If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high dosage steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat Pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor their GI health. As lesions are usually terribly painful, it is likely that pain medication can complicate and exacerbate the GI issues caused by steroids.

All of these drugs may cause severe side effects, so the patient should be closely monitored by doctors. Once the outbreaks are under control, dosage is often reduced, to lessen side effects.

If skin lesions do become infected, antibiotics may be prescribed. Tetracycline antibiotics have a mildly beneficial effect on the disease and are sometimes enough for Pemphigus Foliaceus. In addition, talcum powder is helpful to prevent oozing sores from adhering to bedsheets and clothes. Wound care and treatment is often akin to that used in burn units, including careful use of dressings that don't stick to the wounds, etc.

If paraneoplastic pemphigus is diagnosed with pulmonary disease, a powerful cocktail of immune suppressant drugs is sometimes used in an attempt to halt the rapid progression of bronchiolitis obliterans, including methylprednisolone, ciclosporin, azathioprine, and thalidomide. Plasmapheresis may also be useful.

Most cases of angular cheilitis respond quickly when antifungal treatment is used. In more long standing cases, the severity of the condition often follows a relapsing and remitting course over time. The condition can be difficult to treat and can be prolonged.

There are 4 aspects to the treatment of angular cheilitis. Firstly, potential reservoirs of infection inside the mouth are identified and treated. Oral candidiasis, especially denture-related stomatitis is often found to be present where there is angular cheilitis, and if it is not treated, the sores at the corners of the mouth may often recur. This involves having dentures properly fitted and disinfected. Commercial preparations are marketed for this purpose, although dentures may be left in dilute (1:10 concentration) household bleach overnight, but only if they are entirely plastic and do not contain any metal parts, and with rinsing under clean water before use. Improved denture hygiene is often required thereafter, including not wearing the denture during sleep and cleaning it daily. For more information, see Denture-related stomatitis.

Secondly, there may be a need to increase the vertical dimension of the lower face to prevent overclosure of the mouth and formation of deep skin folds. This may require the construction of a new denture with an adjusted bite. Rarely, in cases resistant to normal treatments, surgical procedures such as collagen injections (or other facial fillers such as autologous fat or crosslinked hyaluronic acid) are used in an attempt to restore the normal facial contour. Other measures which seek to reverse the local factors that may be contributing to the condition include improving oral hygiene, stopping smoking or other tobacco habits and use of a barrier cream (e.g. zinc oxide paste) at night.

Thirdly, treatment of the infection and inflammation of the lesions themselves is addressed. This is usually with topical antifungal medication, such as clotrimazole, amphotericin B, ketoconazole, or nystatin cream. Some antifungal creams are combined with corticosteroids such as hydrocortisone or triamcinolone to reduce inflammation, and certain antifungals such as miconazole also have some antibacterial action. Diiodohydroxyquinoline is another topical therapy for angular cheilitis. If "Staphylococcus aureus" infection is demonstrated by microbiological culture to be responsible (or suspected), the treatment may be changed to fusidic acid cream, an antibiotic which is effective against this type of bacteria. Aside from fusidic acid, neomycin, mupirocin, metronidazole, and chlorhexidine are alternative options in this scenario.

Finally, if the condition appears resistant to treatment, investigations for underlying causes such as anemia or nutrient deficiencies or HIV infection. Identification of the underlying cause is essential for treating chronic cases. The lesions may resolve when the underlying disease is treated, e.g. with a course of oral iron or B vitamin supplements. Patch testing is recommended by some in cases which are resistant to treatment and where allergic contact dermatitis is suspected.

Sunscreen and protective clothing should also be used during the hottest part of the day to avoid blisters from sunburn. Avoiding sunlight during midday is the best way to avoid blisters from sunburn. Protective gloves should be worn when handling detergents, cleaning products, solvents and other chemicals.

Friction blisters, caused by rubbing against the skin, can be prevented by reducing the friction to a level where blisters will not form. This can be accomplished in a variety of ways.

