Diagnosis
Types
Granuloma annulare may be divided into the following types:: 703–5 
Localized granuloma annulare
Generalized granuloma annulare
Patch-type granuloma annulare
Subcutaneous granuloma annulare
Perforating granuloma annulare

Treatment
Because granuloma annulare is usually asymptomatic and self-limiting with a course of about 2 years, initial treatment is generally topical steroids or calcineurin inhibitors; if unimproved with topical treatments, it may be treated with intradermal injections of steroids. If local treatment fails it may be treated with systemic corticosteroids. Treatment success varies widely, with most patients finding only brief success with the above-mentioned treatments. Most lesions of granuloma annulare disappear in pre-pubertal patients with no treatment within two years while older patients (50+) have rings for upwards of 20 years. The appearance of new rings years later is not uncommon. History
The disease was first described in 1895 by Thomas Colcott Fox as a "ringed eruption of the fingers", and it was named granuloma annulare by Henry Radcliffe Crocker in 1902. See also
Granuloma
Necrobiosis lipoidica

References
External links
DermNet dermal-infiltrative/granuloma-annulare
These markers include angiotensin-converting enzyme, cathepsin S, chitotriosidase, and CCL18 in the blood plasma; and tumor necrosis factor alpha in splenic Gaucher cells (engorged macrophages). Diagnosis
Gaucher disease is suggested based on the overall clinical picture. Initial laboratory testing may include enzyme testing. As a result, lower than 15% of mean normal activity is considered to be diagnostic. Decreased enzyme levels will often be confirmed by genetic testing. Numerous different mutations occur; sequencing of the beta-glucosidase gene is sometimes necessary to confirm the diagnosis. Prenatal diagnosis is available and is useful when a known genetic risk factor is present.A diagnosis can also be implied by biochemical abnormalities such as high alkaline phosphatase, angiotensin-converting enzyme, and immunoglobulin levels, or by cell analysis showing "crinkled paper" cytoplasm and glycolipid-laden macrophages.Some lysosomal enzymes are elevated, including tartrate-resistant acid phosphatase, hexosaminidase, and a human chitinase, chitotriosidase. This latter enzyme has proved to be very useful for monitoring Gauchers disease activity in response to treatment, and may reflect the severity of the disease

Classification
Gauchers disease (GD) has three common clinical subtypes. These subtypes have come under some criticism for not taking account of the full spectrum of observable symptoms (the phenotypes). Also, compound heterozygous variations occur which considerably increase the complexity of predicting disease course. GD type I (non-neuropathic) is the most common and least severe form of the disease. Symptoms may begin early in life or in adulthood and mainly affect the liver, spleen, and bone.