Non-sedating antihistamines that block the histamine H1 receptors are the first line of therapy. First generation antihistamines such as diphenhydramine or hydroxyzine block both central and peripheral H1 receptors and can be sedating. Second generation antihistamines such as loratadine, cetirizine, or desloratadine selectively antagonize the peripheral H1 receptors and are less sedating, less anticholinergic, and generally preferred over the first generation antihistamines.

People who don’t respond to the maximum dose of H1 antihistamines may benefit from increasing the dose, then to switching to another non-sedating antihistamine, then to adding a leukotriene antagonist, then to using an older antihistamine, then to using systemic steroids and finally to using ciclosporin or omalizumab.

Treatments for autoimmune disease have traditionally been immunosuppressive, anti-inflammatory, or palliative. Managing inflammation is critical in autoimmune diseases. Non-immunological therapies, such as hormone replacement in Hashimoto's thyroiditis or Type 1 diabetes mellitus treat outcomes of the autoaggressive response, thus these are palliative treatments. Dietary manipulation limits the severity of celiac disease. Steroidal or NSAID treatment limits inflammatory symptoms of many diseases. IVIG is used for CIDP and GBS. Specific immunomodulatory therapies, such as the TNFα antagonists (e.g. etanercept), the B cell depleting agent rituximab, the anti-IL-6 receptor tocilizumab and the costimulation blocker abatacept have been shown to be useful in treating RA. Some of these immunotherapies may be associated with increased risk of adverse effects, such as susceptibility to infection.

Helminthic therapy is an experimental approach that involves inoculation of the patient with specific parasitic intestinal nematodes (helminths). There are currently two closely related treatments available, inoculation with either Necator americanus, commonly known as hookworms, or Trichuris Suis Ova, commonly known as Pig Whipworm Eggs.

T cell vaccination is also being explored as a possible future therapy for autoimmune disorders.

Oral glucocorticoids are effective in controlling symptoms of chronic hives however they have an extensive list of adverse effects such as adrenal suppression, weight gain, osteoporosis, hyperglycemia, etc. Therefore, their use should be limited to a couple of weeks. In addition, one study found that systemic glucocorticoids combined with antihistamines did not hasten the time to symptom control compared with antihistamines alone.

Vitamin D/Sunlight

Omega-3 Fatty Acids

Probiotics/Microflora

Antioxidants

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

AIP often completely resolves with steroid treatment. The failure to differentiate AIP from malignancy may lead to unnecessary pancreatic resection, and the characteristic lymphoplasmacytic infiltrate of AIP has been found in up to 23% of patients undergoing pancreatic resection for suspected malignancy who are ultimately found to have benign disease. In this subset of patients, a trial of steroid therapy may have prevented a Whipple procedure or complete pancreatectomy for a benign disease which responds well to medical therapy. "This benign disease resembles pancreatic carcinoma both clinically and radiographically. The diagnosis of autoimmune pancreatitis is challenging to make. However, accurate and timely diagnosis may preempt the misdiagnosis of cancer and decrease the number of unnecessary pancreatic resections." Autoimmune pancreatitis responds dramatically to corticosteroid treatment.

If relapse occurs after corticosteroid treatment or corticosteroid treatment is not tolerated, immunomodulators may be used. Immunomodulators such as azathioprine, and 6-mercaptopurine have been shown to extend remission of autoimmune pancreatitis after corticosteroid treatment. If corticosteroid and immunomodulator treatments are not sufficient, rituximab may also be used. Rituximab has been shown to induce and maintain remission.

Prevention focuses on improving sanitation of water and food sources.

Treatment focuses on addressing the central components of intestinal inflammation, bacterial overgrowth and nutritional supplementation.

There is evidence for a link between inflammation and depression. Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.

In addition there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode". Classical symptoms of being physically sick like lethargy show a large overlap in behaviors that characterize depression. Levels of cytokines tend to increase sharply during depressive episodes in manics and drop off during remission. Furthermore, it has been shown in clinical trials that anti-inflammatory medicines taken in addition to antidepressants not only significantly improves symptoms but also increases the proportion of subjects positively responding to treatment.

Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites.

Observation is acceptable if the lesions are neither symptomatic nor disfiguring. Intralesional or oral steroids can shrink the nodules, but seldom result in cure.

Cyclosporine has been reported to induce remission in patients with Kimura's disease, but recurrence of the lesions have been observed once this therapy is stopped.

