on his mind then you can cure these psoriasis. jesoga70therapy is the one who witness the power of the divine power , the living light. the word of wisdom from god.
Some of our patient from La Vista subd., Quezon near Atenio De Manila univercity testify how she (they)got the heatingenergy so hot 60 degree Celsius they claimed these people was came from the high class family so classified in character even i my self can't explained how they suffered from these disease. Now our target mission is to build a place which can visited us in term of public service one day a week , so that those poor community can benefited with these vocation. so may the power and mercy full hands of our lord god be with you . thanks arigato.
Food therapy
try omega 3 fatty acid have long been touted as away to help ease psoriasis. But if you prefer your main couse to be a land animal take another look at turkey in one study people who eat a lot of turkey showed marked improvement.
There is no single test for psoriatic arthritis. It is normally diagnosed using a combination of methods - looking at your medical history, physical examinations, blood tests, X-rays and MRI scans.
Psoriatic arthritis can be treated with anti-inflammatory or anti-rheumatic medicines.
Psychological complications
Due to the unpleasant effects psoriasis can have on physical appearance, feelings of low self-esteem and anxiety are common among people living with this condition. These feelings can then trigger depression, especially if the psoriasis worsens.
Your GP or dermatologist will understand that psoriasis has a psychological and emotional impact, so don't be afraid to discuss any concerns or anxieties you may have.
Many people living with psoriasis have found getting involved in support groups may help. Support groups can help increase your self-confidence and reduce any feelings of isolation, while offering practical advice about living with the condition.
How can jesoga70therapy treat or cure psoriasis.
By using the 14 vitality abdominal impulses functioning system all these white scale on your body easily revome until you see healthy body. Psoriasis isn't a hidden problem. and for sure, on one is sure what causes psoriasis. Doctors knows that it doen't spread from person to person., though it does run in the family. Contact Details (private): 09296143292 that's mr Salva mother who suffer long time ago when psoriasis flares up to her , with red scaly sores from her elbows , knees , scalp , chest , and back , legs itching like crazy and defying all attempts she make them to go away but failed even her attending doctor . But because of the power of jesoga70therapy using the electro chemical neuron on her kidney ignited brain manages to stimulate the impulses of uterus/prostate , ovary/testicle , pancreas and pituitary and thryroid these chain fashion rebalance the che or key of all body fluid(oinic) which immidiately stop the intensive flaking of the skin and itches and cure them seventime faster than normal. These condition notice by the patient during therapy medication. her skin sensation became normal seems no resembling fish scale. There's no known cure for these disease ask you good doctor? if i'm saying wrong information to all of you out dear viewers, and any one from you , knows what has god on his mind then you can cure these psoriasis. jesoga70therapy is the one who witness the power of the divine power , the living light. the word of wisdom from god.
Some of our patient from La Vista subd., Quezon near Atenio De Manila univercity testify how she (they)got the heatingenergy so hot 60 degree Celsius they claimed these people was came from the high class family so classified in character even i my self can't explained how they suffered from these disease. Now our target mission is to build a place which can visited us in term of public service one day a week , so that those poor community can benefited with these vocation. so may the power and mercy full hands of our lord god be with you . thanks arigato.
Food therapy
try omega 3 fatty acid have long been touted as away to help ease psoriasis. But if you prefer your main couse to be a land animal take another look at turkey in one study people who eat a lot of turkey showed marked improvement.
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