Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149925 (small cell lung cancer)
 6,491 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 77-year-old man was admitted to our hospital with muscle weakness and shortness of breath. Chest CT showed a mass in the left upper lobe, and electromyography showed waxing phenomenon with high-frequency repetitive stimulation. We diagnosed Lambert-Eaton myasthenic syndrome accompanying small cell lung cancer. He was treated with carboplatin and etoposide, and concurrent thoracic irradiation. Although, the tumor size decreased, his myasthenic symptoms remained. He started taking 3,4-diaminopyridine and his muscle weakness improved dramatically, and he was eventually able to walk finally. In some cases, anti-tumor therapies cannot improve the myasthenic symptoms. In such cases, 3,4-diaminopyridine could improve the quality of life, and should be approved in Japan.
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PMID:[A case of Lambert-Eaton myasthenic syndrome with small cell lung cancer, treated with 3,4-diaminopyridine]. 1919 42

A 58-year-old man complaining of increasing weakness of muscular leg strength, diplopia and ptosis was admitted to our hospital. An electromyogram (EMG) showed typical waxing phenomenon in response to high-frequency repetitive stimulation. A diagnosis of Lambert-Eaton myasthenic syndrome (LEMS) was made from his symptoms and EMG results. A chest CT showed mediastinal lymph node swelling. No abnormal mass was seen in either lung field. His serum levels of a P/Q-type anti-voltage-gated calcium channel (VGCC) antibody, Pro-GRP, and NSE were high. FDG-PET showed accumulation of FDG to the mediastinal and left inguinal lymph nodes. The left inguinal lymphadenopathy was pathologically diagnosed as metastasis of small cell lung carcinoma. No tumor could be detected by bronchofiberscopy. No other distant metastasis was detected by brain MRI, abdominal CT, or FDG-PET. After 6 courses of chemotherapy for SCLC, a partial response and reduction of symptoms were obtained. For assessment of indistinguishable neuropathic symptoms, the possible diagnosis of paraneoplastic syndrome, such as LEMS, and the fact that early treatment for primary disease was effective, should be considered.
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PMID:[A case of small cell lung carcinoma without apparent primary lesion accompanying Lambert-Eaton myasthenic syndrome]. 2005 96

A 75-year-old man had been given a diagnosis of small cell lung cancer (SCLC) in March 2005. He had been treated with chemotherapy consisting of carboplatin and etoposide, and he had showed partial response to treatment. He presented with general fatigue, weakness of the muscles and extremities, skin lesions and finger erythema in April 2006. A muscle biopsy was performed and the pathological findings confirmed dermatomyositis. The findings of his chest X-ray and computed tomography showed an increase in the size of the lung cancer lesion. The tumor size decreased, and creatine kinase and lactate dehydrogenase levels also decreased after irinotecan chemotherapy. He was also given prednisolone (1 mg/kg) for prolonged muscle weakness. There are few cases which report dermatomyositis after a diagnosis of SCLC. In the present case, dermatomyositis appeared when the recurrence of SCLC became evident. We believed that the onset of dermatomyositis might be related to the activity level of SCLC.
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PMID:[A case of dermatomyositis becoming symptomatic after recurrence of small cell lung cancer]. 2018 42

Lambert-Eaton myasthenic syndrome (LEMS) is a neuromuscular disorder in which autoantibodies inhibit the presynaptic release of acetylcholine. Autoantibodies against P/Q-type voltage-gated calcium channels (VGCC) are detected in 85% of patients with LEMS. In addition, autoantibodies to synaptotagmin, an M1-type muscarinic acetylcholine receptor and SOX1 are also found in the sera of patients with LEMS. LEMS is closely associated with small cell lung cancer (SCLC) in 50-60% of patients. Patients with SCLC who have anti-VGCC antibodies have been reported to have a favorable prognosis. In contrast to paraneoplatic LEMS, other forms of LEMS may have an autoimmune aspect because of the established association between human leukocyte antigen and a family history of other autoimmune disorders in this condition. The clinical features of LEMS include proximal weakness, areflexia, ptosis, cerebellar ataxia and autonomic dysfunction. The findings of electrophysiological examination show that LEMS is characterized by compound muscle action potential potentials with a low amplitude and increment upon repetitive nerve stimulation at a high rate. Tumor removal is the primary treatment of LEMS. The efficacy of 3,4-diaminopyridine for the treatment of LEMS has also been established. Patients with LEMS require the immunotherapies such as plasma exchange and the administration of high doses of immunoglobulin and prednisolone.
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PMID:[Lambert-Eaton myasthenic syndrome (LEMS)]. 2042 Jan 83

