FDG positron emission tomography (PET) may be useful to detect the condition early. Other imaging studies including MRI, CT scans, and X-rays may reveal inflammation and/or damaged cartilage facilitating diagnosis.

It is useful to do a full set of pulmonary function tests, including inspiratory and expiratory flow-volume loops. Patterns consistent with either extrathoracic or intrathoracic obstruction (or both) may occur in this disease. Pulmonary function tests (flow-volume loops) provide a useful noninvasive means of quantifying and following the degree of extrathoracic airway obstruction in relapsing polychondritis.

The course of ACA is long-standing, from a few to several years, and it leads to extensive atrophy of the skin and, in some patients, to the limitation of upper and lower limb joint mobility.The outlook is good if the acute inflammatory stage of ACA is treated adequately. The therapeutic outcome is difficult to assess in patients with the chronic atrophic phase, in which many changes are only partially reversible.

Physicians should use serologic and histologic examination to confirm the diagnosis of ACA. Treatment consists of antibiotics including doxycycline and penicillin for up to four weeks in the acute case.

Since AIED symptoms are fairly common to many hearing loss disorders, it may be difficult to diagnose AIED without performing multiple medical tests. Some examples of these tests include:

- Hearing Tests for Progressive Hearing and Balance loss

- Audiometry (measure of hearing acuity and sound intensity)

- Rotatory Chair Test (determines if inner ear is responsible for balance loss)

- Electrocochleography (ECOG) (recording of electrical potential in inner ear due to sound)

- Blood Tests for General Autoimmune Diseases

- Erythrocyte sedimentation rate (test for inflammation)

- Rheumatoid Factor (indicator of autoimmune disorders)

There are also blood tests specific to inner ear disorders:

- Anti-cochlear antibody test (testing for antibodies against cochlear cells)

- Lymphocyte Transformation Assay (testing whether an individual has developed a T-cell response against a certain drug)

Though it has also been proposed that the use of anti heat shock protein 70 antibodies may be useful in the detection and diagnosis of AIED, there is not enough evidence to confirm the reliability of this method.

A vast number of traditional herbal remedies were recommended for "rheumatism". Modern medicine, both conventional and alternative, recognises that the different rheumatic disorders have different causes (and several of them have multiple causes) and require different kinds of treatment.

Nevertheless, initial therapy of the major rheumatological diseases is with analgesics, such as paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs), members of which are ibuprofen and naproxen. Often, stronger analgesics are required.

The ancient Greeks recorded that bee venom had some beneficial effects on some types of rheumatism. Bee and ant stings were known as a folk remedy in the late 19th century, and at least one physician developed a treatment consisting of repeated formic acid injections. Certain Amazonian tribes, including the Zo'é, use fire ant stings as a remedy for aches and pains.

Cod liver oil has also been used as a remedy.

Neem Tree Oil according to East Indian cultures has also been used as a remedy.

The diagnosis of episcleritis is based upon the history and physical examination. The history should be explored for the presence of the diseases associated with episcleritis, and the symptoms they cause, such as rash, arthritis, venereal disease, and recent viral infection. Episcleritis may be differentiated from scleritis by using phenylephrine or neosynephrine eye drops, which causes blanching of the blood vessels in episcleritis, but not in scleritis. A blue color to the sclera suggests scleritis, rather than episcleritis.

After anesthetizing the eye with medication, the conjunctiva may be moved with a cotton swab to observe the location of the enlarged blood vessels.

Costochondritis is a common condition and is responsible for 30% of emergency room chest pain related visits. One-fifth of visits to the primary care physician are for musculoskeletal chest pain; of this 20% of primary care office visits, 13% is due to costochondritis. Costochondritis cases are most often seen in people older than age 40 and occurs more often in women.

Clinical evaluation and identification of characteristics papules may allow a dermatologist to diagnose Degos disease. The papules have a white center and are bordered with a red ring. After lesions begin to appear, the diagnosis for Degos disease can be supported by histological findings. Most cases will show a wedge-shaped connective tissue necoris in the deep corium. This shape is due to the blockage/occlusion of small arteries.

