Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231807 (exertional dyspnea)
 3,402 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 66-year-old man who developed vitamin B1 deficiency polyneuropathy long after a gastrectomy. After a preceding bronchial infection, the patient noticed numbness and weakness in his extremities, followed by generalized edema and exertional dyspnea. He had undergone subtotal gastrectomy due to duodenal ulcer at age 19. His daily oral intake of food was normal without any alcoholic abuse. He was admitted to our hospital with rapidly progressive gait disturbance due to muscle weakness, and sensory disturbance. Neurological examination showed peripheral polyneuropathy with distal dominant muscular weakness and sensory disturbance. Chest X-ray film showed marked cardiomegaly and pleural effusion. Nerve conduction studies showed decreases in the action potentials of both the motor and sensory nerves, with the sensory nerves being more severely affected than the motor nerves. Sural nerve biopsy demonstrated severe axonal degeneration without any inflammatory change. The blood concentration of thiamine (vitamin B1) was slightly decreased below the normal range (19 ng/ml; normal, 20-50), and the serum vascular endothelial growth factor (VEGF) was high (890 pg/ml; normal < 200 pg/ml). Intravenous administration of vitamin B1 (50 mg per day) dramatically improved his symptoms in a few days and the level of VEGF returned to nearly normal. In this gastrectomized patient many years ago, vitamin B1 deficiency neuropathy is warranted in view of a prompt response to thiamine administration. This case suggests that VEGF is involved in the pathogenesis of vitamin B1 deficiency polyneuropathy.
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PMID:[Thiamine deficiency polyneuropathy after gastrectomy associated with high level of serum vascular endothelial growth factor (VEGF). A case report]. 1519 56

A 67-year-old woman who complained of pain and sensory disturbance in the right upper extremity was admitted. Her chest CT showed a mass lesion in the upper lobe of the right lung, indicating invasion to the chest wall. CT-guided tumor biopsy resulted in a diagnosis of squamous cell carcinoma, and FDG-PET scan suggested metastasis to the right supraclavicular lymph node. We diagnosed squamous cell lung cancer (T3N3M0 : stage IIIB) and started chemotherapy using carboplatin and vinorelbine combined with thoracic radiotherapy. At the end of 6th cycles of chemotherapy, exertional dyspnea and palpitations appeared, and she was readmitted. Repeated transthoracic echocardiography showed a deterioration of the thickening of the right ventricular wall. Magnetic resonance imaging and Ga-scintigraphy suggested a neoplastic lesion in the myocardium. Eventually, we diagnosed it as myocardial metastasis from non-small cell lung cancer. Shortly after the beginning of palliative radiotherapy to the myocardial lesion, repeated episodes of ventricular tachycardia emerged. We stopped radiotherapy and managed to control the ventricular tachycardia by initiating amiodarone. Though we administered erlotinib as a second line chemotherapy, the primary tumor and pericardial effusion progressed and pleural effusion appeared, so we discontinued erlotinib. Pericardiocentesis was carried out to improve her symptoms and cytological examination of effusion revealed class IV. Her performance status dropped off and we decided to continue best supportive care. Myocardial metastasis of lung cancer is rarely a clinical problem, but it might have a decisive influence on the patient's prognosis due to serious arrhythmia or some other complications. Therefore, there is a need to consider cardiac involvement in the course of lung cancer.
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PMID:[Case of squamous cell lung cancer with myocardial metastasis complicated with ventricular tachycardia]. 1982 87