Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Valine-depleted amino acid imbalance solution markedly inhibits tumor growth but causes fatty liver as a side effect. However, much remains unknown about the mechanism of the development of fatty liver. Valine-depleted amino acid imbalance solution containing various concentrations of calories was administered to tumor-bearing rats for four days by means of total parenteral nutritional methods to investigate the interaction of caloric intake and the development of fatty liver. Compared with the total parenteral nutrition control group the triglyceride content of the liver rose significantly in the group given valine-depleted amino acid imbalance solution with an increase in caloric intake. Plasma total protein and albumin significantly decreased. The very-low-density lipoprotein concentration in serum was also significantly lower than that in the control group. Valine-depleted amino acid imbalance caused hypoproteinemia, suggesting a fall in synthesis of apolipoproteins in the liver indispensable for lipid release. Along with the increase in the total caloric intake, triglyceride synthesis in the liver increased, resulting in augmentation of fatty content of the liver, probably because of the decreased lipid release.
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PMID:Effects of caloric intake on anticancer therapy in rats with valine-depleted amino acid imbalance. 920 Jan 58

A diversity of coagulation disorders in cancer patients arise from tumor-specific growth characteristics, neoangiogenesis with impaired endothelial lining, defective myelopoiesis, hypoproteinemia or metastatic lesions growth with organ dysfunction. Recent investigations have found a clinically relevant correlation of coagulation disorders and tumor growth. These prompted new therapeutic strategies focused on growth factors with the aim to control tumor metastasis, particularly if used for the treatment of micrometastatic disease. However, such treatment may lead to the life threatening coagulation imbalance. A coagulation homeostasis may become further impaired after nonsurgical cancer therapy, especially after preoperative irradiation, which produces lesions precipitating both bleeding and thrombosis. Anticancer chemotherapy may affect liver function and decrease the synthesis of both procoagulation and anticoagulation factors. The most of chemotherapeutic protocols affect platelet synthesis, which arises as a principal dose-limiting side effect. It was observed both during combined systemic chemotherapy and local antitumor therapy. Although the side effects produced by chemotherapy are reversible, endothelial lesions may persist for many years after the anticancer treatment. Instead of cancer patients, there's a growing cohort of patients with nonmalignant diseases who use cytostatics in the perioperative period, and are candidates for surgical procedures not related to their malignant disease, i.e. hernia repair. In this patient population a special attention must be paid to the preoperative evaluation of coagulation status and thromboprophylaxis. This overview reminds the most common coagulation disorders in cancer patients in the perioperative period. It emphasizes the need for proper patient monitoring which may facilitate the diagnostics and treatment of cancer-related coagulation disorders in the perioperative setting.
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PMID:An overview of coagulation disorders in cancer patients. 1939 16