Individuals may be diagnosed with the benign form if only the papules are present. However, an individual may be diagnosed with the malignant form if involvement of other organs like the lungs, intestine and/or central nervous system occurs. The malignant, or systematic form of this condition may suddenly develop even after having papules present for several years. In order to quickly diagnose this shift to the malignant variant of the disease, it is important for individuals to have consistent follow-up evaluations.In these evaluations, depending on which organs are suspected to be involved, the following procedures and tests may be conducted: skin inspection, brain magnetic resonance tomography, colonoscopy, chest X-ray, and/or abdominal ultrasound.

No consensus criteria exist for the diagnosis of ENS; it is typically diagnosed by ruling out other conditions, with ENS remaining the likely diagnosis if the signs and symptoms are present. A "cotton test" has been proposed, in which moist cotton is held where a turbinate should be, to see if it provides relief; while this has not been validated nor is it widely accepted, it may be useful to identify which people may benefit from surgery.

As of 2015, protocols for using rhinomanometry to diagnose ENS and measure response to surgery were under development, as was a standardized clinical instrument (a well defined and validated questionnaire) to obtain more useful reporting of symptoms.

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.

There has long been said to be a link between "rheumatic" pain and the weather. There appears to be no firm evidence in favour or against; a 1995 questionnaire given to 557 people by A. Naser and others at the Brigham and Women's Hospital's Pain Management Center concludes that "changes in barometric pressure are the main link between weather and pain. Low pressure is generally associated with cold, wet weather and an increase in pain. Clear, dry conditions signal high pressure and a decrease in pain."

Chondritis is inflammation of cartilage.

It takes several forms, osteochondritis, costochondritis, Relapsing polychondritis among them. Costochondritis is notable for feeling like a heart attack.

A positive culture in MacConkey agar is diagnostic, but cultures are only positive in 50–60% of cases. Diagnostic characteristics are most commonly found in the granulomatous stage and are described as being chronic inflammatory cells, Russell bodies, and pseudoepitheliomatous hyperplasia, and groups of large vacuolated histiocytes containing "Klebsiella rhinoscleromatis" (Mikulicz cells).

The papules characteristic for this disease develop due to infractions, or blockages in small-medium arteries and veins. The underlying cause is unknown for this disease. Though not confirmed, some cases have shown signs of inheritance between first-degree relatives. It has been suggested that the disease has a familial inheritance pattern; it is thought to be an autosomal dominant disorder. In most cases of familial inheritance, the benign variant of the disease has been present.

Due to the lack of knowledge of the pathomechanism for this condition prevention strategies are not known. However, in order to prevent worsening of symptoms, consistent evaluations should be conducted by a physician.

Costochondritis may be treated with physical therapy (including ultrasonic, TENS, with or without nerve stimulation) or with medication. Treatment may involve the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or other pain relief medications (analgesics) such as acetaminophen. Severe cases of costochondritis may call for the use of opioid medications such as hydrocodone or oxycodone, tricyclic antidepressant medications such as amitriptyline for pain from chronic costochondritis, or anti-epileptic drugs such as gabapentin may be used. Oral or injected corticosteroids may be used for cases of costochondritis unresponsive to treatment by NSAIDs; however, this treatment has not been the subject of study by rigorous randomized controlled trials and its practice is currently based on clinical experience. Rest from stressful physical activity is often advised during the recovery period.

Patients and their primary care physicians must be made fully aware of the ophthalmic risks and the need for regular screening examinations to detect retinal toxicity at an early stage.

Baseline evaluation for patients beginning treatment with a chloroquine derivative should include a complete eye examination by an eye care professional, retinal photography for follow-up comparisons, and Visual field testing with a white pattern. Central visual field assessment should test the central 10° of vision with a white test target (such as Humphrey 10-2 program).

In patients at risk or those with unclear presentation, optical coherence tomography (loss of IS/OS junctions), fundus autofluorescence (focal hyper or hypoautofluorescence), and multifocal electroretinography (paracentral depressions) may be obtained.

Profound abnormalities detected with visual field and multifocal electroretinography testing can be observed in the presence of a normal retinal appearance. Retinal examinations are advised for documentation, but visible bull's-eye maculopathy is a late change, and the goal of screening is to recognize toxicity at an earlier stage. Annual screening should begin after 5 years (or sooner if there are unusual risk factors).

Cessation of the drug at the first sign of toxicity is recommended. No treatment exists as yet for this disorder, so it is imperative that patients and their ophthalmologists be aware of the best practices for minimizing toxic damage.

Extreme deviation of nasal septum may be accompanied by atrophic rhinitis on the wider side.