Cetirizine is an effective agent in treating its symptoms. Cetirizine's properties of being effective both in the treatment of pruritus (itching) and as an anti-inflammatory agent make it suitable for the treatment of the pruritus associated with these lesions. In a 2005 study, the American College of Rheumatology conducted treatments initially using prednisone, followed by steroid dosages and azathioprine, omeprazole, and calcium and vitamin D supplements over the course of two years. The skin condition of the patient began to improve and the skin lesions lessened. However, there were symptoms of cushingoid and hirsutism observed before the patient was removed from the courses of steroids and placed on 10 mg/day of cetirizine to prevent skin lesions; an agent suitable for the treatment of pruritus associated with such lesions. Asymptomatically, the patient's skin lesions disappeared after treatment with cetirizine, blood eosinophil counts became normal, corticosteroid effects were resolved, and a remission began within a period of two months. It is also thought that the inhibition of eosinophils may be the key to treatment of Kimura's disease due to the role of eosinophils, rather than other cells with regards to the lesions of the skin.

Radiotherapy has been used to treat recurrent or persistent lesions. However, considering the benign nature of this disease, radiation should be considered only in cases of recurrent, disfiguring lesions.

Surgery has been considered the mainstay of therapy. However, recurrence after surgery is common.

In 2011, an eight-year-old boy had presented with a firm, nontender, nonfluctuating 15-12-cm mass on the left side of the neck involving the lateral region of the neck and jaw and a 5- to 7-cm mass on the right side of his neck. He had an eosinophil concentration of 36% (absolute count: 8172/ml), his IgE level was 9187 IU/ml. He was diagnosed with Kimura's disease. Initially treated with corticosteroids, he was given a single dose of intravenous immunoglobulin (IVIG) as a steroid-sparing agent after the disease flared while tapering prednisone. After IVIG administration, improvement was rapid, both left and right cervical masses diminished to less than 1 cm and his eosinophil and IgE levels returned to normal range. He has been free of disease during a six-year follow-up. IVIG may have value in the treatment of Kimura's disease.

A study is going on to assess the efficacy of tacrolimus on Kimura's disease. One case has so far been described. A patient with refractory Kimura's disease after surgery and treatment with prednisone was treated with tacrolimus. Tacrolimus (FK-506) was administered at an initial dosage of 1 mg every 12 hours, and FK-506 concentration in the blood was monitored monthly. FK-506 blood concentration was controlled within 5 to 15 μg/l. After 6 months, the dosage of tacrolimus was reduced to 0.5 mg daily for another 2 months and then treatment was stopped. Swelling of the bilateral salivary glands disappeared within the first week. No serious side effects were noted and the disease has not recurred in the 2 years of follow-up. Tacrolimus may be an effective treatment for patients with Kimura's disease, but more research is needed to determine its long-term efficacy and safety, as well as its mechanism of action.

Antihistamine agents are the typically prescribed drug for the treatment of physical urticaria. They block the effect of histamine, a compound produced by the body which forms a part of the local immune response consequently causing inflammation. Some research has suggested that the use antihistamines and antagonist in synergy are better for the treatment of physical urticarias.

The cascade of events that link the autoantibody-antigen reaction with the production and release of histamine is not well characterized. Therefore, the focus of treatment for physical urticaria has been on characterizing the effectiveness of antihistamines rather than analysis of receptor binding or the pathomechanisms.

Inflammation is usually indicated by adding the suffix "", as shown below. However, some conditions such as asthma and pneumonia do not follow this convention. More examples are available at list of types of inflammation.

Because neuroinflammation has been associated with a variety of neurodegenerative diseases, there is increasing interest to determine whether reducing inflammation will reverse neurodegeneration. Inhibiting inflammatory cytokines, such as IL-1β, decreases neuronal loss seen in neurodegenerative diseases. Current treatments for multiple sclerosis include interferon-B, Glatiramer actetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease. Current treatments for Alzheimer's disease include NSAIDs and glucocorticoids. NSAIDs function by blocking conversion of prostaglandin H2 into other prostaglandins (PGs) and thromboxane (TX). Prostoglandins and thromboxane act as inflammatory mediators and increase microvascular permeability.

Chronic pain is treated with a variety of medications and non-pharmacological interventions. Opioid tolerance and withdrawal can be seen in the NICU and PICU. Other side effects with opioid use can be: cognition deficits, altered mood, and disturbances of endocrine development. Opioid misuse can occur in adolescents and is associated with the use of alcohol, cigarettes and marijuana.

Non-pharmacological treatment for children in helping to relieve periodic pain episodes and severity includes counselling and behavior modification therapy. The American Association of Pediatrics have suggested that parents be educated on providing round the clock medication administration after their children receive surgery.