Blisters on the feet can be prevented by wearing comfortable, well-fitting shoes and clean socks. Inherently ill-fitting or stiffer shoes, such as high heels and dress shoes, present a larger risk of blistering. Blisters are more likely to develop on skin that is moist, so socks that manage moisture or frequent sock changes will aid those with particularly sweaty feet. While exercising or playing sports, special sports socks can help keep feet drier and reduce the chance of blisters. Before going for a long walk, it is also important to ensure that shoes or hiking boots have been properly broken in.

Even before a "hot" or irritated area on the foot is felt, taping a protective layer of padding or a friction-reducing interface between the affected area and the footwear can prevent the formation of a blister. Bandages, moleskin and tapes generally must be applied to the foot daily, and most have a very high coefficient of friction (COF), but a friction-management patch applied to the shoe will remain in place much longer, throughout many changes of socks and insoles. This type of intervention may be used with footwear that is worn daily, with specialty shoes and boots like hockey skates, ice skates, inline skates, ski boots and cleats, or even with orthotic braces and splints. For periods of sustained use such as hiking and trail running, especially where water ingress or moisture build up in the shoe or boot can occur, moisture wicking liner socks can provide the required friction protection.

To avoid friction blisters on the hands, gloves should be worn when using tools such as a shovel or pickaxe, doing manual work such as gardening, or using sports equipment like golf clubs or baseball bats. Oars used for competitive rowing are known for causing frequent blisters on the hands of oarsmen. Weightlifters are also prone to blisters as are gymnasts from the friction developed by the rubbing against the bars. To further reduce the occurrence one can tape the hands, and there are also a number of products on the market that claim to reduce the occurrence of blisters. These are all intended to be worn as a liner underneath a glove. The majority of these offerings simply add padding and create a layer that reduces the coefficient of friction between the skin and the glove.

A lubricant, typically talcum powder, can be used to reduce friction between skin and apparel in the short term. People put talcum powder inside gloves or shoes for this purpose, although this type of lubricant will increase the friction in the long term, as it absorbs moisture. Increased friction makes blisters more likely.

As mentioned above, primary cicatricial alopecias are classified by the predominant type of inflammatory cells that attack the hair follicles: i.e., lymphocytes, neutrophils, or mixed inflammatory cells. Treatment strategies are different for each subtype and detailed treatment options are beyond the scope of this discussion. However, certain general principals are reviewed below.

Treatment of the lymphocytic group of cicatricial alopecias (including lichen planopilaris, frontal fibrosing alopecia, central centrifugal alopecia, and pseudopelade (Brocq) involves use of anti-inflammatory medications. The goal of treatment is to decrease or eliminate the lymphocytic inflammatory cells that are attacking and destroying the hair follicle. Oral medications may include hydroxychloroquine, doxycycline, mycophenolate mofetil, cyclosporine, or corticosteroids. Topical medications may include corticosteroids, tacrolimus, pimecrolimus, or Derma-Smoothe/FS scalp oil. Triamcinolone acetonide, a corticosteroid, may be injected into inflamed, symptomatic areas of the scalp.

Treatment of the neutrophilic group of cicatricial alopecias (folliculitis decalvans, tufted folliculitis) is directed at eliminating the predominant pathogenic microbes that are invariably involved in the inflammatory process. Oral antibiotics are the mainstay of therapy, and topical antibiotics may be used to supplement the oral antibiotics. In dissecting cellulitis, pathogenic microbes are not usually present. Isotretinoin in small doses may be helpful in treating dissecting cellulitis.

Treatment of the mixed group of cicatricial alopecias (folliculitis keloidalis) may include antimicrobials, isotretinoin, and anti-inflammatory medications.

You should discuss any treatment with your dermatologist, who will also explain potential side effects, as well as laboratory tests that are needed before starting treatment and sometimes are monitored during treatment.