The differential diagnosis includes oral lichen planus, erythematous candidiasis, leukoplakia, lupus erythematosus, glossitis, and chemical burns. Atrophic glossitis is usually distinguished from benign migratory glossitis on the basis of the migrating pattern of the lesions and the presence of a whitish border, features which are not present in atrophic glossitis, which instead shows lesions which enlarge rather than migrate. Rarely, blood tests may be required to distinguish from glossitis associated with anemia or other nutritional deficiencies. Since the appearance and the history of the condition (i.e. migrating areas of depapillation) are so striking, there is rarely any need for biopsy. When biopsy is taken, the histopathologic appearance is quite similar to psoriasis:

- Hyperparakeratosis.

- Acanthosis.

- Subepithelial T lymphocyte inflammatory infiltrate.

- Migration of neutrophilic granulocytes into the epithelial layer, which may create superficial microabscesses, similar to the Munro's microabscesses described in pustular psoriasis.

The rash caused by ACA is most evident on the extremities. It begins with an inflammatory stage with bluish red discoloration and cutaneous swelling, and concludes several months or years later with an atrophic phase. Sclerotic skin plaques may also develop.As ACA progresses the skin begins to wrinkle.

Treatment of atrophic rhinitis can be either medical or surgical.

Medical measures include:

- Nasal irrigation using normal saline

- Nasal irrigation and removal of crusts using alkaline nasal solutions prepared by dissolving a spoonful of powder containing one part sodium bicarbonate, one part sodium biborate and two part sodium chloride.

- 25% glucose in glycerine can be applied to the nasal mucosa to inhibit the growth of proteolytic organisms which produce foul smell.

- Local antibiotics, such as chloromycetine.

- Vitamin D (Kemicetine).

- Estradiol spray for regeneration of seromucinous glands and vascularization of mucosa.

- Systemic streptomycin (1g/day) against Klebsiella organisms.

- Oral potassium iodide for liquefaction of secretion.

- Placental extract injected in the submucosa.

Surgical interventions include:

- Young's operation.

- Modified Young's operation.

- Narrowing of nasal cavities, submucosal injection of Teflon paste, section and medial displacement of the lateral wall of the nose.

- Transposition of parotid duct to maxillary sinus or nasal mucosa.

Often, treatment is not necessary, because episcleritis is a self-limiting condition. Artificial tears may be used to help with irritation and discomfort. More severe cases can be treated with either topical corticosteroids or oral non-steroidal anti-inflammatory drugs.

Ketorolac, a topical NSAID, may be used, but it is not more effective than artificial tears and it causes more side effects.

The diagnosis is usually made on the clinical appearance, and tissue biopsy is not usually needed. The histologic picture is one of superficial candidal hyphal infiltration and a polymorphonuclear leukocytic inflammatory infiltrate present in the epithelium. The rete ridges are elongated and hyperplastic (pseudoepitheliomatous hyperplasia, which may be mistaken for carcinoma).

Initial treatment is similar to atrophic rhinitis, namely keeping the nasal mucosa moist with saline or oil-based lubricants and treating pain and infection as they arise; adding menthol to lubricants may be helpful in ENS, as may be use of a cool mist humidifer at home. For people with anxiety, depression, or who are obsessed with the feeling that they can't breathe, psychiatric or psychological care may be helpful.

In some people, surgery to restore missing or reduced turbinates may be beneficial.

A 2015 meta-analysis identified 128 people treated with surgery from eight studies that were useful to pool, with an age range of 18 to 64, most of whom had been suffering ENS symptoms for many years. The most common surgical approach was creating a pocket under the mucosa and implanting material - the amount and location were based on the judgement of the surgeon. In about half the cases a filler such as noncellular dermis, a medical-grade porous high-density polyethylene, or silastic was used and in about 40% cartilage taken from the person or from a cow was used. In a few cases hyaluronic acid was injected and in a few others tricalcium phosphate was used. There were no complications caused by the surgery, although one person was over-corrected and developed chronic rhinosinusitis and two people were under-corrected. The hyaluronic acid was completely resorbed in the three people who received it at the one year follow up, and in six people some of the implant came out, but this did not affect the result as enough remained. About 21% of the people had no or marginal improvement but the rest reported significant relief of their symptoms. Since none of the studies used placebo or blinding there may be a strong placebo effect or bias in reporting.

Fluorescein angiography is usually performed for diagnosis and follow-up of patients with POHS.