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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle weakness is a common complaint in clinical practice. If this symptom is combined with focal liver lesions there is a broad spectrum of differential diagnoses for the gastroenterologist to consider. Tumors of neuroendocrine origin such as small-cell lung carcinoma (SCLC) produce a wide array of peptide hormones and are common causes of paraneoplastic syndromes. We report on a 68-year-old woman who presented with progressing muscle fatigue and multiple liver lesions on ultrasonography. Hypertension, hyperglycemia, hypokalemia and metabolic alkalosis prompted consideration of underlying hypercortisolism. Further work-up demonstrated an acute ectopic ACTH syndrome as paraneoplastic manifestation of a small cell lung carcinoma. The woman deteriorated rapidly and finally died from intracranial tumor spread and septic complications. This case stresses the diagnostic and therapeutic difficulties of acute ectopic ACTH syndrome in the setting of SCLC.
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PMID:Making sense of muscle fatigue and liver lesions. 1762 Feb 25

A 54-year old man was admitted with general fatigue, muscle weakness and dyspnea on effort. Medical examinations led to a diagnosis of small cell lung carcinoma (SCLC) with Lambert-Eaton myasthenic syndrome (LEMS). Marked improvement of SCLC and symptoms of LEMS were recognized twice during chemoradiotherapy. On his third admission, he showed muscle weakness, dysaethesia, and neurodysfunction of the bladder and rectum. We initially considered these symptoms to be due to spinal metastasis because MRI findings showed multiple spinal metastases. However, electoromyogram and nerve conduction study demonstrated that his muscle weakness resulted from LEMS though dysethesia and neurodysfunction of bladder and rectum were caused by spinal metastasis. We believe that it is important to perform electomyogram and nerve conduction studies, not only radiographic findings, to detect the "hidden" symptoms of LEMS.
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PMID:[A case of small cell lung carcinoma complicated by Lambert-Eaton myasthenic syndrome]. 1840 71

The Lambert-Eaton myasthenic syndrome (LEMS) is a disease of neuromuscular transmission in which autoantibodies against the P/Q-type voltage-gated calcium channel (VGCC) at the presynaptic nerve terminal play a major role in decreasing quantal release of acetylcholine (ACh), resulting in skeletal muscle weakness and autonomic symptoms. It is associated with cancer, particularly small-cell lung carcinoma (SCLC), in 50-60% of LEMS patients; the nerve terminal and carcinoma cells apparently share a common antigen (VGCC), suggesting an immunological cross-reactivity that may lead to the neurological abnormality. Non-tumor LEMS has a strong association with HLA-DR3-B8. In approximately 15% of LEMS patients, no anti-P/Q-type VGCC antibodies are found, suggesting recognition of other targets(s). The VGCC-associated protein synaptotagmin could be one candidate, because it acts as an exocytotic calcium receptor, is implicated in fast ACh release; its N-terminus is exposed extracellularly during exocytosis and it is expressed in SCLC. Antibodies against synaptotagmin-1 were detected in both anti-VGCC-positive and -negative LEMS patients (20%), and it can be immunogenic, allowing induction of an animal model of LEMS. Another candidate target is the M1-type presynaptic muscarinic ACh receptor (M1 mAChR), also expressed extracellularly on motor nerve terminals; it modulates cholinergic transmission, linking to P/Q-type VGCC. In our series of 25 LEMS patients with and without SCLC, anti-M1 mAChR antibodies were prevalent in both anti-VGCC-positive and -negative LEMS patients. Autonomic symptoms seemed more frequent in the latter; serum from one of them passively transferred LEMS-type electrophysiological defects to mice. As a compensatory mechanism, researchers in Oxford suggested a shift in the dependence of ACh release from the P/Q-type to other types of VGCC. We have also focused on G protein-coupled mAChRs and neurotrophins, which may affect both P/Q-type VGCC and clathrin-independent "kiss-and-run" synaptic vesicle recycling (fast-mode of endocytosis) via protein kinase C activation. We hypothesize that these signaling cascades help to compensate for the immune-mediated defects in calcium entry in LEMS, compensation that may frequently be restricted by the coincident anti-M1 mAChR antibodies in this disease.
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PMID:Lambert-Eaton myasthenic syndrome: search for alternative autoimmune targets and possible compensatory mechanisms based on presynaptic calcium homeostasis. 1865 48

