Systemic Lupus Erythematosus Rash Causes

Systemic Lupus Erythematosus (SLE or lupus) is a chronic autoimmune disease that can be fatal, though with recent medical advances, fatalities are becoming increasingly rare. It may affect the skin, joints, kidneys, and other organs. Systemic lupus erythematosus involves chronic inflammation that can affect many parts of the body. SLE (lupus) is an autoimmune disease. This means there is a problem with the body’s normal immune system response. Normally, the immune system helps protect the body from harmful substances. Fever occurs in 90% of patients with SLE and is usually caused by the inflammatory process of the disease, not by infection. It is low-grade except during an acute lupus crisis. SLE may be mild or severe enough to cause death.

SLE often begins with a skin rash over the nose and cheeks that is shaped like a butterfly and made worse by exposure to the sun. This may be accompanied by tiredness and joint pains. SLE symptoms may develop slowly over months or years, or they may appear suddenly. Symptoms tend to be worse during winter months, perhaps because prolonged exposure to sunlight in the summer causes a gradual build-up of factors that trigger symptoms months later. SLE is one of several diseases known as the great imitator because its symptoms vary so widely it often mimics or is mistaken for other illnesses. There are an estimated 50,000 people with SLE in the UK. Women are nine times more likely to be affected than men. SLE commonly starts in the teens and 20s.

About 90% of people who have lupus are young women in their late teens to 30s. Older men and women can also be affected. SLE or lupus occurs in all parts of the world but may be more common in blacks and in Asians. Treatment depends on which organs are affected and whether the lupus is mild or severe. Immunosuppressants may be used to relieve symptoms and control the disease, while physiotherapy can help to relieve joint problems. Sun exposure should be avoided and infections treated promptly. Bone marrow transplant autologous stem cell transplants are under investigation as a possible cure. Nonsteroidal anti-inflammatory drugs for fever, arthritis, and headache. Antimalarial drugs for pleurisy, mild kidney involvement, and inflammation of the tissue surrounding the heart

Lupus Erythematosus Treatment and Prevention Tips

1. Nonsteroidal anti-inflammatory medications (NSAIDs) are used.

2. Corticosteroid creams are used to treat skin rashes.

3. Sun exposure should be avoided and infections treated promptly.

4. Immunosuppressants may be used to relieve symptoms and control the disease.

5. Hydroxychloroquine (Plaquenil) is an antimalarial medication found to be particularly effective for SLE patients.


Systemic Lupus Erythematosus Diagnosis Criteria

What is lupusc
Systemic lupus erythematosus, also known as SLE, or simply lupus, is a disease that is characterized by periodic episodes of inflammation of and damage to the joints, tendons, other connective tissues, and organs, including the heart, lungs, blood vessels, brain, kidneys, and skin. The heart, lungs, kidneys, and brain are the organs most affected. Lupus affects each individual differently and the effects of the illness range from mild to severe. Lupus is an autoimmune disease that occurs in about one in 1,000 people. It is much more common in women of childbearing age, especially African-American women.
What are the symptoms of lupusc
The following are the most common symptoms of lupus. However, each individual may experience symptoms differently. Symptoms may include:
malar rash – a rash shaped like a butterfly that is usually found on the bridge of the nose and the cheeks.discoid rash – a raised rash found on the head, arms, chest, or back.feverinflammation of the jointssunlight sensitivityhair lossmouth ulcersfluid around the lungs, heart, or other organskidney problemslow white blood cell or low platelet countRaynaud phenomenon – a condition in which the blood vessels of the fingers and toes go into spasm when triggered by factors such as cold, stress, or illness.weight lossnerve or brain dysfunctionanemia
The symptoms of lupus may resemble other medical conditions or problems. Always consult your physician for a diagnosis.
How is lupus diagnosedc
In addition to a complete medical history and physical examination, lupus may be diagnosed by symptoms and by blood tests for antibodies specific for the disease. The course of the disease ranges from mild to severe and most people have periods of increased symptoms called flares.
How does pregnancy affect lupusc
Pregnancy may or may not increase the symptoms of, or change the course of, lupus. Flares may occur at any time in pregnancy or the postpartum period (after delivery), but are usually mild.
How does lupus affect pregnancyc
Lupus can affect pregnancy at any stage. It is not clear whether the severity of the disease or the type of medication causes problems. However, there are higher pregnancy risks associated with lupus. The rate of miscarriage is higher, ranging from 9 to 40 percent. Later pregnancy loss may also be more likely. Pregnancy complications that may be increased in women with lupus include, but are not limited to, the following:
miscarriagepreterm delivery, especially with a lupus flarepremature rupture of membranes (early breaking of the amniotic sac)pregnancy-induced hypertension (high blood pressure of pregnancy)intrauterine growth restriction (poor fetal growth)stillbirth
It is thought that high levels of antiphospholipid antibodies (antibodies that cause abnormal blood clotting) may be linked with stillbirth. Pregnancy loss may also be associated with the severity of lupus at the time of conception, or if lupus begins during pregnancy. It is also thought that kidney disease with lupus may play a role in pregnancy loss.

A rare condition called neonatal lupus erythematosus (NLE) may affect babies of mothers with lupus. Symptoms may include:
congenital heart block – a problem in the heart’s electrical system that causes the heart to be slower than normal. This affects about 5 percent of newborns who have no other heart defect.skin rashes on the face, scalp, chest and upper back (these usually go away in the first year)blood abnormalities including anemia, low platelets, and lowered white blood cell countManagement of lupus during pregnancy:
Because of the higher risks for pregnancy loss with lupus, mothers need close monitoring of the disease. More frequent prenatal visits are often needed.

Medications used to treat lupus may need to be changed (type and/or dosage), during pregnancy. Consult your physician for more information.