The course of cicatricial alopecia is usually prolonged. Treatment is continued until the symptoms and signs of scalp inflammation are controlled, and progression of the condition has been slowed. In other words, itching, pain, tenderness, and burning have cleared, scalp redness, scaling, and/or pustules are no longer present, and the progression of the hair loss has been stopped or slowed. Treatment may then be stopped. Unfortunately, the cicatricial alopecias may reactivate after a quiet period and treatment may have to be repeated.

Surgical treatment for cosmetic benefit is an option in some cases after the disease has been inactive for one to two or more years. Hair restoration surgery or scalp reduction may be considered in these instances.

Adenitis is a general term for an inflammation of a gland. Often it is used to refer to lymphadenitis which is the inflammation of a lymph node.

Following a successful induction of remission, maintenance therapy might be given in some cases, for example when there is a high risk of relapse or in patients with organ-threatening manifestations. Common maintenancy therapy is prednisolone 2.5–5 mg per day, or use of a steroid-sparing agent instead.

Hair will not regrow once the follicle is destroyed. However, it may be possible to treat the inflammation in and around surrounding follicles before they are destroyed, and for this reason it is important to begin treatment as early as possible to halt the inflammatory process. Minoxidil solution (2% or 5%) applied twice daily to the scalp may be helpful to stimulate any small, remaining, unscarred follicles. The progression of hair loss is unpredictable. In some cases, progression is slow and there is always sufficient hair remaining to cover the affected scalp areas; in other cases, progression can be rapid and extensive.

Superficial lymphatic malformation (also known as "Lymphangioma circumscriptum") is a congenital malformation of the superficial lymphatics, presenting as groups of deep-seated, vesicle-like papules resembling frog spawn, at birth or shortly thereafter.

Relapses are common, and a previous history of relapse appears to be a strong predictor of future relapse. When relapse occurs while off therapy and there has been a prolonged disease remission following initial glucocorticoid induction, then the relapse can usually be managed successfully with a re-induction strategy using glucocorticoids. Introducing a steroid-sparing agent might also need to be considered for relapses; however, none has been tested in prospective, controlled studies, and evidence for their efficacy beyond that offered by concomitant glucocorticoid therapy is scarce.

In one retrospective cohort study, baseline concentrations of serum IgG4, IgE and blood eosinophils were found to be independently predictive of relapse risk following treatment with rituximab with or without glucocorticoids; the higher the baseline values, the greater the relapse risk and the shorter the time to relapse.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

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.

The main infectious agents are Enterobacteriaceae (such as Escherichia coli and Klebsiella), Neisseria gonorrhoeae and Chlamydia trachomatis.

One study has shown that men with MAGI who have lower serum levels of total testosterone tend to have a more complicated form of MAGI, such as involving more than one site, than those with normal levels.

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues. Failure to do so results in chronic inflammation, and cellular destruction. Resolution of inflammation occurs by different mechanisms in different tissues.

Mechanisms that serve to terminate inflammation include:

Cat-scratch disease can be primarily prevented by taking flea control measures and washing hands after handling a cat or cat feces; since cats are mostly exposed to fleas when they are outside, keeping cats inside can prevent infestation.

Treatment of aortitis depends on the underlying cause. Infectious causes commonly require antibiotic treatment, while those associated with autoimmune vasculitides are generally treated with steroids.

Management includes the following treatment priorities: stop the inflammation, treat complications, prevent and monitor for re-occurrence.

Keratoconjunctivitis is inflammation ("-itis") of the cornea and conjunctiva.

When only the cornea is inflamed, it is called "keratitis"; when only the conjunctiva is inflamed, it is called "conjunctivitis".

There are several potential causes of the inflammation:

- Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.) It occurs with 20% of rheumatoid arthritis patients.

- The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.

- "Atopic keratoconjunctivitis" is one manifestation of atopy.

- "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.

- "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria "Moraxella bovis".

- "Pink eye in sheep and goat" is another infectious keratoconjunctivitis of veterinary concern, mostly caused by "Chlamydophila pecorum"

- "Superior limbic keratoconjunctivitis" is thought to be caused by mechanical trauma.