The use of medications to treat acute, chronic, recurrent and neuropathic pain is most common. Most instances of pain in children are treated with analgesics. These include acetaminophen, NSAIDs, local anesthetics, opioids, and medications for neuropathic pain. The most effective approach to pain management in children is to provide medicine around the clock instead of providing pain relief as needed. Regional anesthesia is also effective and recommended whenever possible. Opioids are effective too but often depress breathing in infants.

Antidepressants are "associated with improvements in pain, depression, fatigue, sleep disturbances, and health-related quality of life in people with FMS." The goal of antidepressants should be symptom reduction and if used long term, their effects should be evaluated against side effects. A small number of people benefit significantly from the SNRIs duloxetine and milnacipran and the tricyclic antidepressants (TCAs), such as amitriptyline. However, many people experience more adverse effects than benefits. While amitriptyline has been used as a first line treatment, the quality of evidence to support this use is poor.

It can take up to three months to derive benefit from the antidepressant amitriptyline and between three and six months to gain the maximal response from duloxetine, milnacipran, and pregabalin. Some medications have the potential to cause withdrawal symptoms when stopping so gradual discontinuation may be warranted particularly for antidepressants and pregabalin.

There is tentative evidence that the benefits and harms of SSRIs appear to be about similar.

The anti-convulsant drugs gabapentin and pregabalin may be used to reduce pain. Gabapentin may be of significant benefit for pain relief in about 35% of people with fibromyalgia. It is not possible to predict who will benefit, and a short trial may be recommended to test the effectiveness of this type of medication. Approximately 6/10 people who take gabapentin to treat pain related to fibromyalgia experience unpleasant side effects such as dizziness, abnormal walking, or swelling from fluid accumulation. Pregabalin demonstrates a substantial benefit in about 9% of people. Pregabalin reduced time off work by 0.2 days per week.

There are many causes of toothache and its diagnosis is a specialist topic, meaning that attendance at a dentist is usually required. Since many cases of toothache are inflammatory in nature, over the counter non-steroidal anti-inflammatory drugs (NSAIDs) may help (unless contraindicated, such as with a peptic ulcer). Generally, NSAIDs are as effective as aspirin alone or in combination with codeine. However, simple analgesics may have little effect on some causes of toothache, and the severe pain can drive individuals to exceed the maximum dose. For example, when acetaminophen (paracetamol) is taken for toothache, an accidental overdose is more likely to occur when compared to people who are taking acetaminophen for other reasons. Another risk in persons with toothache is a painful chemical burn of the oral mucosa caused by holding a caustic substance such as aspirin tablets and toothache remedies containing eugenol (such as clove oil) against the gum. Although the logic of placing a tablet against the painful tooth is understandable, an aspirin tablet needs to be swallowed to have any pain-killing effect. Caustic toothache remedies require careful application to the tooth only, without coming into excessive contact with the soft tissues of the mouth.

For the dentist, the goal of treatment generally is to relieve the pain, and wherever possible to preserve or restore function. The treatment depends on the cause of the toothache, and frequently a clinical decision regarding the current state and long-term prognosis of the affected tooth, as well as the individual's wishes and ability to cope with dental treatment, will influence the treatment choice. Often, administration of an intra-oral local anesthetic such as lidocaine and epinephrine is indicated in order to carry out pain-free treatment. Treatment may range from simple advice, removal of dental decay with a dental drill and subsequent placement of a filling, to root canal treatment, tooth extraction, or debridement.

Corticosteroids are administered through IV or orally. They cause lymphocytopenia, a condition where white blood cell levels are abnormally low. Corticosteroids cause white blood cell death, lowering their numbers throughout the body. They also cause white blood cells to recirculate away from the area of damage (the retina). This minimizes damage caused by the antibodies produced by the white blood cells. Often, this is treatment is combined with plasmapheresis. Instead of treating the plasma and blood cells, they are replaced with a healthy donor mixture. Patients who respond positively show improved visual fields and an almost complete disappearance of anti-retinal antibodies.

This is the condition where the pulp is irreversibly damaged. The pulp can not recover from the insult and damage. For example, decay that has reached the pulp of the tooth introduces bacteria into the pulp. The pulp is still alive, but the introduction of bacteria into the pulp will not allow the pulp to heal and it will ultimately result in necrosis, or death, of the pulp tissue.

Symptoms associated with irreversible pulpitis may include dull aching, pain from hot or cold (though cold may actually provide relief) lingering pain after removal of a stimulus, spontaneous pain, or referred pain.