Testing during pregnancy with lupus may include the following:
blood tests for lupus (specific antibodies that help track the severity of the disease)monitoring for signs of pregnancy-induced hypertensionultrasound – a diagnostic imaging technique which uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are used to view internal organs as they function, and to assess blood flow through various vessels used to monitor fetal growth and development.fetal heart monitoring (to check the fetal heart rate for signs of distress)
Women with lupus can increase their chances for a healthy pregnancy by getting early prenatal care and working with their healthcare providers in the management of their disease.
Lupus death rate jumps:
There has been a sharp increase in deaths from lupus that is concerning government health officials. Reported in the Morbidity and Mortality Weekly Report from the Centers for Disease Control and Prevention (CDC), the death rate from lupus increased by 35 percent over two decades. The greatest increase occurred among middle-aged black women, among whom the death toll rose by almost 70 percent.

Unfortunately experts have no clear explanation for the increase in the death rate. The CDC is considering establishing a special registry, which may help determine whether the increased death rate is real or comes from better recognition of the condition.

Discover How You Can Treat Infertility Naturally, Without Drugs or Surgery

Systemic Lupus Erythematosus Symptoms Causes

Systemic Lupus Erythematosus (SLE or lupus) is a chronic autoimmune disease that can be fatal, though with recent medical advances, fatalities are becoming increasingly rare. It may affect the skin, joints, kidneys, and other organs. Systemic lupus erythematosus involves chronic inflammation that can affect many parts of the body. SLE (lupus) is an autoimmune disease. This means there is a problem with the body’s normal immune system response. Normally, the immune system helps protect the body from harmful substances. Fever occurs in 90% of patients with SLE and is usually caused by the inflammatory process of the disease, not by infection. It is low-grade except during an acute lupus crisis. SLE may be mild or severe enough to cause death.

SLE often begins with a skin rash over the nose and cheeks that is shaped like a butterfly and made worse by exposure to the sun. This may be accompanied by tiredness and joint pains. SLE symptoms may develop slowly over months or years, or they may appear suddenly. Symptoms tend to be worse during winter months, perhaps because prolonged exposure to sunlight in the summer causes a gradual build-up of factors that trigger symptoms months later. SLE is one of several diseases known as the great imitator because its symptoms vary so widely it often mimics or is mistaken for other illnesses. There are an estimated 50,000 people with SLE in the UK. Women are nine times more likely to be affected than men. SLE commonly starts in the teens and 20s.

About 90% of people who have lupus are young women in their late teens to 30s. Older men and women can also be affected. SLE or lupus occurs in all parts of the world but may be more common in blacks and in Asians. Treatment depends on which organs are affected and whether the lupus is mild or severe. Immunosuppressants may be used to relieve symptoms and control the disease, while physiotherapy can help to relieve joint problems. Sun exposure should be avoided and infections treated promptly. Bone marrow transplant autologous stem cell transplants are under investigation as a possible cure. Nonsteroidal anti-inflammatory drugs for fever, arthritis, and headache. Antimalarial drugs for pleurisy, mild kidney involvement, and inflammation of the tissue surrounding the heart

Lupus Erythematosus Treatment and Prevention Tips

1. Nonsteroidal anti-inflammatory medications (NSAIDs) are used.

2. Corticosteroid creams are used to treat skin rashes.

3. Sun exposure should be avoided and infections treated promptly.

4. Immunosuppressants may be used to relieve symptoms and control the disease.

5. Hydroxychloroquine (Plaquenil) is an antimalarial medication found to be particularly effective for SLE patients.


Systemic Lupus Erythematosus And Pregnancy Symptoms

What is lupusc
Systemic lupus erythematosus, also known as SLE, or simply lupus, is a disease that is characterized by periodic episodes of inflammation of and damage to the joints, tendons, other connective tissues, and organs, including the heart, lungs, blood vessels, brain, kidneys, and skin. The heart, lungs, kidneys, and brain are the organs most affected. Lupus affects each individual differently and the effects of the illness range from mild to severe. Lupus is an autoimmune disease that occurs in about one in 1,000 people. It is much more common in women of childbearing age, especially African-American women.
What are the symptoms of lupusc
The following are the most common symptoms of lupus. However, each individual may experience symptoms differently. Symptoms may include:
malar rash – a rash shaped like a butterfly that is usually found on the bridge of the nose and the cheeks.discoid rash – a raised rash found on the head, arms, chest, or back.feverinflammation of the jointssunlight sensitivityhair lossmouth ulcersfluid around the lungs, heart, or other organskidney problemslow white blood cell or low platelet countRaynaud phenomenon – a condition in which the blood vessels of the fingers and toes go into spasm when triggered by factors such as cold, stress, or illness.weight lossnerve or brain dysfunctionanemia
The symptoms of lupus may resemble other medical conditions or problems. Always consult your physician for a diagnosis.
How is lupus diagnosedc
In addition to a complete medical history and physical examination, lupus may be diagnosed by symptoms and by blood tests for antibodies specific for the disease. The course of the disease ranges from mild to severe and most people have periods of increased symptoms called flares.
How does pregnancy affect lupusc
Pregnancy may or may not increase the symptoms of, or change the course of, lupus. Flares may occur at any time in pregnancy or the postpartum period (after delivery), but are usually mild.
How does lupus affect pregnancyc
Lupus can affect pregnancy at any stage. It is not clear whether the severity of the disease or the type of medication causes problems. However, there are higher pregnancy risks associated with lupus. The rate of miscarriage is higher, ranging from 9 to 40 percent. Later pregnancy loss may also be more likely. Pregnancy complications that may be increased in women with lupus include, but are not limited to, the following:
miscarriagepreterm delivery, especially with a lupus flarepremature rupture of membranes (early breaking of the amniotic sac)pregnancy-induced hypertension (high blood pressure of pregnancy)intrauterine growth restriction (poor fetal growth)stillbirth
It is thought that high levels of antiphospholipid antibodies (antibodies that cause abnormal blood clotting) may be linked with stillbirth. Pregnancy loss may also be associated with the severity of lupus at the time of conception, or if lupus begins during pregnancy. It is also thought that kidney disease with lupus may play a role in pregnancy loss.

