We noticed that her ankle pain disappeared Alpelisib molecular weight once she had resumed walking. Radiography and computed tomography images revealed that union of the ankle had been achieved (Fig. 2c, d). No side effects attributable to the drug were observed during treatment, and her subsequent laboratory findings continued to be normal. At 6 months, the patient could walk without a brace and without any pain. Plain images taken at this time revealed complete healing of the fractured and nonunion sites. Discussion A major problem for patients with chronic diabetes mellitus is the development of peripheral neuropathy. Sensory loss leads to
neuropathic ulceration, which is aggravated in the presence of foot and ankle deformities and causes excessive pressure on deformed areas, a condition that is known as Charcot arthropathy or diabetic ankle [5, 6]. The main aims when treating Charcot arthropathy of the foot and ankle
are to correct the deformity so that there is an appropriate distribution of pressure for healing and to prevent skin ulceration . Surgical correction with internal fixation for Charcot arthropathy is associated with a high rate of complications and failure because of infection, bone softening, resorption, fragmentation, and breakage of the implant . Our patient with severe Type selleck inhibitor I diabetes mellitus and Charcot arthropathy had undergone two failed operations. Ankle union was not achieved even after the second operation, and the patient sustained a femoral shaft fracture. Nonunion is a severe complication and has a negative impact on the quality of life; undoubtedly, a second intervention is therefore necessary, but it is not exempt from further risks and potential
complications . It is therefore important that some treatment that can resolve this problem should be undertaken, but a third surgery to fix nonunion is extremely difficult as the ankle needs to be stabilized and the bone needs to be strengthened. Teriparatide (rhPTH 1–34) is an anabolic agent that is administered subcutaneously. Its anabolic effect is attributable to the stimulation of osteoblasts, which causes a net increase in both cancellous Janus kinase (JAK) and cortical bone, thus improving the bone architecture [10, 11]. Teriparatide has different effects on trabecular and cortical bone. Because of the high degree of PRI-724 nmr remodeling and apoptosis of trabecular bone osteoblasts, teriparatide has a more profound effect on trabecular than on cortical bone, which has a lower degree of osteoblastic apoptosis . Teriparatide also accelerates fracture healing by improving the biomechanical properties of the fracture callus and by increasing endochondral ossification and bone remodeling in animal models . This effect has also been observed in several other clinical case reports [12–14].