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Treatment should be directed towards the specific underlying cause of the vasculitis. If no underlying cause is found and the vasculitis is truly limited to the skin then treatment is primarily supportive. Such treatment involves measures such as leg elevation, stockings, and topical steroids to relieve itching/burning. If the vasculitis does not self-resolve within 3–4 weeks, more aggressive treatment may be warranted. Oral colchicine or dapsone are often used for this purpose. If rapid control of symptoms is needed, a short course of high-dose oral steroids may be given. Immunosuppressive agents such as methotrexate and azathioprine may be used in truly refractory cases not responsive to colchicine or dapsone.
Erythema multiforme is frequently self-limiting and requires no treatment. The appropriateness of glucocorticoid therapy can be uncertain, because it is difficult to determine if the course will be a resolving one.
The basis of management is to find and correct the underlying cause. Many times cats with EGC will respond to treatment with corticosteroids or to ciclosporin.
Topical treatment for the skin changes of scleroderma do not alter the disease course, but may improve pain and ulceration. A range of NSAIDs (nonsteroidal anti-inflammatory drugs) can be used to ease painful symptoms, such as naproxen. There is limited benefit from steroids such as prednisone. Episodes of Raynaud's phenomenon sometimes respond to nifedipine or other calcium channel blockers; severe digital ulceration may respond to prostacyclin analogue iloprost, and the dual endothelin-receptor antagonist bosentan may be beneficial for Raynaud's phenomenon. The skin tightness may be treated systemically with methotrexate and ciclosporin. and the skin thickness treated with penicillamine.
There are no permanent cures for urticaria pigmentosa. However, treatments are possible. Most treatments for mastocytosis can be used to treat urticaria pigmentosa. Many common anti-allergy medications are useful because they reduce the mast cell's ability to react to histamine.
At least one clinical study suggested that nifedipine, a calcium channel blocker used to treat high blood pressure, may reduce mast cell degranulation in patients with urticaria pigmentosa. A 1984 study by Fairly et al. included a patient with symptomatic urticaria pigmentosa who responded to nifedipine at dose of 10 mg po tid. However, nifedipine has never been approved by the FDA for treatment of urticaria pigmentosa.
Another mast cell stabilizer Gastrocrom, a form of cromoglicic acid has also been used to reduce mast cell degranulation.
Scleroderma renal crisis, the occurrence of acute renal failure and malignant hypertension (very high blood pressure with evidence of organ damage) in people with scleroderma, is effectively treated with drugs from the class of the ACE inhibitors. The benefit of ACE inhibitors extends even to those who have to commence dialysis to treat their kidney disease, and may give sufficient benefit to allow the discontinuation of renal replacement therapy.
Hospitalization for the diseased person is suggested because of the controlled environment because it may prevent nutritional deficiencies and skin infections. A decrease in severity of symptoms usually happens after a few weeks when treated redness and scaliness usually do not recur. In 10 percent of cases, the result of uncontrolled infections or severe electrolyte loss may be fatal.
Other than identifying and treating any underlying conditions in secondary livedo, idiopathic livedo reticularis may improve with warming the area.
Intertrigo is treated by addressing associated infections, by removing moisture from the site, and by using substances at the site to help maintain skin integrity. If the individual is overweight, losing weight may also help. Relapses of intertrigo are common.
Keeping the area of the intertrigo dry and exposed to the air can help prevent recurrences, as can removing moisture from the area using absorbent fabrics or body powders, including plain cornstarch and judiciously used antiperspirants.
Greases, oils, and barrier ointments, may help by protecting skin from moisture and from friction. Antifungal powders, most commonly clotrimazole 1%, may also be used in conjunction with a barrier ointment. Diaper rash ointment can also help.
Fungal infections associated with intertrigo may be treated with prescription antifungals applied directly to the skin (in most cases) or systemic antifungals, including fluconazole, nystatin, and griseofulvin.
Intertrigo is also a known symptom of vitamin B6 deficiency.
Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general.
Ursodeoxycholic acid has been used successfully as a treatment for cases with liver involvement. Thalidomide has also been tried successfully as a treatment for treatment-resistant lupus pernio in a clinical trial, which may stem from its anti-TNF activity, although it failed to exhibit any efficacy in a pulmonary sarcoidosis clinical trial. Cutaneous disease may be successfully managed with antimalarials (such as chloroquine and hydroxychloroquine) and the tetracycline antibiotic, minocycline. Antimalarials have also demonstrated efficacy in treating sarcoidosis-induced hypercalcemia and neurosarcoidosis. Long-term use of antimalarials is limited, however, by their potential to cause irreversible blindness and hence the need for regular ophthalmologic screening. This toxicity is usually less of a problem with hydroxychloroquine than with chloroquine, although hydroxychloroquine can disturb the glucose homeostasis.