A rare condition called neonatal lupus erythematosus (NLE) may affect babies of mothers with lupus. Symptoms may include:
congenital heart block – a problem in the heart’s electrical system that causes the heart to be slower than normal. This affects about 5 percent of newborns who have no other heart defect.skin rashes on the face, scalp, chest and upper back (these usually go away in the first year)blood abnormalities including anemia, low platelets, and lowered white blood cell countManagement of lupus during pregnancy:
Because of the higher risks for pregnancy loss with lupus, mothers need close monitoring of the disease. More frequent prenatal visits are often needed.

Medications used to treat lupus may need to be changed (type and/or dosage), during pregnancy. Consult your physician for more information.

Testing during pregnancy with lupus may include the following:
blood tests for lupus (specific antibodies that help track the severity of the disease)monitoring for signs of pregnancy-induced hypertensionultrasound – a diagnostic imaging technique which uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are used to view internal organs as they function, and to assess blood flow through various vessels used to monitor fetal growth and development.fetal heart monitoring (to check the fetal heart rate for signs of distress)
Women with lupus can increase their chances for a healthy pregnancy by getting early prenatal care and working with their healthcare providers in the management of their disease.
Lupus death rate jumps:
There has been a sharp increase in deaths from lupus that is concerning government health officials. Reported in the Morbidity and Mortality Weekly Report from the Centers for Disease Control and Prevention (CDC), the death rate from lupus increased by 35 percent over two decades. The greatest increase occurred among middle-aged black women, among whom the death toll rose by almost 70 percent.

Unfortunately experts have no clear explanation for the increase in the death rate. The CDC is considering establishing a special registry, which may help determine whether the increased death rate is real or comes from better recognition of the condition.

Discover How You Can Treat Infertility Naturally, Without Drugs or Surgery

Systemic Lupus Erythematosus Nursing Diagnosis

Pleurisy, also called pleuritis, is an inflammation of the pleura. Pleurisy can be generated by a variety of infectious and non-infectious causes. Pleurisy is caused by swelling and irritation of the membrane that surrounds the lungs. Certain autoimmune diseases (such as systemic lupus erythematosus) can irritate the pleura. It is usually a symptom of another illness. It is also called Pleuritic Chest Pain. Pleurisy can develop from many things, including bacterial or viral infections of the lungs (such as pneumonia), TB, lupus, chest injury or trauma, a blood clot in the lung, or cancer. Sometimes a cause cannot be found. The effects of pleurisy can often be felt long after the condition has gone away.The hallmark of pleurisy is severe chest pain that starts suddenly.

The pain is often strong or stabbing when you take a deep breath. It usually subsides or disappears between breaths. It’s usually felt on one side of the stomach area or lower chest. Deep breathing and coughing often make it worse. Pleurisy causes fluid to collect inside the lung area. Breathing may be rapid and shallow because deep breathing induces pain; the muscles on the painful side move less than those on the other side. When an accumulation of fluids (pleural effusion) is associated with pleurisy, the pain usually disappears because the fluid serves as a lubricant. Treatment depends on what is causing the pleurisy. Bacterial infections are treated with antibiotics.

Rheumatoid arthritis is an inflammatory form of arthritis that causes joint pain and damage. It affecting more than two million people in the United States. Rheumatoid arthritis attacks the lining of your joints (synovium) causing swelling that can result in aching and throbbing and eventually deformity. Sometimes rheumatoid arthritis symptoms make even the simplest activities – such as opening a jar or taking a walk – difficult to manage. Rheumatoid arthritis is two to three times more common in women than in men and generally occurs between the ages of 40 and 60. But rheumatoid arthritis can also affect young children and older adults. It is commonly polyarticular; that is, it affects many joints.

About seventy-five percent of those affected are women, and 1-3% of women may develop rheumatoid arthritis is their lifetime. The disease most often begins between the fourth and sixth decades of life; however, RA can develop at any age. RA usually affects joints on both sides of the body equally. Wrists, fingers, knees, feet, and ankles are the most commonly affected.Rheumatoid arthritis is two to three times more common in women than in men and generally occurs between the ages of 40 and 60. But rheumatoid arthritis can also affect young children and older adults. Inflammation, soft tissue swelling, and the involvement of multiple joints are common signs and symptoms that distinguish rheumatoid and other inflammatory arthritis from non-inflammatory arthritis such as osteoarthritis.

Treatments include medicine, lifestyle changes and surgery. These can slow or stop joint damage and reduce pain and swelling. To quickly reduce joint inflammation and symptoms, first-line treatment usually consists of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin and others), naproxen (Naprosyn, Aleve), celecoxib (Celebrex) and many others.


Diagram Of Pathophysiology Of Systemic Lupus Erythematosus

Dermatitis herpetiformis in India is very affordable-Complete Information Introduction Background
Dermatitis herpetiformis (DH ) is an autoimmune blistering disorder associated with a gluten-sensitive enteropathy (GSE). The disease was described and named in 1884 by Dr. Louis Duhring at the University of Pennsylvania. It is characterized by grouped excoriations; erythematous, urticarial plaques; and papules with vesicles. These are located on the extensor surfaces of the elbows, knees, buttocks, and back. It is exquisitely pruritic, and the vesicles are often excoriated to erosions by the time of physical examination. Diagnosis requires direct immunofluorescence of a skin biopsy specimen showing deposition of immunoglobulin A (IgA) in a granular pattern in the upper papillary dermis. Although most patients are asymptomatic, more than 90% have an associated GSE upon endoscopic examination. Among patients with celiac disease, 15-25% develop DERMATITIS HERPETIFORMIS . The mainstays of treatment are dapsone and a gluten-free diet.
Pathophysiology
DERMATITIS HERPETIFORMIS is a disease of the skin caused by the deposition of IgA in the papillary dermis, which triggers an immunologic cascade, resulting in neutrophil recruitment and complement activation. It has been hypothesized that DERMATITIS HERPETIFORMIS is the result of an immunologic response to chronic stimulation of the gut mucosa by dietary gluten with subsequent activation of cutaneous endothelial cells and circulating inflammatory cells, including neutrophils.

