Relationship to Menieres Disease
The data on how often progression to Menieres disease occurs is mixed, but the majority of recent studies suggest a low likelihood. A 1984 study from Japan looked at patients with Menieres disease and classified them into subcategories based on their first symptoms. The study found that the majority of patients with Menieres disease (104 out of 163, or 63.80%) presented vertigo with their first symptoms, and only 59 out of 163 (36.19%) of patients presented with cochlear symptoms first, such as "tinnitus or deafness." However, the study found that 59 out of 74 (79.72%) patients who started out with a cochlear hydrops diagnosis progressed to Menieres disease, and concluded that "cochlear Menieres disease frequently develops into Menieres disease. "Conversely, A 2006 study from doctors at the House Ear Institute found that “conversion from cochlear hydrops to Menieres disease occurred in 33%” of diagnosed patients in a study including 46 subjects. A 2009 study from Japan found that only about 10% of their diagnosed patients with sudden low-frequency hearing loss (SLFHL) went on to develop full Menieres disease, and about 18% with recurring SLFHL developed Menieres disease. From this study, about 70% of patients who did not develop Menieres Disease maintained their hearing in the end.
6-MP is metabolized analogously to natural purines, giving thioguanosine triphosphate (TGTP) and thiodeoxyguanosine triphosphate (TdGTP) via thioinosine monophosphate (TIMP) and several further intermediates. On a second path, the sulfur atom of 6-MP and TIMP is methylated. The end products of azathioprine metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine. Mechanism of action
Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression. Azathioprine is converted within tissues to 6-MP, some of which is converted, in turn, to 6-thioguanine by the addition of an amino group. Both 6-MP and 6-thioguanine are conjugated with ribose, and then phosphorylated to form the nucleotides  thioinosinic acid and thioguanylic acid, respectively. These nucleotides masquerade, respectively, as inosinic acid and guanylic acid; the former is the starting point for purine nucleotide biosynthesis, while the latter is one of the building blocks of DNA and RNA. The nucleotides are  incorporated into newly synthesized (but nonfunctional) DNA, halting replication. The nucleotides act to inhibit glutamine-phosphoribosyl pyrophosphate amidotransferase (GPAT), one of the enzymes involved in purine biosynthesis, one of the earlier steps in the synthesis of DNA and RNA. They achieve GPAT inhibition through a form of negative feedback called product inhibition.