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

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
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PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

In two men presenting with muscle weakness and disturbances of equilibrium neurophysiological examination by repeated stimulations revealed responses suggestive of Lambert-Eaton syndrome. In the first month of the disease very high levels of anti-Hu antibody were found in the serum and CSF, betraying a malignant lesion. This was confirmed by autopsy 4 months later in one patient and by bronchial biopsy 16 months later in the other patient. Both had small-cell lung carcinoma associated with paraneoplastic encephalomyelitis.
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PMID:[Paraneoplastic encephalomyelitis and Lambert-Eaton syndrome]. 133 34

The clinical and electrophysiological data of 18 consecutive adult patients with paraneoplastic Lambert-Eaton myasthenic syndrome (LMES) have been reviewed. The cancer associated with LEMS was small-cell lung carcinoma (SCLC) in 15 cases and epidermoid lung carcinoma in 3 cases. The main clinical neurological features were proximal lower limb weakness (100%), depressed tendon reflexes (94%) and dryness of the mouth (66%). The results of repetitive nerve stimulation (RNS) were not statistically different in the paraneoplastic LEMS group and in a group of 6 LMS patients in whom no carcinoma had been detected. Low-amplitude compound muscle action potential (CMAP) was present in all cases; decremental response at low stimulation rates was present in 13/15 cases. An abnormal incremental response at high stimulation rates was observed in all cases. A close correlation between CMAP amplitude and clinical condition was found in 4 cases during the long-term follow-up. In one patient the RNS electrical pattern could be misinterpreted as myasthenia gravis in only one muscle tested. We underline the usefulness of a 50 Hz stimulation during 4 seconds to establish the diagnosis unequivocally, and that of post-exercise facilitation in routine detection among an SCLC population. Our results suggest that CAMP amplitude and RNS test could be used to evaluate the short-term improvement of LMS under treatment and, in some cases, for the long-term follow-up. The infraclinical axonal neuropathy detected in 8 patients probably was another associated autoimmune paraneoplastic complication.
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PMID:[Lambert-Eaton syndrome: clinical and electrophysiological study of 18 cases associated with lung cancer]. 144 71

Malignant tumors of the pituitary gland may mimic pituitary adenomas both in clinical presentation and in imaging, and often present with neurologic findings including visual field loss and extraocular movement palsies. We describe a 58-year-old woman without known malignancy who presented with extraocular movement weakness, loss of facial sensation, and a sellar plasmacytoma; a 49-year-old woman with oculomotor palsy, no known malignancy, and rapidly failing vision who had metastatic lung carcinoma; and a 70-year-old woman with metastatic breast carcinoma who presented with rapidly failing vision and a metastasis to the anterior lobe of the pituitary. These cases illustrate several important features of malignancy in the pituitary fossa: that it can mimic a "nonfunctioning" pituitary adenoma in clinical presentation and imaging; that rapidly progressive visual loss, extraocular movement palsies, or facial sensory loss may help to distinguish it from a benign adenoma; and that when the pathologist evaluates an alleged "nonsecretory" or "nonfunctional" adenoma, metastases should be included in the differential diagnosis.
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PMID:Malignant tumors in the pituitary gland. 158 Aug 20

Eaton-Lambert myasthenic syndrome is a rare disorder of neuromuscular transmission. We are unaware of previous New Zealand reports and present two patients. Characteristic abnormalities in compound muscle action potential amplitude following repetitive nerve stimulation and on single fibre electromyography were present. Both patients also showed mild patchy abnormalities in peripheral nerve conduction. The clinical picture resembled Guillain-Barre syndrome in one patient who developed severe generalised weakness and respiratory failure. In both patients the neurological presentation lead to the recognition of a previously asymptomatic small cell lung carcinoma.
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PMID:Eaton-Lambert myasthenic syndrome: two cases with typical and atypical features. 216 Jun 29

A 63-year-old man with Eaton-Lambert syndrome manifested by marked respiratory failure was reported. He began to notice blepharoptosis and diplopia in September, 1987, followed by weakness and easy fatigability in bulbar, neck and limb muscles in association with impotence by February, 1988. On admission in August, 1988, Gowers' sign, decreased tendon reflexes and muscle weakness improved by the injection of edrophonium were found. Anti-acetylcholine receptor antibody was negative. Single muscle action potential evoked in the thenar muscle was abnormally low in amplitude with the stimulation of the median nerve: repetitive nerve stimulation study revealed the waning at the low rates, but the waxing at the high rate (30 Hz), suggesting the diagnosis of Eaton-Lambert syndrome. Early gastric cancer (adenocarcinoma) was diagnosed from needle biopsy specimens in August, 1988, but no other neoplasm including thymoma or lung cancer was found. After subtotal gastric resection in September, 1988, he failed into respiratory failure, requiring artificial ventilation for seven months. Plasmapheresis and drugs such as anticholinesterase, guanidine hydrochloride, and corticosteroid were ineffective for the recovery from weakness in respiratory muscle. Lung cancer was suspected, based on a chest X-ray in March, 1989, and one month later he died of pneumonia. At autopsy, small cell carcinoma of the lung was observed, but there was neither recurrence nor metastasis of the gastric cancer. Emphasis was placed on the respiratory failure in Eaton-Lambert syndrome which has rarely been reported.
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PMID:[Eaton-Lambert syndrome manifested by respiratory failure associated with small cell carcinoma of the lung]. 217 52