An underlying genetic predisposition to the development of DERMATITIS HERPETIFORMIS has been demonstrated. Both DERMATITIS HERPETIFORMIS and celiac disease (CD) show an increased expression of HLA-A1, HLA-B8, HLA-DR3, and HLA-DQ2 haplotypes. Environmental factors are also important; monozygotic twins may have DERMATITIS HERPETIFORMIS , CD, and/or GSE with variable symptomatology.

Evidence is mounting that epidermal transglutaminase 3 (TGase3), a cytosolic enzyme involved in cell envelope formation during keratinocyte differentiation, is the autoantigen of DERMATITIS HERPETIFORMIS . Theoretically, DERMATITIS HERPETIFORMIS is caused by dermal deposition of circulating immune complexes containing both IgA and TGase3. This is supported by the finding that precipitates of skin-bound IgA from DERMATITIS HERPETIFORMIS lesions contain TGase3. In addition, it has been demonstrated that serum from DERMATITIS HERPETIFORMIS patients contains high-affinity anti-TGase IgA autoantibodies. Skin and gut TGases are both highly homologous, and serum from patients with GSE, with or without skin disease, contains IgA antibodies to both skin and gut types. The target autoantigen of TGase3 has not been demonstrated in normal papillary dermis, suggesting it is part of the circulating complex that is deposited in the papillary dermis, rather than originating from the papillary dermis.

The leading theory for DERMATITIS HERPETIFORMIS is that a genetic predisposition for gluten sensitivity, coupled with a diet high in gluten, leads to the formation of IgA antibodies to gluten-TGase complexes. These antibodies cross-react with TGase3, and IgA/TGase3 complexes deposit within the papillary dermis to cause the lesions of DERMATITIS HERPETIFORMIS . These IgA deposits can disappear after long-term (up to 10 y) avoidance of dietary gluten.

Cutaneous IgA deposits in DERMATITIS HERPETIFORMIS have been shown to function in vitro as a ligand for neutrophil migration and attachment. Although IgA deposition is pivotal for disease, an increased serum IgA is not necessary for pathogenesis; in fact, case reports describeDERMATITIS HERPETIFORMIS in patients with a partial IgA deficiency. When the disease is active, circulating neutrophils have a higher level of CD11b and an increased ability to bind IgA. In fact, the characteristic histologic finding of DERMATITIS HERPETIFORMIS is neutrophil accumulation at the dermoepidermal junction, frequently localizing to the papillary tips of the basement membrane zone.

Collagenase and stromelysin 1 may be induced in basal keratinocytes by either cytokines released from neutrophils or by contact with keratin from damaged basement membrane matrix. Stromelysin 1 may contribute to blister formation.

One study found levels of E-selectin mRNA expression in normal-appearing skin of patients with DERMATITIS HERPETIFORMIS to be 1271 times greater that that of controls. Additionally, the same study observed increased soluble E-selectin, IgA antitissue transglutaminase antibodies, tumor necrosis factor-alpha, and serum interleukin 8 levels in patients with DERMATITIS HERPETIFORMIS , providing further evidence of endothelial cell activation and a systemic inflammatory response as part of the pathogenic mechanism of the disease. Mild local trauma may also induce the release of cytokines and attract the partially primed or activated neutrophils, which is consistent with the typical location of DERMATITIS HERPETIFORMIS lesions on frequently traumatized areas, such as the knees and elbows.

Deposits of C3 also may be present in a similar pattern at the dermoepidermal junction. The membrane attack complex, C5-C9, also has been identified in perilesional skin, although it may be inactive and not contribute to cell lysis.

Hormonal factors may also play a role in the pathogenesis of DERMATITIS HERPETIFORMIS , and 2recent reports describe DERMATITIS HERPETIFORMIS induced by treatment with leuprolide acetate, a gonadotropin-releasing hormone analog. Androgens have a suppressive effect on immune activity, including decreased autoimmunity, and androgen deficient states may be a potential trigger for DERMATITIS HERPETIFORMIS exacerbation.

Apoptosis may contribute to the pathogenesis of epidermal changes in DERMATITIS HERPETIFORMIS , and recent research demonstrates a markedly increased apoptotic rate within the epidermal compartment in DERMATITIS HERPETIFORMIS . In addition, Bax and Bcl-2 proteins were increased in the dermal perivascular compartment and Fas proteins showed epidermal staining in DERMATITIS HERPETIFORMIS lesions.

Most patients with DERMATITIS HERPETIFORMIS have histologic evidence of enteropathy, even in the absence of symptoms of malabsorption. In one recent study, all DERMATITIS HERPETIFORMIS patients had increased intestinal permeability (as measured by the lactulose/mannitol ratio) and up-regulation of zonulin, a regulator of tight junctions. Thus, increased expression of zonulin may be involved in the pathogenesis of enteropathy in patients with DERMATITIS HERPETIFORMIS .
Frequency
United States

The only US study showed a prevalence of 11.2 cases per 100,000 population.