Recently selective phosphodiesterase 4 (PDE4) inhibitors like apremilast (a thalidomide derivative), roflumilast, and the less subtype-selective PDE4 inhibitor, pentoxifylline, have been tried as a treatment for sarcoidosis, with successful results being obtained with apremilast in cutaneous sarcoidosis in a small open-label study. Pentoxifylline has been used successfully to treat acute disease although its use is greatly limited by its gastrointestinal toxicity (mostly nausea, vomiting, and diarrhea). Case reports have supported the efficacy of rituximab, an anti-CD20 monoclonal antibody and a clinical trial investigating atorvastatin as a treatment for sarcoidosis is under-way. ACE inhibitors have been reported to cause remission in cutaneous sarcoidosis and improvement in pulmonary sarcoidosis, including improvement in pulmonary function, remodeling of lung parenchyma and prevention of pulmonary fibrosis in separate case series'. Nicotine patches have been found to possess anti-inflammatory effects in sarcoidosis patients, although whether they had disease-modifying effects requires further investigation. Antimycobacterial treatment (drugs that kill off mycobacteria, the causative agents behind tuberculosis and leprosy) has also proven itself effective in treating chronic cutaneous (that is, it affects the skin) sarcoidosis in one clinical trial. Quercetin has also been tried as a treatment for pulmonary sarcoidosis with some early success in one small trial.
Because of its uncommon nature, the treatment of male reproductive tract sarcoidosis is controversial. Since the differential diagnosis includes testicular cancer, some recommend orchiectomy, even if evidence of sarcoidosis in other organs is present. In the newer approach, testicular, epididymal biopsy and resection of the largest lesion has been proposed.
As the granulomas are caused by collections of immune system cells, particularly T cells, there has been some success using immunosuppressants (like cyclophosphamide, cladribine, chlorambucil, and cyclosporine), immunomodulatory (pentoxifylline and thalidomide), and anti-tumor necrosis factor treatment (such as infliximab, etanercept, golimumab, and adalimumab).
In a clinical trial cyclosporine added to prednisone treatment failed to demonstrate any significant benefit over prednisone alone in people with pulmonary sarcoidosis, although there was evidence of increased toxicity from the addition of cyclosporine to the steroid treatment including infections, malignancies (cancers), hypertension, and kidney dysfunction. Likewise chlorambucil and cyclophosphamide are seldom used in the treatment of sarcoidosis due to their high degree of toxicity, especially their potential for causing malignancies. Infliximab has been used successfully to treat pulmonary sarcoidosis in clinical trials in a number of persons. Etanercept, on the other hand, has failed to demonstrate any significant efficacy in people with uveal sarcoidosis in a couple of clinical trials. Likewise golimumab has failed to show any benefit in persons with pulmonary sarcoidosis. One clinical trial of adalimumab found treatment response in about half of subjects, which is similar to that seen with infliximab, but as adalimumab has better tolerability profile it may be preferred over infliximab.
Antihistamines are used primarily to reduce itching, if present. However, research studies suggest that some antihistamines have anti-inflammatory properties.
The topical antifungal medications ketoconazole and ciclopirox have the best evidence. It is unclear if other antifungals are equally effective as this has not been studied.
Treatment consists primarily of immunosuppressive drugs (e.g., hydroxychloroquine and corticosteroids). An interesting second line drug is methotrexate in its low-dose schedule. In 2011, the U.S. Food and Drug Administration (FDA) approved the first new drug for lupus in more than 50 years to be used in the US, belimumab. In addition to medicative therapy, due to the psychological and social impacts that Lupus may have on an individual, Cognitive Behavioural Therapy (CBT) has also been demonstrated to be effective in reducing stress, anxiety, and depression in lupus sufferers.
The culprit can be both a prescription drug or an over-the-counter medication.
Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.
Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.
If the cradle cap is not severe, it could simply be combed out gently after bathing. The softened scales can then be brushed away with a soft brush, comb or cloth, but if not done very gently, this could worsen the condition and bring about temporary hair loss. Applying petroleum jelly (e.g., Vaseline) liberally overnight is another popular treatment. The softened scales either fall off during the night, or can be brushed off in the morning. Making a paste from sodium bicarbonate (baking soda) and leaving it on the affected area for 10 minutes can also help lift the scales. There have been no studies done on these treatments.