Hyponatremia is the most common electrolyte derangement occurring in hospitalized patients. The study presents a case of severe hyponatremia (range 93.2 mEq/l) in 67-year-old women presented weakness and neurological abnormalities. Laboratory tests showed additional electrolyte abnormalities such as hypokaliemia, hypomphosphatemia and hypomagnesemia. The cause of syndrome of inadequate antidiuretic hormone secretion (SIADH) in reported patient was lung carcinoma.
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PMID:[Severe hyponatremia in patient with tumor of mediastinum]. 1894 36

Spinal leptomeningeal metastasis occurs rarely in solid tumors, and the prognosis is extremely poor. Adenocarcinomas and small-cell carcinomas are the most common histological type detected among lung tumors. A 58-year-old man with a history of squamous-cell lung carcinoma with mediastinal invasion and brain metastasis was examined because of his low back pain and weakness in both lower limbs. Spinal MRI revealed subpial enhancement in the spinal cord; and innumerable nodules with thickening of the cauda equina fibres. To our knowledge, this is the second reported case of squamous cell lung cancer with spinal leptomeningeal metastasis.
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PMID:Spinal leptomeningeal metastasis in a patient with squamous cell lung cancer. 1902 1

Lambert-Eaton myasthenic syndrome is a paraneoplastic syndrome that may reveal a primitive tumor. Neuroblastoma in children and small cell lung carcinoma in adults are the leading tumors revealed or expressed by paraneoplastic phenomena. The clinical neurologic manifestations of Lambert-Eaton myasthenic syndrome are muscular weakness, sleepiness, absence of reflexes, and dysautonomia. Neurologic manifestations are explained by the induction of an autoimmune response because of the presence of antigens that are expressed by the tumor. Neurologic paraneoplastic disorders may also be the result of toxicity of drugs, coagulopathy, infection, or metabolic diseases. We describe the case of a 13-month-old child with unusual neurologic symptoms because of the presence of an abdominal neuroblastoma.
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PMID:Lambert-Eaton myasthenic syndrome revealing an abdominal neuroblastoma. 1963 90

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

Our understanding of transmission at the neuromuscular junction has increased greatly in recent years. We now recognise a wide variety of autoimmune and genetic diseases that affect this specialised synapse, causing muscle weakness and fatigue. These disorders greatly affect quality of life and rarely can be fatal. Myasthenia gravis is the most common disorder and is most commonly caused by autoantibodies targeting postsynaptic acetylcholine receptors. Antibodies to muscle-specific kinase (MuSK) are detected in a variable proportion of the remainder. Treatment is symptomatic and immunomodulatory. Lambert-Eaton myasthenic syndrome is caused by antibodies to presynaptic calcium channels, and approximately 50% of cases are paraneoplastic, most often related to small cell carcinoma of the lung. Botulism is an acquired disorder caused by neurotoxins produced by Clostridium botulinum, impairing acetylcholine release into the synaptic cleft. In addition, several rare congenital myasthenic syndromes have been identified, caused by inherited defects in presynaptic, synaptic basal lamina and postsynaptic proteins necessary for neuromuscular transmission. This review focuses on recent advances in the diagnosis and treatment of these disorders.
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PMID:Myasthenia and related disorders of the neuromuscular junction. 2054 29

Pulmonary carcinoma was diagnosed in an 18+-year-old captive female great horned owl (Bubo virginianus). The owl presented with a history of progressive weakness and sudden onset of frank blood in the droppings. On physical examination, the owl had multiple white to yellow plaques in the oral cavity, decreased air sac sounds on the right side, dyspnea (during manual restraint), and reduced pectoral musculature. Whole-body radiographs revealed obliteration of the right-sided air sacs, a soft tissue plaque/density in the left caudal thoracic air sac, soft tissue opacity over the coelomic organs, and increased medullary opacity in the distal right humerus. The owl died during anesthetic recovery, and the body was submitted for necropsy. Although the clinical signs, physical examination results, radiographic signs, and gross pathology supported a diagnosis of mycotic infection, such as aspergillosis, histopathology confirmed pulmonary carcinoma with metastases to the air sacs and humerus.
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PMID:Pulmonary carcinoma in a great horned owl (Bubo virginianus). 2072 57

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.
Lung Cancer 2011 Mar
PMID:Acute onset of brain atrophy and dementia in a patient with small cell lung cancer: a case report. 2121 22


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