International

Prevalence has been reported as high as 10 cases per 100,000 population.
Mortality/Morbidity
Patients with DERMATITIS HERPETIFORMIS were followed (152 total) from the date of diagnosis to the end of 1989 for mortality and from 1971 or the date of diagnosis (if later) to 1986 for cancer incidence. Death occurred in 38 patients younger than 85 years, slightly fewer than expected on the basis of national general population rates. Cancer incidence was significantly increased. Cancer of the small intestine caused 1 death, and lymphoma caused 1 death. A 30-year population-based study of 1147 CD and DERMATITIS HERPETIFORMIS patients in Finland also revealed an overall good prognosis for patients with DERMATITIS HERPETIFORMIS . The total occurrence of malignancies was equal to that of the general population in both CD and DERMATITIS HERPETIFORMIS , but an increased incidence of non-Hodgkin lymphoma was noted among both CD and DERMATITIS HERPETIFORMIS patients with standardized incidence ratios of 3.2 and 6.0, respectively. Overall mortality was actually decreased in DERMATITIS HERPETIFORMIS patients compared to that in the general population.

DERMATITIS HERPETIFORMIS lesions are extremely pruritic. Morbidity results from scarring, discomfort, and insomnia due to itching. Secondary infection may also develop, requiring antibiotic therapy.
Race
DERMATITIS HERPETIFORMIS occurs more frequently in individuals of Northern European ancestry and is rare in Asians and persons of African descent. It is most common in Ireland and Sweden. This can be attributed to the shared HLA associations of DERMATITIS HERPETIFORMIS and CD including DQA1*0501 and B1*-02, which encode HLA-DQ2 heterodimers.
Sex
US studies show a male-to-female ratio of 1.44:1, but international studies have demonstrated a male-to-female ratio up to 2:1. In one study of patients with GSE, 16% of the men and 9% of the women had DERMATITIS HERPETIFORMIS .
Age
Typically, the onset of DERMATITIS HERPETIFORMIS is in the second to fourth decade; however, persons of any age may be affected.
Clinical History
Patients typically present with a waxing and waning, pruritic eruption on the arms, knees, and buttocks. Small vesicles may have been noted. They may have associated worsening of disease with dietary intake of gluten. Many do not report any GI symptoms until prompted.
Physical
The diagnosis is suspected based on the distribution of the eruption.
Flesh-coloredtoerythematous excoriated papules or plaques with herpetiform (ie, small, clustered) vesicles are symmetrically distributed over extensor surfaces, including the elbows, knees, buttocks, and shoulders. It rarely occurs on the posterior (nuchal) scalp and face. Lesions occur infrequently on the oral mucosa, but males are more likely than females to have involvement of the oral and genital membranes. Palms and soles are spared. Digital purpura resembling vasculitis can occur. Erythematous papules and urticarialike plaques occur less frequently; bullae are rare. The eruption is intensely pruritic; patients often present with erosions and crusts in the absence of vesicles, which have ruptured due to excoriation. Typical symptoms include burning, stinging, and intense itching. Rarely, if ever, are patients totally asymptomatic, although the degree of itching varies. DERMATITIS HERPETIFORMIS is a lifelong disease, although periods of exacerbation and remission are common. Causes
DERMATITIS HERPETIFORMIS has recently been proposed as a cutaneous manifestation of asymptomatic-to-mild CD. The genetic predisposition to the development of gluten sensitivity underlies the disease.
Gluten is a protein present in grasses of the species Triticeae, which includes barley, rye, and wheat. Rice and oats belong to different species and are generally well tolerated. Strict compliance with a gluten-free diet results in normalization of the small bowel mucosal changes and control of the cutaneous manifestations of DERMATITIS HERPETIFORMIS in most patients. The GSE does not cause symptoms in most DERMATITIS HERPETIFORMIS patients. Less than 10% exhibit symptoms of bloating, diarrhea, or malabsorption. However, greater than 90% show abnormalities upon endoscopic examination. Two thirds have villous atrophy detected on intestinal biopsy specimens. The other third shows elevated intraepithelial lymphocyte counts, increased T-cell receptor gamma/delta intraepithelial lymphocyte counts, or both. The critical role of associated GSE in the pathogenesis of DERMATITIS HERPETIFORMIS is confirmed by the fact that resumption of a gluten-containing diet in patients with DERMATITIS HERPETIFORMIS results in a return of the characteristic skin disease. Mild steatorrhea or other signs of mild malabsorption (eg, altered D-xylose absorption, iron or folate deficiency) can be demonstrated in 20-30% of patients with DERMATITIS HERPETIFORMIS . Patients with DERMATITIS HERPETIFORMIS and no apparent GI disease can be induced into developing DERMATITIS HERPETIFORMIS by increasing gluten intake, which is often termed latent GSE (CD). IgA circulating immune complexes are present in 25-35% of patients with DERMATITIS HERPETIFORMIS , although no association with disease severity has been noted. These immune complexes also have been noted in patients with isolated GSE and are believed to be related to the presence of the gut disease. IgA antibodies to gliadin (a portion of wheat protein), reticulum, and smooth muscle endomysium have also been noted in patients with DERMATITIS HERPETIFORMIS and in those with isolated GSE. IgA endomysial antibodies are most specific for gluten sensitivity and are found in 80% of patients with DERMATITIS HERPETIFORMIS and greater than 95% of patients with CD. The presence of IgA antiendomysial antibodies correlates with the extent of the gut disease; however, some DERMATITIS HERPETIFORMIS patients do not have detectable IgA antiendomysial antibodies, even during episodes of active skin disease. The criterion standard for the diagnosis of DERMATITIS HERPETIFORMIS remains the presence of granular deposits of IgA in normal-appearing perilesional skin. Patients with bullous pemphigoid, cicatricial pemphigoid, Henoch-Schnlein purpura, and alcoholic liver disease also may have IgA deposits in normal skin; however, the pattern of IgA deposits is different from that seen in patients with DERMATITIS HERPETIFORMIS . In patients with DERMATITIS HERPETIFORMIS , 10-15% of their first-degree relatives have DERMATITIS HERPETIFORMIS or CD. HLA studies have conclusively established the presence of a genetic predisposition for DERMATITIS HERPETIFORMIS . Patients with DERMATITIS HERPETIFORMIS have an increased expression of the HLA-A1, HLA-B8, HLA-DR3, and HLA-DQ2 haplotypes. This is identical to the HLA association found in patients with isolated GSE. Most persons with these HLA types do not have DERMATITIS HERPETIFORMIS or GSE. Associations of HLA and DERMATITIS HERPETIFORMIS are as follows: For HLA-B8, the association with DERMATITIS HERPETIFORMIS is 58-87%, versus 20-30% for control patients. For HLA-DR3, the association with DERMATITIS HERPETIFORMIS is 90-95%, versus 23% for control patients. For HLA-DQ2, the association with DERMATITIS HERPETIFORMIS is 95-100%, versus 40% for control patients. Other associations include the following: Associated GI conditions include gluten enteropathy, gastric atrophy, gastric hypochlorhydria, and pernicious anemia. Associated autoimmune diseases include dermatomyositis, type 1 diabetes mellitus, myasthenia gravis, rheumatoid arthritis, Sjgren syndrome, systemic lupus erythematosus, and thyroid abnormalities. Thyroid abnormalities are present in as many as 50% of DERMATITIS HERPETIFORMIS patients and include hypothyroidism, hyperthyroidism, thyroid nodules, and thyroid cancer. Associated neoplastic conditions include GI lymphomas and non-Hodgkin lymphoma; patients are at increased risk of developing these cancers. A gluten-free diet may reduce incidence of DERMATITIS HERPETIFORMIS -associated lymphomas. CD usually involves more severe and widespread intestinal involvement. CD has been associated with genetic abnormalities, including Down syndrome, Turner syndrome, and William syndrome. Liver disease, neurologic disorders, and other skin diseases are also increased in CD, possibly due to common HLA regions on chromosome 6 or immune molecule cross-reactivity. Gastric manipulation (surgery) may induce DERMATITIS HERPETIFORMIS . Several chemicals have been associated with induction of DERMATITIS HERPETIFORMIS , including potassium iodide and cleaning solutions. Case reports have describedDERMATITIS HERPETIFORMIS induced by treatment with leuprolide acetate.
Differential Diagnoses

