Treatment protocol is not well established. Some sources report that approximately half of the patients will fully recover after lengthy (mean time 14.5 months, range 2–24 months) expectant management.

Treatment with steroids is lengthy and usually requires about 6 months. While some source report very good success with steroids most report a considerable risk of recurrence after a treatment with steroids alone. Steroids are known to cause elevation of prolactin levels and increase risk of several conditions such as diabetes, and other endocrinopathies which in turn increase the risk of IGM. Treatment with topical steroids to limit side effects was also reported in one case. For surgical treatment recurrence rates of 5-50% have been reported.

A 1997 literature review article recommended complete resection or corticosteroid therapy, stating also that long-term follow-up was indicated due to a high rate of recurrence.

Treatment with a combination of glucocorticoids and prolactin lowering medications such as bromocriptine or cabergoline was used with good success in Germany. Prolactin lowering medication has also been reported to reduce the risk of recurrence. In cases of drug-induced hyperprolactinemia (such as antipsychotics) prolactin-sparing medication can be tried.

Methotrexate alone or in combination with steroids has been used with good success. Its principal mechanism of action is immunomodulating activity, with a side effect profile that is more favorable for treating IGM.

Colchicine, azathioprine and NSAIDs have also been used.

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.

Antimetabolites, also categorized as steroid-sparing agents, such as azathioprine, methotrexate, mycophenolic acid, and leflunomide are often used as alternatives to corticosteroids. Of these, methotrexate is most widely used and studied. Methotrexate is considered a first-line treatment in neurosarcoidosis, often in conjunction with corticosteroids. Long-term treatment with methotrexate is associated with liver damage in about 10% of people and hence may be a significant concern in people with liver involvement and requires regular liver function test monitoring. Methotrexate can also lead to pulmonary toxicity (lung damage), although this is fairly uncommon and more commonly it can confound the leukopenia caused by sarcoidosis. Due to these safety concerns it is often recommended that methotrexate is combined with folic acid in order to prevent toxicity. Azathioprine treatment can also lead to liver damage. Leflunomide is being used as a replacement for methotrexate, possibly due to its purportedly lower rate of pulmonary toxicity. Mycophenolic acid has been used successfully in uveal sarcoidosis, neurosarcoidosis (especially CNS sarcoidosis; minimally effective in sarcoidosis myopathy), and pulmonary sarcoidosis.

In lactation mastitis, antibiotics are not needed in the overwhelming majority of cases and should be used only for bacterial infections. Dicloxacillin or cephalexin are sometimes recommended. The effects of antibiotics has not been well studied as of 2013.

Anti-tumour necrosis factor α antagonists (e.g. infliximab)

Dietary restriction of a particular suspected or proven antigen may be involved in the management of OFG, such as cinnamon or benzoate-free diets.

Most women with fibrocystic changes and no symptoms do not need treatment, but closer follow-up may be advised.

There is no widely accepted treatment or prevention strategy for fibrocystic condition. When treatment of symptoms is necessary it follows the same strategies as treatment for cyclical breast pain.

It is controversial whether benign breast conditions improve or worsen with oral contraceptives or hormone replacement therapy.

A few small-scale studies have indicated that the fibrocystic condition may be improved by dietary changes (especially by a reduced intake of caffeine and related methylxanthines or by a reduced intake of salt) and by vitamin supplements.

Small, preliminary studies have shown beneficial effects of iodine supplementation (such as reducing the presence of breast cysts, fibrous tissue plaques and breast pain) in women with fibrocystic breast changes, with elemental iodine (I) being more effective than iodide (I). It is noted that iodine supplementation, via an iodine-based modulation of estrogen influence in the breast, also appears to inhibit early cancer progression in small studies done on breast cancer cells in a lab.. Since treatment success in a lab is often not replicated in humans, more human research is necessary to determine if iodine supplementation prevents breast cancer

A U.S. National Institutes of Health fact sheet of 2011 reported on a randomized, double-blind, placebo-controlled clinical trial performed on 111 women affected by fibrosis and having a history of breast pain. In this trial, daily doses of iodine led to decreased in breast pain, tenderness and nodularity. It was emphasized that further research to clarify iodine's role in fibrocystic breast disease is needed and that large doses of iodine should only be used under the guidance of a physician.

In lactation mastitis, frequent emptying of both breasts by breastfeeding is essential. Also essential is adequate fluid supply for the mother and baby. Use of pumps to empty the breast is now considered somewhat controversial.