Clinical signs may include reduced response to electronic pulp testing and painful response to thermal stimuli. Today electronic pulp testers are rarely used for diagnosis of the reversibility of pulpitis due to their unreliable nature. Instead they should only be used to test the vitality of teeth.

The pulp of a tooth with irreversible pulpitis may not be left alone to heal. That is at least the general viewpoint of the dental profession, and not every dentist would agree that a dead tooth must be treated. No statistics are known but it is possible to have a trouble-free tooth after irreversible pulpitis, albeit a dead tooth. The tooth may be endodontically treated whereby the pulp is removed and replaced by gutta percha. An alternative is extraction of the tooth. This may be required if there is insufficient coronal tissue remaining for restoration once the root canal therapy has been completed.

In-office treatments may be much more complex and they may include the application of dental sealants, having fillings put over the exposed root that is causing the sensitivity, or a recommendation to wear a specially made night guard or retainer if the problems are a result of teeth grinding.

Other possible treatments include fluorides are also used because they decrease permeability of dentin "in vitro". Also, potassium nitrate can be applied topically in an aqueous solution or an adhesive gel. Oxalate products are also used because they reduce dentin permeability and occlude tubules more consistently. However, while some studies have showed that oxalates reduced sensitivity, others reported that their effects did not differ significantly from those of a placebo. Nowadays, dentin hypersensitivity treatments use adhesives, which include varnishes, bonding agents and restorative materials because these materials offer improved desensitization.

Low-output lasers are also suggested for dentin hypersensitivity, including GaAlAs lasers and . They are thought to act by producing a transient reduction in action potential in C-fibers in the pulp, but Aδ-fibers are not affected.

At-home treatments include desensitizing toothpastes or dentifrices, potassium salts, mouthwashes and chewing gums.

A variety of toothpastes are marketed for dentin hypersensitivity, including compounds such as strontium chloride, strontium acetate, arginine, calcium carbonate, hydroxyapatite and calcium sodium phosphosilicate. Desensitizing chewing gums and mouthwashes are also marketed.

Potassium-containing toothpastes are common; however, the mechanism by which they may reduce hypersensitivity is unclear. Animal research has demonstrated that potassium ions placed in deep dentin cavities cause nerve depolarization and prevent re-polarization. It is not known if this effect would occur with the twice-daily, transient and small increase in potassium ions in saliva that brushing with potassium-containing toothpaste creates. In individuals with dentin hypersensitivity associated with exposed root surfaces, brushing twice daily with toothpaste containing 5% potassium nitrate for six to eight weeks reduces reported sensitivity to tactile, thermal and air blast stimuli. However, meta analysis reported that these individuals' subjective report of sensitivity did not significantly change after six to eight weeks of using the potassium nitrate toothpaste.

Desensitizing toothpastes containing potassium nitrate have been used since the 1980s while toothpastes with potassium chloride or potassium citrate have been available since at least 2000. It is believed that potassium ions diffuse along the dentinal tubules to inactivate intradental nerves. However, , this has not been confirmed in intact human teeth and the desensitizing mechanism of potassium-containing toothpastes remains uncertain. Since 2000, several trials have shown that potassium-containing toothpastes can be effective in reducing dentin hypersensitivity, although rinsing the mouth after brushing may reduce their efficacy.

Studies have found that mouthwashes containing potassium salts and fluorides can reduce dentine hypersensitivity, although rarely to any significant degree. , no controlled study of the effects of chewing gum containing potassium chloride has been made, although it has been reported as significantly reducing dentine hypersensitivity.

Nano-hydroxyapatite (nano-HAp) is considered one of the most biocompatible and bioactive materials, and has gained wide acceptance in dentistry in recent years. An increasing number of reports have shown that nano-hydroxyapatite shares characteristics with the natural building blocks of enamel having the potential, due to its particle size, to occlude exposed dentinal tubules helping to reduce hypersensitivity and enhancing teeth remineralization.

For this reason, the number of toothpastes and mouthwashes that already incorporate nano-hydroxyapatite as a desensitizing agent is increasing.

There are multiple large-field, multi-country research initiatives focusing on strategies to prevent and treat EE.

- The MAL-ED project

- The Alive and Thrive nutrition project

- The Sanitation, Hygiene and Infant Nutrition Efficacy (SHINE) Trial (ClinicalTrials.gov identifier: NCT01824940)

- The WASH Benefits Study

Since each case is different, the following are possible treatments that patients might receive in the management of myelitis.