Bullous Pemphigoid
Erythema Multiforme
Linear IgA Dermatosis
Neurotic Excoriations
Scabies
Transient Acantholytic Dermatosis

Other Problems to Be Considered

Eczema
Papular urticaria

Workup

Laboratory Studies
The diagnosis is made on the basis of skin biopsy results. However, other tests should be performed depending on the presence of symptoms of associated syndromes. Serum markers, such as IgA endomysial antibodies, are negative in up to 10-30% of patients with DERMATITIS HERPETIFORMIS . Arguments have been made in favor of testing for tissue transglutaminase for diagnosis, but tissue transglutaminase enzyme-linked immunosorbent assay positivity can occur in many autoimmune diseases because of impurities and cross-reactivity.
Procedures
The diagnosis is made after observing characteristic findings from skin biopsy specimens. The biopsy sample should be taken from the edge of a lesion for hematoxylin and eosin staining and from normal-appearing perilesional skin for direct immunofluorescence staining. Direct immunofluorescence of lesional skin is often falsely negative. The vigorous immune response degrades the IgA antibody at the site. Therefore, biopsy specimens for the direct immunofluorescence studies should be taken from healthy-appearing skin.
Histologic Findings

Biopsy specimens of lesional skin reveal neutrophils in the dermal papillae, with fibrin deposition, neutrophil fragments, and edema. Eosinophils may be present. Papillary microabscesses form and progress to subepidermal vacuolization and vesicle formation. Vesicles form in the lamina lucida, the weakest portion of the dermoepidermal junction, due to neutrophil lysosomal enzymes

The histologic differential diagnosis of early skin lesions includes bullous lupus erythematosus, bullous pemphigoid, epidermolysis bullosa acquisita, and linear IgA disease. The histologic differential diagnosis of late skin lesions includes bullous drug eruption, bullous pemphigoid, erythema multiforme, and herpes gestationis.

Granular IgA deposits in dermal papillae of perilesional skin observed by direct immunofluorescence is the criterion standard of diagnosis. Inflammation in lesional skin degrades the immunoreactants and is usually negative for the diagnostic granular pattern. Because deposits are found throughout normal-appearing skin, the standard practice is to obtain biopsy specimens from normal-appearing perilesional skin for direct immunofluorescent staining.

Treatment

Medical Care

Control of the skin disease can be achieved with medications, dietary avoidance of gluten, or both.
A gluten-free diet is very difficult to achieve; however, limiting intake of wheat, barley, or rye products can lessen the symptoms. Dapsone (diaminodiphenyl sulfone) and sulfapyridine are the primary medications used to treat DERMATITIS HERPETIFORMIS . Before easy availability of direct immunofluorescence, rapid improvement after dapsone therapy was a chief diagnostic criterion for the disease. However, many diseases respond to dapsone, and this should not be used as the only diagnostic criterion. Dapsone is readily available at most pharmacies and is the first-line drug therapy. For patients unable to tolerate dapsone, particularly those who develop hemolysis, sulfapyridine may be substituted. The mechanism for therapeutic effect of dapsone in DERMATITIS HERPETIFORMIS is unclear. It may be related to the inhibition of neutrophil migration into the area, thus, decreasing the inflammatory response. Improvement may be dramatic; symptomatic improvement of skin lesions often begins within hours. No new lesions form for up to 2 days after a dose of dapsone; however, dapsone does not improve GI mucosal pathology. Other, less effective treatments for DERMATITIS HERPETIFORMIS include colchicine, cyclosporine, azathioprine, and prednisone. UV light may provide some symptomatic relief. Cyclosporine should be used with caution in patients with DERMATITIS HERPETIFORMIS because of a potential increase in the risk of developing intestinal lymphomas. One case report describedresolution of DERMATITIS HERPETIFORMIS after initiation of the Atkins diet. Nonsteroidal anti-inflammatory drugs may exacerbate DERMATITIS HERPETIFORMIS ; however, ibuprofen appears to be safe. Iodides may elicit or exacerbate DERMATITIS HERPETIFORMIS .
Consultations
Consider consultation with a gastroenterologist for evaluation and for recommendations regarding GSE. Consult with a dietitian regarding patients who are modifying dietary intake to avoid gluten or who are instituting an elemental diet.
Diet