For breastfeeding women with light mastitis, massage and application of heat prior to feeding can help as this may aid unblocking the ducts. However, in more severe cases of mastitis heat or massage could make the symptoms worse and cold compresses are better suited to contain the inflammation.

Nonpuerperal mastitis is treated by medication and possibly aspiration or drainage (see in particular treatment of subareolar abscess and treatment of granulomatous mastitis). According to a BMJ best practice report, antibiotics are generally to be used in all nonpuerperal mastitis cases, with replacement of the antibiotics by an antifungal agent such as fluconazole in cases of deep fungal infections, and corticosteroids are to be used in case of granulomatous mastitis (with differential diagnosis to tuberculosis infection of the breast).

The condition is usually self-limiting, and thus not indicated for surgery.

Danazol, an estrogen biosynthesis inhibitor, tamoxifen, an antagonistic modulator of the estrogen receptor, and bromocriptine, a prolactin-lowering D receptor agonist, are the main drugs used in the treatment of mastodynia and are effective.

Other medications and supplements have been found to be of benefit. Spironolactone (Aldactone), low dose oral contraceptives, low-dose estrogen have helped to relieve pain. Topical anti-inflammatory medications can be used for localized pain. For anti hormonal treatment, danazol (Danocrine) can be helpful. Tamoxifen citrate is used in some cases of severe breast pain. Vitamin E is not effective in relieving pain nor is Evening primrose oil. Vitamin B and Vitamin A have not been consistently found to be beneficial. Flaxseed has shown some activity in the treatment of cyclic mastalgia.

Pain may be relieved by the use of nonsteroidal anti-inflammatory drugs or, for more severe localized pain, by local anaesthetic. Pain may be relieved psychologically by reassurance that it does not signal a serious underlying problem, and an active life style can also effect an improvement.

Information regarding how the pain is real but not necessarily caused by disease can help to understand the problem. Learning breast self-examination helps to orient the woman to normal and expected texture and structure of the breast and nipple. Yearly breast exams may be suggested. Counseling can also be to describe changes that vary during the monthly cycle. Women on hormone replacement therapy may benefit from a dose adjustment. Another non-pharmacological measure to help relieve symptoms of pain may be to use good bra support. Breasts change during adolescence and menopause and refitting may be beneficial. Applying heat and/or ice can bring relief. Dietary changes may also help with the pain. Methylxanthines can be eliminated from the diet to see if a sensitivity is present. Some clinicians recommending a reduction in salt, though no evidence supports this practice.

Treatment is possible with long-acting antibiotics, but milk from such cows is not marketable until drug residues have left the cow's system. Antibiotics may be systemic (injected into the body), or they may be forced upwards into the teat through the teat canal (intramammary infusion). Cows being treated may be marked with tape to alert dairy workers, and their milk is syphoned off and discarded. To determine whether the levels of antibiotic residuals are within regulatory requirements, special tests exist. Vaccinations for mastitis are available, but as they only reduce the severity of the condition, and cannot prevent reoccurring infections, they should be used in conjunction with a mastitis prevention program.

Incision drainage with proper evacuation of the fluid followed by anti-tubercular medication.

The standard treatment for GPA is cyclophosphamide and high dose corticosteroids for remission induction and less toxic immunosuppressants like azathioprine, leflunomide, methotrexate or mycophenolate mofetil. Trimethoprim/sulfamethoxazole may also help prevent relapse. Rituximab may be substituted for cyclophosphamide in inducing remission.

A systematic review of 84 trials examined the evidence for various treatments in GPA. Many trials include data on pooled groups of people with GPA and microscopic polyangiitis. In this review, cases are divided between localised disease, non-organ threatening, generalized organ-threatening disease and severe kidney vasculitis and immediately life-threatening disease.

- In generalised non-organ-threatening disease, remission can be induced with methotrexate and steroids, where the steroid dose is reduced after a remission has been achieved and methotrexate used as maintenance.

- In case of organ-threatening disease, pulsed intravenous cyclophosphamide with steroids is recommended. Once remission has been achieved, azathioprine and steroids can be used to maintain remission.

- In severe kidney vasculitis, the same regimen is used but with the addition of plasma exchange.

- In pulmonary haemorrhage, high doses of cyclophosphamide with pulsed methylprednisolone may be used, or alternatively CYC, steroids, and plasma exchange.