A 59-year-old man who was diagnosed with small cell lung cancer (SCLC), achieved a complete response to the induction chemoradiotherapy and received prophylactic cranial irradiation (PCI) (25 Gy at 250 cGy per fraction) in October 2008. Three months later, he complained of anorexia, weight loss, fatigue, and short-term memory loss and developed dementia and systemic muscle weakness. Magnetic resonance imaging in April and July 2009 revealed the progression of the diffuse brain atrophy without evidence of the metastasis of SCLC. Paraneoplastic neurological syndrome was suspected because anti-Hu antibody was detected in his serum and cerebrospinal fluid, but the adverse effects of chemotherapy and/or radiotherapy were also suspected as the cause of his neurological disorder.
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PMID:Acute onset of brain atrophy and dementia in a patient with small cell lung cancer: a case report. 2121 22

Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease of the neuromuscular junction, and approximately 60% of patients with LEMS have a tumor, mostly small cell lung cancer (SCLC), as a paraneoplastic neurological syndrome. The clinical data of Japanese patients in the present study are as follows: the ratio of men to women is 3: 1 (mean age, 62 years; age range, 17-80 years). Of the patients with LEMS, 61% have SCLC, whereas the others do not have cancer. Clinical symptoms are usually characterized by proximal muscle weakness and dysautonomia. In less than 10% of the patients, there are signs of cerebellar dysfunctions (paraneoplastic cerebellar degeneration with LEMS; PCD-LEMS), and these are usually associated with SCLC. The diagnosis can be confirmed by detecting a specific antibody in a radioimmunoprecipitation assay and finding reduced amplitude of compound muscle action potential that increases by over 100% after maximum voluntary activation or 50Hz of nerve stimulation. The pathomechanism of LEMS is characterized by impaired transmission across the neuromuscular junction because of autoantibodies directed against the presynaptic P/Q-type voltage-gated calcium channels (P/Q-VGCCs). Histopathologic evaluation of the cerebellum in patients with PCD-LEMS showed a reduced number of P/Q-type VGCCs in the molecular layer. Therefore, it was hypothesized that P/Q-VGCC antibodies may induce cerebellar dysfunction after entering the CNS in patients with PCD-LEMS. Specific tumor therapy in patients with LEMS as well as cancer often improves the neurologic deficit. Tumor removal is the primary treatment for LEMS. If the result of the primary screening is negative, screening should be repeated after 3-6 months and thereafter every 6 months for up to 2 years. Most patients benefit from 3, 4-diaminopyridine administered with pyridostigmine. In those with severe weakness, intravenous gamma globulin (IVIg) or plasmapheresis confers short-term benefits. Prednisone when administered alone or in combination with immunosuppressive drugs can achieve long-term control of the disorder.
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PMID:[Lambert-Eaton myasthenic syndrome]. 2174 45

In Lambert-Eaton myasthenic syndrome (LEMS), antibodies against presynaptic voltage-gated calcium channels reduce the quantal release of acetylcholine, causing muscle weakness and autonomic dysfunction. More than half of the affected patients have associated small cell lung cancer, and thorough screening for an underlying malignancy is crucial. The mainstay of treatment for LEMS is symptomatic but immunotherapy is needed in more severely affected patients. Symptomatic therapies aim at increasing the concentration of acetylcholine at the muscle endplate. While acetylcholinesterase inhibitors were the first drugs to be used for the amelioration of symptoms, 3,4-diaminopyridine (3,4-DAP, amifampridine) has been shown to be more effective. 3,4-DAP blocks presynaptic potassium channels, thereby prolonging the action potential and increasing presynaptic calcium concentrations. This then results in increased quantal release of acetylcholine. The efficacy of 3,4-DAP for increasing muscle strength and resting compound muscle action potentials has been demonstrated by four placebo-controlled trials. Side effects are usually mild, and the most frequently reported are paresthesias. The most common serious adverse events are epileptic seizures. 3,4-DAP is currently the treatment of choice in patients with Lambert-Eaton myasthenic syndrome.
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PMID:Update on treatment options for Lambert-Eaton myasthenic syndrome: focus on use of amifampridine. 2182 85