- Intravenous steroids

High-dose intravenous methyl-prednisolone for 3–5 days is considered as a standard of care for patients suspected to have acute myelitis, unless there are compelling reasons otherwise. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of 5 days of steroids.

- Plasma exchange (PLEX)

Patients with moderate to aggressive forms of disease who don’t show much improvement after being treated with intravenous and oral steroids will be treated with PLEX. Retrospective studies of patients with TM treated with IV steroids followed by PLEX showed a positive outcome. It also has been shown to be effective with other autoimmune or inflammatory central nervous system disorders. Particular benefit has been shown with patients who are in the acute or subacute stage of the myelitis showing active inflammation on MRI. However, because of the risks implied by the lumbar puncture procedure, this intervention is determined by the treating physician on a case-by-case basis.

- Immunosuppressants/Immunomodulatory agents

Myelitis with no definite cause seldom recurs, but for others, myelitis may be a manifestation of other diseases that are mentioned above. In these cases, ongoing treatment with medications that modulate or suppress the immune system may be necessary. Sometimes there is no specific treatment. Either way, aggressive rehabilitation and long-term symptom management are an integral part of the healthcare plan.

First-line treatment for CIDP is currently intravenous immunoglobulin (IVIG) and other treatments include corticosteroids (e.g. prednisone), and plasmapheresis (plasma exchange) which may be prescribed alone or in combination with an immunosuppressant drug. Recent controlled studies show subcutaneous immunoglobin (SCIG) appears to be as effective for CIDP treatment as IVIG in most patients, and with fewer systemic side effects.

IVIG and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. IVIG is probably the first-line CIDP treatment, but is extremely expensive. For example, in the U.S., a single 65 g dose of Gamunex brand in 2010 might be billed at the rate of $8,000 just for the immunoglobulin—not including other charges such as nurse administration. Gamunex brand IVIG is the only U.S. FDA approved treatment for CIDP, as in 2008 Talecris, the maker of Gamunex, received orphan drug status for this drug for the treatment of CIDP.

Immunosuppressive drugs are often of the cytotoxic (chemotherapy) class, including rituximab (Rituxan) which targets B cells, and cyclophosphamide, a drug which reduces the function of the immune system. Ciclosporin has also been used in CIDP but with less frequency as it is a newer approach. Ciclosporin is thought to bind to immunocompetent lymphocytes, especially T-lymphocytes.

Non-cytotoxic immunosuppressive treatments usually include the anti-rejection transplant drugs azathioprine (Imuran/Azoran) and mycophenolate mofetil (Cellcept). In the U.S., these drugs are used as "off-label" treatments for CIDP, meaning that their use here is accepted by the FDA, but that CIDP treatment is not explicitly indicated or approved in the drug literature. Before azathioprine is used, the patient should first have a blood test that ensures that azathioprine can safely be used.

Anti-thymocyte globulin (ATG), an immunosuppressive agent that selectively destroys T lymphocytes is being studied for use in CIDP. Anti-thymocyte globulin is the gamma globulin fraction of antiserum from animals that have been immunized against human thymocytes. It is a polyclonal antibody.

Although chemotherapeutic and immunosuppressive agents have shown to be effective in treating CIDP, significant evidence is lacking, mostly due to the heterogeneous nature of the disease in the patient population in addition to the lack of controlled trials.

A review of several treatments found that azathioprine, interferon alpha and methotrexate were not effective. Cyclophosphamide and rituximab seem to have some response. Mycophenolate mofetil may be of use in milder cases. Immunoglobulin and steroids are the first line choices for treatment. Rarely bone marrow transplantation has been performed.

Physical therapy and occupational therapy may improve muscle strength, activities of daily living, mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

Lymphocytic and collagenous colitis have both been shown in randomized, placebo-controlled trials to respond well to budesonide, a glucocorticoid. Budesonide formulated to be active in the distal colon and rectum is effective for both active disease and in the prevention of relapse. However, relapse occurs frequently after withdrawal of therapy.

Studies of a number of other agents including antidiarrheals, bismuth subsalicylate (Pepto-Bismol), mesalazine/mesalamine (alone or in combination with cholestyramine), systemic corticosteroids, cholestyramine, immunomodulators, and probiotics have shown to be less effective than budesonide for treating both forms of microscopic colitis.

Anti-TNF inhibitors. split ileostomy, diverting ileostomy, and subtotal colectomy are options for management of steroid-dependent or refractory microscopic colitis. Currently, the need to resort to surgery is limited considering the improvement of drug therapy options. However, surgery is still considered for patients with severe, unresponsive microscopic colitis.