Therapy for GPA and MPA has two main components: induction of remission with initial immunosuppressive therapy, and maintenance of remission with immunosuppressive therapy for a variable period to prevent relapse.

The mainstay of treatment for granulomatosis with polyangiitis (GPA) is a combination of corticosteroids and cytotoxic agents.

- Medications

- Side effect treatments

- Plasma exchange

- Kidney transplant

The customary treatment involves long term dosage of prednisone, alternated or combined with cytotoxic drugs, such as cyclophosphamide or azathioprine.

Plasmapheresis may also be indicated in the acute setting to remove ANCA antibodies.

Rituximab has been investigated, and in April 2011 approved by the FDA when used in combination with glucocorticoids in adult patients.

The cause is currently unknown. The histology is suggestive of an autoimmune reaction. The high rate of relapses as well as relatively high proportion of bilateral cases is highly suggestive of a systemic predisposition.

Presently most evidence points towards an important role of elevated prolactin levels or overt hyperprolactinemia with additional triggers such as local trauma or irritation. Alpha 1-antitrypsin deficiency was documented in one case, interferon-alpha therapy in another case. Similar cases of granulomatous mastitis were reported in IgG4-related disease though the exact relationship to IGM remains to be elucidated. Other contributing factors of IGM were investigated such as oral contraceptives usage. Many cases were reported after use of prolactin elevating medications such as antipsychotics.

Elevated prolactin levels have the direct effects of increasing secretory activity of breast lobules, maintaining tight junctions of the ductal epithelium, preventing involution of the breast gland after weaning and are known to stimulate the immune system, contributing to both physiological and pathological granulomatous lesions and non-caseating granulomas. PRL is also secreted locally in the breast and local secretion by lymphocytes may be enhanced during inflammatory reactions.

Autoimmune reaction to extravasated fat and protein rich luminal fluid (denaturized milk) resulting from the secretory activity is assumed to be one of the triggers of IGM. Several other hormones can contribute to PRL signaling in the breast gland, high levels of insulin caused for example by peripheral insulin resistance (resulting from pregnancy, gestational diabetes or developing diabetes mellitus type 2) will enhance the galactogenic and antiapoptotic effects of PRL and growth hormone by acting synergistically with IGF-1.

Practices such as good nutrition, proper milking hygiene, and the culling of chronically infected cows can help.

Ensuring that cows have clean, dry bedding decreases the risk of infection and transmission. Dairy workers should wear rubber gloves while milking, and machines should be cleaned regularly to decrease the incidence of transmission.

There are usually no adverse side effects to this condition. In almost all cases it subsides after menopause. A possible complication arises through the fact that cancerous tumors may be more difficult to detect in women with fibrocystic changes.

Physicians often prescribe the antibiotic trimethoprim-sulfamethoxazole to prevent bacterial infections. This drug also has the benefit of sparing the normal bacteria of the digestive tract. Fungal infection is commonly prevented with itraconazole, although a newer drug of the same type called voriconazole may be more effective. The use of this drug for this purpose is still under scientific investigation.

It is not lethal in nature and is responsive to tetracycline or ciprofloxacin. Surgical treatment include rhinoplasty. However, if left untreated the disease can lead to sepsis, bleeding, or other chronic conditions that can be fatal.

Interferon, in the form of interferon gamma-1b (Actimmune) is approved by the Food and Drug Administration for the prevention of infection in CGD. It has been shown to reduce infections in CGD patients by 70% and to decrease their severity. Although its exact mechanism is still not entirely understood, it has the ability to give CGD patients more immune function and therefore, greater ability to fight off infections. This therapy has been standard treatment for CGD for several years.

Treatment is targeted to the underlying cause. However, most vasculitis in general are treated with steroids (e.g. methylprednisolone) because the underlying cause of the vasculitis is due to hyperactive immunological damage. Immunosuppressants such as cyclophosphamide and azathioprine may also be given.

A systematic review of antineutrophil cytoplasmic antibody (ANCA) positive vasculitis identified best treatments depending on whether the goal is to induce remission or maintenance and depending on severity of the vasculitis.

The mother must remove the breast milk. If the baby can attach well and suckle, then she should breastfeed as frequently as the baby is willing. If the baby is not able to attach and suckle effectively, she should express her milk by hand or with a pump a few times until the breasts are softer, so that the baby can attach better, and then get them to breastfeed frequently.