A 65-year-old man had suffered from systemic erythema from November 2008 and had noticed gradually progressing weakness in the upper and lower limbs. He received medical treatment in another hospital but his symptoms did not improve. He was admitted to our hospital for treatment of diabetes in June 2009, and his chest X-ray images and CT scans showed a mass shadow in the right upper lobe with hilar and mediastinal lymphadenopathy. We performed bronchoscopy, and diagnosed small cell lung cancer (T2N2M1, stage IV). However, he had hand grip weakness and continuing upper and lower limb muscle weakness, and therefore electromyography was performed, which showed the presence of waxing in the right leg. Subsequently, a diagnosis of Lambert-Eaton myasthenic syndrome was made. As he also showed ataxia of the left lower extremity, we also diagnosed paraneoplastic cerebellar degeneration. We gave the patient chemotherapy consisting of carboplatin and etoposide which resulted in the disappearance of his waxing, and his grip strength and erythema immediately improved with regression of the tumor after 1 course of chemotherapy. We report a case of small cell lung cancer associated with Lambert-Eaton myasthenic syndrome, paraneoplastic cerebellar degeneration and erythema which presented as paraneoplastic syndrome, which improved with chemotherapy.
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PMID:[A case of small cell lung cancer that presented with paraneoplastic syndrome]. 2184 89

The neuromuscular junction lacks the protection of the blood-nerve barrier and is vulnerable to antibody-mediated disorders. Myasthenia gravis (MG) is caused by the failure of neuromuscular transmission mediated by autoantibodies against acetylcholine receptors (AChR) and muscle-specific receptor tyrosine kinase (MuSK)/LDL-receptor related protein 4 which are AChR-associated transmembrane post-synaptic proteins involved in AChR aggregation. The seropositivity rates for AChR positive and MuSK positive MG in Japan are 80-85% and 5-10%/less than 1%,respectively. The incidence of late-onset MG, defined as onset after age 50 years, has been increasing worldwide. A nationwide epidemiological survey in Japan also revealed that the rates of late-onset MG had increased from 20% in 1987 to 42% in 2006. In 2010, a guideline for standard treatments of late-onset MG was published by the Japanese Society of Neurological Therapeutics. Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease of the neuromuscular junction and approximately 60% of LEMS patients have a tumor, mostly small cell lung cancer (SCLC), as a paraneoplastic neurological syndrome. The clinical pictures of Japanese LEMS patients are as follows; male dominant sex ratio (3 : 1), mean age 62 years (17-80 years), 61% of LEMS have SCLC, and the remaining are without cancer. In less than 10% of cases there are signs of cerebellar dysfunctions (paraneoplastic cerebellar degeneration with LEMS; PCD-LEMS) as well, often associated with SCLC. Most patients benefit from 3, 4-diaminopyridine plus pyridostigmine. In paraneoplastic LEMS, treatment of the tumor often results in neurological improvement. In non-paraneoplastic LEMS, prednisone alone or combined with immunosuppressants are treatment options. In both MG and LEMS, where weakness is severe, plasma exchange or intravenous immunoglobulin treatment may provide short-term benefit.
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PMID:[The pathophysiology and treatment of autoimmune neuromuscular junction diseases]. 2227 98

We present the first case of small cell lung cancer with Lambert-Eaton myasthenic syndrome during hemodialysis (HD). A 72-year-old male patient receiving HD experienced progressive muscle weakness. He was diagnosed with small cell lung cancer with Lambert-Eaton myasthenic syndrome due to an increased serum level of anti-voltage-gated calcium channel antibody and aspiration cytology on endobronchial ultrasonography for the swelling of a subcarinal lymph node. He received chemotherapy consisting of carboplatin (300 mg/m(2)) and etoposide (50 mg/m(2)), to which he had a partial response. However, the second therapy course could not be administered because of the unexpected development of severe hematological adverse events, which also prevented him from undergoing further HD. This case indicates that caution should be taken when using chemotherapy for such patients because of hypotension due to chemotherapy, with which it is impossible to undergo HD.
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PMID:Hypotension due to Chemotherapy in a Patient with Small Cell Lung Cancer and Lambert-Eaton Myasthenic Syndrome Undergoing Hemodialysis: A First Case Report. 2242 46


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