RESUMO
Post-traumatic stress disorder (PTSD) is a mental disorder that develops after individual exposure to one or more traumatic events.Natural disasters and war are the major primers of PTSD.Tt is affracting more attention due to the high prevalence in war veterans and natural disasters.The risk factors range from gender,environment to physiology.Hypothalamic-pituitary-adrenal (HPA) axis plays an important role in stress reaction and dysfunction of HPA axis leads to disorder of neuroendocrine.In addition,chronic inflammation,including adaptive and innate immune response disorder,has been reported in many PTSD studies.Neural imaging studies have found that there are significant changes in the brain structure and neural circuits of PTSD patients.However,the biological mechanism underlying PTSD is largely unknown.Currently,based on the clinic symptoms of PTSD patients,anti-depression and anxiety drugs are the first choice for treatment,but the outcomes are diverse.Some potential therapeutic drugs or avenues that are derived from the identified targets are still under investigation.In this review,we overview and summarize the biological changes of PTSD,focusing on disorder of neuroendocrine,chronic inflammation,brain structure and circuits changes and therapeutic strategies in clinical and preclinical trials.This review aims to will provide new ideas for revelation of PTSD mechanisms and develop novel therapies.
RESUMO
Tumor-induced osteomalacia (TIO), or oncogenic osteomalacia (OOM), is a rare acquired paraneoplastic disease characterized by renal phosphate wasting and hypophosphatemia. Recent evidence shows that tumor-overexpressed fibroblast growth factor 23 (FGF23) is responsible for the hypophosphatemia and osteomalacia. The tumors associated with TIO are usually phosphaturic mesenchymal tumor mixed connective tissue variants (PMTMCT). Surgical removal of the responsible tumors is clinically essential for the treatment of TIO. However, identifying the responsible tumors is often difficult. Here, we report a case of a TIO patient with elevated serum FGF23 levels suffering from bone pain and hypophosphatemia for more than three years. A tumor was finally located in first metacarpal bone by octreotide scintigraphy and she was cured by surgery. After complete excision of the tumor, serum FGF23 levels rapidly decreased, dropping to 54.7% of the preoperative level one hour after surgery and eventually to a little below normal. The patient's serum phosphate level rapidly improved and returned to normal level in four days. Accordingly, her clinical symptoms were greatly improved within one month after surgery. There was no sign of tumor recurrence during an 18-month period of follow-up. According to pathology, the tumor was originally diagnosed as "lomangioma" based upon a biopsy sample, "proliferative giant cell tumor of tendon sheath" based upon sections of tumor, and finally diagnosed as PMTMCT by consultation one year after surgery. In conclusion, although an extremely rare disease, clinicians and pathologists should be aware of the existence of TIO and PMTMCT, respectively.