Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphangioleiomyomatosis (LAM) is a rare multisystem disease, occurs in women, usually premenopausal, caused by the proliferation of neoplastic smooth muscle-derived cells. Mutations in the tuberous sclerosis complex genes, lead to the activation of mammalian target of rapamycin kinase (mTOR), results in proliferation of LAM cells, its increasing motility, and survival. Polycystic lung destruction, extensive involvement of lymphatic channels, chylothorax, chyloperitoneum, and renal angiomyolipomas can develop in LAM patients. The new, promising treatment strategies have been recently introduced due to discovery of the genetic and molecular mechanisms of LAM. Comprehension of the disease pathogenesis has resulted in the implementation of other therapeutic agents such as mTOR inhibitors, VEGF-D inhibitors, statins, interferon, chloroquine analogs, cyclin-dependent kinase inhibitors, matrix metalloproteinase inhibitors, aromatase inhibitors, and their combinations. The mTOR inhibitors appear to be the most important, and the efficacy of sirolimus in LAM treatment has been proved. The article discussed the new control studies with mTOR inhibitors, doxycycline, simvastatin, and combination of them in LAM patients.
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PMID:Lymphangioleiomyomatosis: New Treatment Perspectives. 2598 May 93

Chylous ascites (CA) is an uncommon entity with several etiologies. Only a few cases of CA have been reported as a complication after liver transplantation (LT). Most of these cases occurred within 1 month after surgery and typically resulted from traumatic intraoperative injury leading to disruption of lymphatics. Although peripheral lymphedema has been frequently correlated with use of calcineurin inhibitors, associated spontaneous CA has only been reported in a few cases after renal transplantation. We report a case of delayed spontaneous CA after LT caused by the use of the mammalian target of rapamycin (mTOR) inhibitor everolimus. Everolimus was introduced in our patient early after transplantation because of tacrolimus-induced microangiopathy, and years later the patient presented with spontaneous CA. After excluding other causes of CA, everolimus was discontinued, and immunosuppression was maintained by increasing prednisone and continuing mycophenolate mofetil. Additionally, the patient was treated with percutaneous drain placement and began a low-fat, high-protein diet. One month later the patient had complete resolution of symptoms with no recurrence of ascites. To our knowledge, this is the first case of delayed-onset CA caused by everolimus after LT.
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PMID:Spontaneous Chylous Ascites After Liver Transplantation Secondary to Everolimus: A Case Report. 3202 15