There is broad disagreement regarding the role of shampoos. Some sources warn against frequent shampooing, others recommend it. Mild baby shampoo is often recommended, but the exact denotation of the label "mild" in this context is not quite clear. Baby shampoos often contain detergent surfactants, perfumes, quaternium-15 and other eczemagenic irritants. Again, no studies have been performed on non-prescription shampoos.
In stubborn cases some doctors may recommend keratolytic (dandruff) shampoos (e.g. with sulfur, selenium, zinc pyrithione, or salicylic acid) while others warn against the use of medicated shampoos in newborns due to systemic absorption. Dandruff shampoos often contain sodium dodecyl sulfate, a noted skin irritant.
Steroid and tar preparations have also been used but may have drawbacks. Immunomodulators (tacrolimus/Protopic, pimecrolimus/Elidel) have not been approved for babies under two years.
Ketoconazole shampoos and creams are currently shown to be the most effective medical treatment of moderate to serious cradle cap. Research indicates that this anti-fungal medication is not absorbed into the bloodstream.
Typical medical advice is to use diluted baby shampoo on a cotton swab to cleanse the eyelid. There is no agreement on the dilution, which ranges from a few drops to a half cup warm water, to a 50/50 mix.
Unfortunately, treatment for the anti-synthetase syndrome is limited, and usually involves immunosuppressive drugs such as glucocorticoids. For patients with pulmonary involvement, the most serious complication of this syndrome is pulmonary fibrosis and subsequent pulmonary hypertension.
Additional treatment with azathioprine and/or methotrexate may be required in advanced cases.
Prognosis is largely determined by the extent of pulmonary damage.
Both lyme disease and STARI can be treated with antibiotics, particularly doxycyclin.
The cause of this disease is unknown; some infants may have a severe case, others may have immunodeficiency.
CREST syndrome can be noted in up to 10% of patients with primary biliary cirrhosis.
Early stage sepsis-associated purpura fulminans may be reversible with quick therapeutic intervention. Treatment is mainly removing the underlying cause and degree of clotting abnormalities and with supportive treatment (antibiotics, volume expansion, tissue oxygenation, etc.). Thus, treatment includes aggressive management of the septic state.
Purpura fulminans with disseminated intravascular coagulation should be urgently treated with fresh frozen plasma (10–20 mL/kg every 8–12 hours) and/or protein C concentrate to replace pro-coagulant and anticoagulant plasma proteins that have been depleted by the disseminated intravascular coagulation process.
Protein C in plasma in the steady state has a half life of 6- to 10-hour, therefore, patients with severe protein C deficiency and presenting with purpura fulminans can be treated acutely with an initial bolus of protein C concentrate 100 IU/kg followed by 50 IU /kg every 6 hours. A total of 1 IU/kg of protein C concentrate or 1 mL/kg of fresh frozen plasma will increase the plasma concentration of protein C by 1 IU/dL. Cases with comorbid pathological bleeding may require additional transfusions with platelet concentrate (10–15 mL/kg) or cryoprecipitate (5 mL/kg).
Established soft tissue necrosis may require surgical removal of the dead tissue, fasciotomy, amputation or reconstructive surgery.
Alpha-1 antitrypsin deficiency panniculitis is a panniculitis associated with a deficiency of the α-antitrypsin enzyme.
Many suspected aetiologic factors have been reported to cause EM.
- Infections: Bacterial (including Bacillus Calmette-Guérin (BCG) vaccination, haemolytic "Streptococci", legionellosis, leprosy, "Neisseria meningitidis, Mycobacterium, "Pneumococcus, "Salmonella" species, "Staphylococcus" species, "Mycoplasma pneumoniae), "Chlamydial.
- Fungal (Coccidioides immitis)
- Parasitic ("Trichomonas" species, "Toxoplasma gondii), "
- Viral (especially Herpes simplex)
- Drug reactions, most commonly to: antibiotics (including, sulphonamides, penicillin), anticonvulsants (phenytoin, barbiturates), aspirin, antituberculoids, and allopurinol and many others.
- Physical factors: radiotherapy, cold, sunlight
- Others: collagen diseases, vasculitides, non-Hodgkin lymphoma, leukaemia, multiple myeloma, myeloid metaplasia, polycythemia
EM minor is regarded as being triggered by HSV in almost all cases. A herpetic aetiology also accounts for 55% of cases of EM major. Among the other infections, "Mycoplasma" infection appears to be a common cause.
Herpes simplex virus suppression and even prophylaxis (with acyclovir) has been shown to prevent recurrent erythema multiforme eruption.