A 57-year-old man presented with muscle stiffness and weakness accompanied by small cell carcinoma of the lung. The electromyogram showed the characteristic pattern for a Lambert-Eaton myasthenic syndrome (LEMS). The tumor of the lung was reduced in size by one-half with chemotherapy, but the muscle weakness improved only a little.
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PMID:A case of Lambert-Eaton myasthenic syndrome accompanied by a small cell carcinoma of the lung. 217 2

There has been increased recognition of adenosquamous lung carcinoma since the 1982 modification of World Health Organization (WHO) histologic criteria. However, data on clinical features of this histologic subtype were nonexistent. Medical records of 127 patients with adenosquamous lung carcinoma were reviewed to determine the clinical features, namely, age, race, sex, smoking history, asbestos exposure, symptoms present at the time of diagnosis, stage, treatments, and survival. The age distribution was: less than 40 yr, 3%; 40 to 49, 17%; 50 to 59, 28%; 60 to 69, 32%; 70 to 79, 18%; greater than or equal to 80, 2%. Men constituted 72%, and 90% were smokers. Four smokers had documented asbestos exposure. The symptoms in order of decreasing frequency were cough, weight loss, expectoration, anorexia, chest pain, dyspnea, weakness, hemoptysis, pneumonia, fever, nausea, vomiting, dizziness, and chills. Stage could be ascertained in 120 (95%) patients. Local stage constituted 10%, regional constituted 30%, and distant constituted 60%. Local stage had the best survival, with a projected 5-yr survival of 62%. Median survivals in regional and distant stages were 8 and 4 months, respectively. Symptoms of adenosquamous lung carcinoma were similar to other histologies. Most patients present in regional or distant stages. Local-stage patients had a good long-term survival after surgical excision of the tumor.
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PMID:Clinical features of adenosquamous lung carcinoma in 127 patients. 236 69

A seventy-year-old woman was admitted to the hospital because of paresthesias and progressive weakness of the extremities. Ten months previously, tightness in the thighs and numbness in the fingers developed, with subsequent tingling sensations of the hands and feet. Three months before entry, she had difficulty in walking because of severe paresthesias in the extremities. She was found to have an abnormal mass in a X-ray film of the chest, and transferred to our hospital. Neurological examination showed generalized hyporeflexia, marked loss of deep and discriminative sensations in the distal portion of the limbs, positive Romberg sign and severely ataxic gait. Cerebellar sign was negative. Cytologic examination of a transbronchial lung biopsy disclosed small cell carcinoma of the lung. A sural nerve biopsy showed severe loss of myelinated fibers accompanied by axonal degeneration of residual fibers. Immunohistochemically antineuronal antibody was found in the serum but not in the CSF, which reacted to nuclei and cytoplasm of the dorsal root ganglion neurons as well as Purkinje cells. Titers of this autoantibody in the serum were markedly reduced after chemotherapy and irradiation. Western blot analysis demonstrated that autoantibody in the serum recognized neuronal antigen with single band at 38 kd. Pathogenesis of carcinomatous neuropathy is still unexplained, but the findings here presented have given rise to the speculation that antineuronal antibody may be a contributory factor in carcinomatous neuropathy.
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PMID:[Antineuronal antibody in carcinomatous neuropathy]. 256 Apr 16

Respiratory muscle function was assessed in six patients with the Lambert-Eaton myasthenic syndrome. Five had histologically proved small cell carcinoma of the lung; the sixth later developed metastases from an unknown primary site. Two patients had ventilatory failure, one without respiratory symptoms; another, who had emphysema, had dyspnoea and orthopnoea. The remaining three patients had no respiratory symptoms. Four patients had limb muscle weakness as judged by the maximal voluntary contraction of the quadriceps muscle (range for all subjects 32-100% predicted). Transdiaphragmatic pressure (Pdi) was measured during a maximal unoccluded sniff (Pdi: sniff), a maximal sustained inspiratory effort against a closed airway (Pdi: Pimax), and phrenic nerve stimulation (Pdi: twitch). Mild to moderate diaphragmatic weakness was present in all six patients in proportion to the degree of leg weakness (Pdi: sniff 30-64% predicted; r = 0.6; Pdi:Pimax 6-69% predicted, r = 0.8); this was associated with very low or absent Pdi:twitch during phrenic nerve stimulation. Four patients had weakness of the expiratory muscles. Improvement in muscle strength was documented in two patients after tumour chemotherapy and specific treatment with 3,4-diaminopyridine and prednisolone; one patient was still alive five years from first diagnosis. It is concluded that the respiratory muscles may be implicated in this condition more often than has previously been recognised. As the lack of mobility may cause respiratory symptoms to be minimised, the presence of respiratory muscle weakness may remain undiagnosed unless formal measurement of respiratory muscle function is made.
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PMID:Respiratory muscle weakness in the Lambert-Eaton myasthenic syndrome. 259 31


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