Dietary intake of gluten causes the disease, and elimination improves it.
Most patients (as many as 80%) respond to gluten-free diet with control of their skin disease. Some patients are able to totally discontinue dapsone therapy. Compliance with a gluten-free diet is difficult and requires a motivated patient, and the best treatment response occurs with absolute gluten restriction in the diet. Strict dietary vigilance may be required for 5-12 months before the dapsone dose can be reduced. Maintaining a gluten-free diet is the only sustainable method of eliminating the disease, not only from the skin, but also from the GI mucosa. Patients on a gluten-reduced diet may experience a decrease in symptoms; therefore, diet reduces the dosage of dapsone required for disease control. Neither IgA deposition nor circulating antibodies correlate with gluten intake in short-duration studies; however, some studies have suggested a correlation with complement deposition. Avoidance of dietary gluten for 10 years or more has resulted in loss of cutaneous IgA deposits, which then return upon reinstitution of gluten in the diet. Elemental diets may improve the disease within weeks. These diets consist of free amino acids, small amounts of triglycerides, and short-chain polysaccharides; they are marketed by pharmaceutical companies. One report has suggested that this improvement may be independent of gluten ingestion; however, this finding has not been confirmed.
Follow-up

Further Outpatient Care
Dietitians and gastroenterologists are helpful in addressing the GSE.
Complications
Complications are related to the GSE, the risk of developing lymphomas, and the potential adverse effects of medications (dapsone).
Prognosis
DERMATITIS HERPETIFORMIS is an ongoing disease process of variable severity. The prognosis is good for patients who can tolerate dapsone and the few who can maintain a gluten-free diet (which may decrease the risk of lymphoma).
Patient Education
Educate patients regarding the use of a gluten-free diet as well as the adverse effects and complications of dapsone.
Miscellaneous

Medicolegal Pitfalls
Failure to consider and diagnose DERMATITIS HERPETIFORMIS can result in the continuation of a distressing disease in a patient who can be treated successfully with dapsone. Failure to mention the association of DERMATITIS HERPETIFORMIS with gluten sensitivity and the association with lymphoma can result in further distress to the patient. Although maintenance of a gluten-free diet demands a motivated patient, it should always be offered as an option. Failure to diagnose DERMATITIS HERPETIFORMIS with immunofluorescence can result in an erroneous diagnosis and the concomitant associated adverse effects of medications (eg, dapsone) used ineffectively. Patients must be monitored when using dapsone or sulfapyridine. Very commonly, patients’ hemoglobin levels drop by 1-2 g/dL while taking dapsone. Larger decreases may be seen. Patients should be counseled regarding the signs of a pronounced hemolytic anemia or methemoglobinemia, including malaise, shortness of breath, tachycardia, or jaundice. Most patients can continue the dapsone if the anemia is mild and they are asymptomatic.
Special Concerns
Polymorphic lesions and an atypical presentation, including a paucity of the characteristic vesicles may make clinical diagnosis difficult. Histopathologic and immunologic confirmation of clinically suspected disease is mandatory for diagnosis.

Drug Induced Systemic Lupus Erythematosus

Lupus is a rare condition, but it can be a very difficult one. When you suffer from lupus, more than one of your organs may be affected. There are three lupus types that one can suffer from: systemic, discoid and lupus induced by drugs.

The discoid form of lupus affects only somebody’ s skin. To diagnose this kind of lupus, the doctor has to do a biopsy of the rash that you are suffering. Because discoid lupus affects only the skin in form of a rash, this is the only proper way to diagnose lupus. The biopsy of the skin affected by lupus will show some abnormalities that otherwise will not be found in a type of skin that has not been affected by lupus. This type of lupus does not affect the internal organs. So a blood test will not be able to confirm if you have discoid lupus or not. Blood tests are used to detect another lupus type, the systematic lupus. There are lupus patients that will show a positive result in their blood test, even if they are suffering from discoid lupus. However, the levels of tiver in their blood will be very little. Although the discoid form of lupus only affects your skin, this lupus type can evolve and become the systemic type of lupus. This particular lupus type can affects almost all your internal organs. Systemic lupus can also atack your nervous system. Unfortunately, this change from discoid lupus to systemic lupus can not be prevented. Even if your treat your discoid type of lupus, you can to prevent it from developing into the systemic lupus type.

Many of the people that go on to have systemic lupus, probably suffered from this form of lupus from the beginning, and the discoid lupus was just one of the symptoms. Normally, there are not two people that suffer from systemic lupus and have the same symptoms. However, many of the lupus symptoms that they have can be similar. The third type of lupus, that induced by drugs, usually sets off after you use a certain drug. The signs of the drug induced type of lupus are very similar to the systemic lupus type. The drugs that are more related with lupus are those used for high blood pressure. Drugs that are used to treat an irregular heart beat are also thought to cause lupus.

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Systemic Lupus Erythematosus Treatment Chennai

Scleroderma is the prototype of the fibrotic skin diseases. It may manifest either as systemic and localized forms. Progressive systemic sclerosis (PSS) is a generalized connective tissue disorders, the fibrotic process of affecting not only the skin but also the heart, lungs, kidneys, and the gastrointestinal tract. The overall female to male incidence of scleroderma is 3:1. The average age of onset is 40 to 50 years. In women, however, the average age of onset lies in the child bearing age between 30 and 39. Men and older patients with systemic scleroderma tend to have a shorter survival rate and thus a poorer prognosis.