She can apply warm compresses to the breast or take a warm shower before expressing, which helps the milk to flow. She can use cold compresses after feeding or expressing, which helps to reduce the oedema.

Engorgement occurs less often in baby-friendly hospitals which practise the Ten Steps and which help mothers to start breastfeeding soon after delivery.

Regular breastfeeding can be continued. The treatment for breast engorgement can be divided into non-medical and medical methods. The non-medical methods include hot/cold packs, Gua-Sha (scraping therapy), acupuncture and cabbage leaves whereas medical methods are proteolytic enzymes such as serrapeptase, protease, and subcutaneous oxytocin. Evidence from published clinical trials on the effectiveness of treatment options is of weak quality and is not strong enough to justify a clinical recommendation.

The clinical management of a cyst of Montgomery depends upon the symptoms of the patient.

If there are no signs of infection, a cyst of Montgomery can be observed, because more than 80% resolve spontaneously, over only a few months. However, in some cases, spontaneous resolution may take up two years. In such cases, a repeat ultrasonography may become necessary. If, however, the patient has signs of an infection, for example reddening (erythema), warmth, pain and tenderness, a treatment for mastitis can be initiated, which may include antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs). With treatment, inflammatory changes usually disappear quickly. In rare cases, drainage may become necessary. A surgical treatment of a cyst of Montgomery, i.e. a resection, may become necessary only if a cyst of Montgomery persists, or the diagnosis is questioned clinically.

The prognosis seems to be excellent. In one series, all adolescent patients with a cyst of Montgomery had a favourable outcome.

The term nonpuerperal mastitis describes inflammatory lesions of the breast (mastitis) that occur unrelated to pregnancy and breastfeeding.

It is sometimes equated with duct ectasia, but other forms can be described.

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or as oral therapy. Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluoresence dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis increases T-regulatory cells in the eye, which likely contributes to disease regression.

In some cases an injection of posterior subtenon triamcinolone acetate may also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatments with Infliximab or other anti-TNF infusions may prove helpful.

The anti-diabetic drug metformin is reported to inhibit the process that causes the inflammation in uveitis.

In the case of herpetic uveitis, anti-viral medications, such as valaciclovir or aciclovir, may be administered to treat the causative viral infection.

"Duct ectasia" in the literal sense (literally: duct widening) is a very common and thus rather unspecific finding, increasing with age. However, in the way in which the term is mostly used, duct ectasia is an inflammatory condition of the larger-order lactiferous ducts. It considered likely that the condition is associated with aseptic (chemical) inflammation related to the rupture of ducts or cysts. It is controversial whether duct dilation occurs first and leads to secretory stasis and subsequent periductal inflammation or whether inflammation occurs first and leads to an inflammatory weakening of the duct walls and then stasis. When the inflammation is complicated by necrosis and secondary bacterial infection, breast abscesses may form. Subareolar abscess, also called Zuska's disease (only nonpuerperal case), is a frequently aseptic inflammation and has been associated with squamous metaplasia of the lactiferous ducts.

The duct ectasia—periductal mastitis complex affects two groups of women: young women (in their late teens and early 20s) and perimenopausal women. Women in the younger group mostly have inverted nipples due to squamous metaplasia that lines the ducts more extensively compared to other women and produces keratin plugs which in turn lead to duct obstruction and then duct dilation, secretory stasis, inflammation, infection and abscess. This is not typically the case for women in the older group; in this group, there is likely a multifactorial etiology involving the balance in estrogen, progesterone and prolactin.

Treatment of mastitis and/or abscess in nonlactating women largely the same as that of lactational mastitis, generally involving antibiotics treatment, possibly surgical intervention by means of fine-needle aspiration and/or incision and drainage and/or interventions on the lactiferous ducts (for details, "see also" the articles on treatment of mastitis, of breast abscess and of subareolar abscess). Additionally, an investigation for possible malignancy is needed, normally by means of mammography, and a pathological investigation such as a biopsy may be necessary to exclude malignant mastitis. Although no "causal" relation with breast cancer has been established, there appears to be an increased statistical risk of breast cancer, warranting a long-term surveillance of patients diagnosed with non-puerperal mastitis.

Nonpuerperal breast abscesses have a higher rate of recurrence compared to puerperal breast abscesses. There is a high statistical correlation of nonpuerperal breast abscess with diabetes mellitus (DM). On this basis, it has recently been suggested that diabetes screening should be performed on patients with such abscess.