After evaluation of a persons history, risk factors, physical examination, laboratory testing and imaging, management begins depending on suspected diagnoses. Depending upon the diagnosis, a person may be placed in the intensive care unit, admitted to the hospital, or be treated outpatient. For persons with suspected cardiac chest pain or acute coronary syndrome, or other emergent diagnoses such as pneumothorax, pulmonary embolism, or aortic dissection, admission to the hospital is most often recommended for further treatment. Outpatient care
For people with non-cardiac chest pain, cognitive behavioral therapy might be helpful on an outpatient basis. A 2015 Cochrane review found that cognitive behavioral therapy might reduce the frequency of chest pain episodes the first three months after treatment. For persons with chest pain due to gastroesophageal reflux disease, a proton-pump inhibitor has been shown to be the most effective treatment. However, treatment with proton pump inhibitors has been shown to be no better than placebo in persons with noncardiac chest pain not caused by gastroesophageal reflux disease. For musculoskeletal causes of chest pain, manipulation therapy or chiropractic therapy, acupuncture,  or a recommendation for increased exercise are often used as treatment. Studies have shown conflicting results on the efficacy of these treatments. A combination therapy of nonsteroidal anti-inflammatory drugs and manipulation therapy with at-home exercises has been shown to be most effective in treatment of musculoskeletal chest pain. Epidemiology
Chest pain is a common presenting problem.
This deficient mechanism is probably located at the level of the B30.2 domain (exon 10) where most of the pathogenic mutations associated with FMF are located. It is probably the interaction of this domain with the cytoskeleton (microtubules) that is failing, as suggested by the efficacy of colchicine.It is not conclusively known what exactly sets off the attacks, and why overproduction of IL-1 would lead to particular symptoms in particular organs (e.g. joints or the peritoneal cavity). Diagnosis
The diagnosis is clinically made on the basis of the history of typical attacks, especially in patients from the ethnic groups in which FMF is more highly prevalent. An acute phase response is present during attacks, with high C-reactive protein levels, an elevated white blood cell count and other markers of inflammation. In patients with a long history of attacks, monitoring the kidney function is of importance in predicting chronic kidney failure.A genetic test is also available to detect mutations in the MEFV gene. Sequencing of exons 2, 3, 5, and 10 of this gene detects an estimated 97% of all known mutations.A specific and highly sensitive test for FMF is the "metaraminol provocative test (MPT)", whereby a single 10 mg infusion of metaraminol is administered to the patient. A positive diagnosis is made if the patient presents with a typical, albeit milder, FMF attack within 48 hours. As MPT is more specific than sensitive, it does not identify all cases of FMF, although a positive MPT can be very useful.