Clinical Features Systemic cleroderma may involve all connective tissue containing organs; however, some represent the main target of the disease. These include the skin, gastrointestinal tract, heart, lungs, and kidneys.

Cutaneous Manifestations are usually early symptoms. They may either proceeds or accompany Raynaud’s disease.They may be divided into an early edemaous phase, sclerotic phase, and late atrophic phase.

Raynaud’s phenomenon It occurs in over 90 percent of patients with scleroderma and may be the initial symptom. It is characterized by a triphasic color reaction involving the distal digits.

Gastrointestinal tract Most systemic scleroderma patients may develop dysphagia, regurgitation, peptic esophagitiss, and fibrotic strictures.

Heart Primary cardiac involvement is common in systemic scleroderma. However, it is frequently overlooked.

Lungs Pulmonary involvement is one of the most important clinical features in systemic scleroderma. In addition to X- ray procedures and functional tests, scintigraphy and the bronchoalveolar lavage have offered new insights into the pathophysiologic events.

Kidneys The presence of renal involvement in scleroderma is regarded as one of the features associated with the poorest prognosis. The clinical criteria for renal disease in scleroderma include persistent proterinuria (> 500 mg/ 24 hr), hypertension (> 140/ 90 mm Hg), and azotemia (blood urea nitrogen BUN > 25 mg/ 100 mL).

Systemic Lupus Erythematosus Treatment-related Complications Superimposed Chronic Disease

RHEUMATOID ARTHRITIS Rheumatoid arthritis is an autoimmune disease in which the body ‘attack on the immune system itself. The pattern of joints affected is usually symmetrical, involves the hands and other joints and is worse in the morning.

Rheumatoid arthritis is a systemic disease, involving other organs, whereas osteoarthritis is limited to the joints. Over time, both forms of arthritis can be crippling. SLE Systemic Lupus erythematosus and rheumatoid arthritis (RA). The etiology of cardiovascular disease probably involved an interaction between risk factors traditional and inflammation induced immune-mediated vascular injury, and hormonal and treatment-related factors.

autoimmune and chronic inflammatory nature of both RA and SLE may contribute to atherogenesis. However, there are enough differences in the pathogenesis, organ involvement, and the modalities of treatment of SLE and RA suggest that the differences may exist in the development of atherosclerosis in each of these diseases
Entries the disease is often progressive, with fatigue, morning stiffness (with a duration of more than one hour), diffuse muscle pain, loss of appetite and weakness. Finally, joint pain appears, with warmth, swelling, tenderness, and stiffness of the joint after inactivity.

The cause of rheumatoid arthritis (RA) is unknown. However, RA involves an attack on the body’s own immune cells (autoimmune disease). Different cases may have different causes. Infectious, genetic and hormonal factors may play a role.RA usually affects the joints on both sides of the body also — wrists, fingers, knees, feet and ankles are the most affected.

Difformits result from the destruction of cartilage, bone erosions, and tendon inflammation and fracture. A joint life-threatening complications can occur when the cervical spine becomes unstable as a result of RA.Rheumatoid arthritis is a systemic autoimmune disease that attacks the first synovium, a connective tissue membrane that lines the cavity between joints and secret liquid lubrication.

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Systemic Lupus Erythematosus Causes Treatment

Lupus Overview

Systemic lupus erythematosus (lupus, SLE) is an autoimmune disease in which a person’s immune system attacks various organs or cells of the body causing damage and dysfunction. Lupus is called a multisystem disease because it can affect many different tissues and organs in the body. Some patients with lupus have a very mild condition, which can be treated with simple medications, whereas others can have serious, life-threatening complications. Lupus is more common in women than men, and its peak incidence is after pubertythe reason for this is unknown.

What is lupus nephritisc

Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. SLE typically causes harm to the skin, joints, kidneys, and brain.
The causes of SLE are unknown. Many factors may play a role, including
genderSLE is more common in women than men
hereditya gene passed down by a parent
infections
viruses
environmental causes

Systemic lupus erythematosus(SLE) is the most common form of lupus. “Systemic” means it can affect several parts of the body. A subtype of SLE is drug-induced lupus. Some medications uncommonly used for high blood pressure, heart disease and tuberculosis can cause this condition.
What are Neurological Sequelae Of Lupusc

Lupus (also called systemic lupus erythematosus) is a disorder of the immune system. Normally, the immune system protects the body against invading infections and cancers. In lupus, the immune system is over-active and produces increased amounts of abnormal antibodies that attack the body’s tissues and organs. Lupus can affect many parts of the body, including the joints, skin, kidneys, lungs, heart, nervous system, and blood vessels. The signs and symptoms of lupus differ from person to person; the disease can range from mild to life threatening.

What is the outlookc

Some people with lupus have only minor symptoms that need no treatment. Others can have multiple symptoms that are severe.
The course of the disease is different for each person. In some it will disappear completely, for others the condition waxes and wanes or gets progressively worse.

Lupus can be difficult to diagnose because the symptoms and disease pattern varies so much from person to person.
However, there are blood tests available to help spot the condition.

What causes Lupusc

Despite many years of research, the cause of lupus is still not known. Scientists believe there are several things that may trigger the formation of the antibodies, including genetic, hormonal and environmental factors. Some of the possible triggers include:

– Hormones (females between the age of 15 and 45 are most commonly affected)
– Certain medications
– Dietary factors
– Viruses and bacteria
– Stress
– Genetics
– Pregnancy
– Exposure to UV light

Signs and symptoms

No two cases of lupus are exactly alike. Signs and symptoms may come on suddenly or develop slowly, may be mild or severe, and may be temporary or permanent. Most people with lupus experience episodes called “flares” of worsening signs and symptoms that eventually improve or even disappear completely for a time.
The signs and symptoms of lupus that you experience will depend on which body systems are affected by the disease.