- "Keratoconjunctivitis photoelectrica" (arc eye) means inflammation caused by photoelectric UV light. It is a type of ultraviolet keratitis. Such UV exposure can be caused by arc welding without wearing protective eye glass, or by high altitude exposure from sunlight reflected from snow ("snow blindness"). The inflammation will only appear after about 6 to 12 hours. It can be treated by rest, as the inflammation usually heals after 24–48 hours. Proper eye protection should be worn to prevent keratoconjunctivitis photoelectrica.

Male Accessory Gland Infection (MAGI), also known as Male Accessory Gland Inflammation, is a condition with signs of inflammation involving one or more sites in the male genital tract. Diagnosis is made according to parameters defined by the World Health Organisation, and it is particularly made in relation to infectious or inflammatory causes of male infertility.

Although it is usually caused by infection spreading from the urethra, non-infectious causes also exist.

"Lymph adenitis" or "lymph node adenitis" is caused by infection in lymph nodes. The infected lymph nodes typically become enlarged, warm and tender. A swelling of lymph nodes due to growth of lymph cells is called lymphadenopathy. Types include:

- Neck

- Cervical adenitis is an inflammation of a lymph node in the neck.

- Tuberculous adenitis (scrofula) is a tuberculous infection of the skin of the neck caused by "Mycobacterium tuberculosis". Non-tuberculous adenitis can also be caused by "Mycobacterium scrofulaceum" or "Mycobacterium avium".

- Abdomen

- Mesenteric adenitis is an inflammation of the mesenteric lymph nodes in the abdomen. It can be caused by the bacterium "Yersinia enterocolitica". If it occurs in the right lower quadrant, it can be mistaken for acute appendicitis, often preceded by a sore throat.

Most healthy people clear the infection without treatment, but in 5 to 14 percent of individuals, the organisms disseminate and infect the liver, spleen, eye, or central nervous system. Although some experts recommend not treating typical CSD in immunocompetent patients with mild to moderate illness, treatment of all patients with antimicrobial agents (Grade 2B) is suggested due to the probability of disseminated disease. The preferred antibiotic for treatment is azithromycin since this agent is the only one studied in a randomized controlled study.

Azithromycin is preferentially used in pregnancy to avoid the teratogenic side effects of doxycycline. However, doxycycline is preferred to treat "B. henselae" infections with optic neuritis due to its ability to adequately penetrate the tissues of the eye and central nervous system.

A new investigation has identified a seemingly successful treatment for LRBA deficiency by targeting CTLA4. Abatacept, an approved drug for rheumatoid arthritis, mimics the function of CTLA4 and has found to reverse life-threatening symptoms. The study included nine patients that exhibited improved clinical status and halted inflammatory conditions with minimal infectious or autoimmune complications. The study also suggests that therapies like chloroquine or hydroxychloroquine, which inhibit lysosomal degradation, may prove to be effective, as well. Larger cohorts are required to further validate these therapeutic approaches as effective long-term treatments for this disorder.

The most common side effects of bicalutamide monotherapy in men are breast pain/tenderness and gynecomastia. These side effects may occur in as many as 90% of men treated with bicalutamide monotherapy, but gynecomastia is generally reported to occur in 70 to 80% of patients. In the trial, at a median follow-up of 7.4 years, breast pain and gynecomastia respectively occurred in 73.6% and 68.8% of men treated with 150 mg/day bicalutamide monotherapy. In more than 90% of affected men, bicalutamide-related breast events are mild-to-moderate in severity. It is only rarely and in severe and extreme cases of gynecomastia that the proportions of the male breasts become so marked that they are comparable to those of women. In the trial, 16.8% of bicalutamide patients relative to 0.7% of controls withdrew from the study due to breast pain and/or gynecomastia. The incidence and severity of gynecomastia are higher with estrogens (e.g., diethylstilbestrol) than with like bicalutamide in the treatment of men with prostate cancer.