For this reason many of the antithrombin structures stored in the protein data bank and presented in this article show variable glycosylation patterns. Antithrombin begins in its native state, which has a higher free energy compared to the latent state, which it decays to on average after 3 days. The latent state has the same form as the activated state - that is, when it is inhibiting thrombin. As such it is a classic example of the utility of kinetic vs thermodynamic control of protein folding. Function
Antithrombin is a serpin (serine protease inhibitor) and is thus similar in structure to most other plasma protease inhibitors, such as alpha 1-antichymotrypsin, alpha 2-antiplasmin and Heparin cofactor II. The physiological target proteases of antithrombin are those of the contact activation pathway (formerly known as the intrinsic pathway), namely the activated forms of Factor X (Xa), Factor IX (IXa), Factor XI (XIa), Factor XII (XIIa) and, to a greater extent, Factor II (thrombin) (IIa), and also the activated form of Factor VII (VIIa) from the tissue factor pathway (formerly known as the extrinsic pathway). The inhibitor also inactivates kallikrein and plasmin, also involved in blood coagulation. However it inactivates certain other serine proteases that are not involved in coagulation such as trypsin and the C1s subunit of the enzyme C1 involved in the classical complement pathway.Protease inactivation results as a consequence of trapping the protease in an equimolar complex with antithrombin in which the active site of the protease enzyme is inaccessible to its usual substrate.
Diagnosis
Differential diagnosis
The disease is often misdiagnosed as Blastomyces dermatitidis or Paracoccidiodes brasiliensis due to its similar morphology. Treatment
Surgical excision or cryosurgery is the treatment of choice. Treatment with antifungals has been considered ineffective, but the use of clofazimine and dapsone in patients with leprosy and lobomycosis has been found to improve the latter. This treatment regimen, with concomitant itraconazole, has been used to prevent recurrence after surgery. Other animals
Lesions in dolphins occur on the dorsal fin, head, flukes, and peduncle. In January 2006, a potential epidemic of lobomycosis was reported in dolphins of the Indian River Lagoon in Florida. See also
List of cutaneous conditions

References
Further reading
Bermudez, L., M.F. van Bressem, O. Reyes-Jaimes, A.J. Sayegh & A.E. Paniz Mondolfi (2009) Lobomycosis in man and lobomycosis-like disease in bottlenose dolphin, Venezuela. Emerg. Infect. Dis., 15: 1301–1303. Carvalho, K. A. D., Floriano, M. C., Enokihara, M. M. S., & Mascarenhas, M. R. M. (2015). Jorge Lobo’s disease. Anais brasileiros de dermatologia, 90(4), 586–588. Esperon, F., D. Garcia-Parraga, E.N. Belliere & J.M. Sanchez-Vizcaino (2012) Molecular diagnosis of lobomycosis-like disease in a bottlenose dolphin in captivity. Med. Mycol., 50: 106–109. Francesconi, V. A., Klein, A. P., Santos, A. P. B. G., Ramasawmy, R., & Francesconi, F (2014) Lobomycosis: epidemiology, clinical presentation, and management options. Therapeutics and Clinical Risk Management, 10, 851. Rodríguez-Toro G (May 1993). "Lobomycosis". Int. J. Dermatol. (Review). 32 (5): 324–32. doi:10.1111/j.1365-4362.1993.tb01466.x. PMID 8505156. S2CID 221814305. Paniz-Mondolfi, A., C. Talhari, L.S. Hoffmann, D.L. Connor and S. Talhari & al. (2012) Lobomycosis: An emerging disease in humans and delphinidae.