Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

Lambert-Eaton myasthenic syndrome is a rare autoimmune neuromuscular and autonomic disease that produces fluctuating muscle weakness, hyporeflexia, and autonomic dysfunction, and often is associated with small-cell lung cancer. The pathophysiology is understood quite well; antibodies to voltage-gated calcium channels in motor and autonomic nerve terminals disrupt calcium influx and reduce acetylcholine release. The diagnosis may be suspected clinically, but must be confirmed with electrophysiologic testing. Initial and then periodic screening for malignancy is essential. Tumors other than small-cell lung cancer occasionally are found. Effective tumor treatment may induce remission. Active disease may respond to agents that enhance neuromuscular transmission or to immunosuppression. Combined therapy frequently is needed and control is often marginal despite this. It is expected that availability of 3,4-DAP will improve significantly the response to treatment in most patients.
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PMID:Diagnosis and treatment of Lambert-Eaton myasthenic syndrome. 804 48

A 76-yr-old male patient with carcinomatous neuropathy associated with hepatic cell carcinoma, whose initial symptom was deep sensory disturbance followed by muscle weakness is described. The onset was subacute, followed by slow progression. Sural nerve biopsy, as well as electrophysiological examinations, revealed severe axonal degeneration without any evidence of demyelination. The autopsy findings were similar to findings described in the literature on carcinomatous neuropathy. Although carcinomatous neuropathy is usually associated with lung cancer, this report describes an association with hepatic cell carcinoma. The patient also had motor nerve involvement with positive serum anti-GM1 ganglioside antibody which decreased after immunosuppressant therapy in parallel with recovery of muscle weakness. The anti-GM1 ganglioside antibody may be involved in the pathogenesis of motor disturbance in the present case.
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PMID:Carcinomatous neuropathy associated with hepatic cell carcinoma: an autopsy case report. 840 Aug 64

Intracerebral uptake of methylene diphosphonate (MDP) was unexpectedly found in metastatic work-up of lung cancer. The history of the 52-year-old patient revealed a sudden onset of weakness of right limbs 10 days ago. Technetium-99m diethylenetriamine pentaacetate (Tc-99m DTPA) brain scan and Tc-99m hexamethyl propylene amine oxime (HMPAO) brain single photon emission computed tomography (SPECT) were done, and both showed abnormality in the left temporoparietooccipital region corresponding to the territory of left middle cerebral artery. A repeated bone scan four months later showed complete resolution of the intracerebral Tc-99m MDP uptake. We present this case to emphasize the importance of complementary and enhanced radionuclide images.
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PMID:Tc-99m MDP uptake in cerebral infarction: comparison with Tc-99m DTPA brain scan and Tc-99m HMPAO brain SPECT. 854 73

The Lambert-Eaton myasthenic syndrome (LEMS) is a rare condition in which weakness results from a presynaptic abnormality of acetylcholine release at the neuromuscular junction. It was first described as a paraneoplastic syndrome in patients with lung cancer but we now know about half of the patients with LEMS do not have cancer. The diagnosis is made on the basis of the clinical findings and characteristic electromyographic patterns. Recent evidence indicates that LEMS results from an autoimmune attack directed against the voltage-gated calcium channels on the presynaptic motor nerve terminal. In patients with LEMS who have cancer, effective treatment of the underlying tumor frequently produces marked improvement of weakness as well. Otherwise, treatment involves the use of agents that improve neuromuscular transmission by increasing the release of neurotransmitter, and immunosuppression.
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PMID:Lambert-Eaton myasthenic syndrome: clinical diagnosis, immune-mediated mechanisms, and update on therapies. 896 18

Both experimental and clinical data have shown that coagulation disorders are common in patients with cancer although clinical symptoms occur rarely. A prethrombotic state is probably involved in the mechanism of metastatic spread. Anticoagulant treatment, with either warfarin or heparin, has been shown to have a positive influence in small cell lung cancer. The purpose of this study was to evaluate the prethrombotic state as a possible marker of the outcome of lung cancer. Pretreatment prothrombin time (PT), partial thromboplastin time (PTT), antithrombin III (AT-III), platelet blood count (P), fibrinogen (F) and D-dimer (DD) were prospectively recorded in a series of 286 consecutive patients with a new primary lung cancer. Other recorded variables (32 in all) consisted of a set of anthropometric, clinical, physical, laboratory, radiological and pathological data. All patients were carefully followed up, and their subsequent clinical course recorded. Spearman rank correlation tests between coagulation factors were weakly significant, or more often non-significant. The best correlation index was that between PT and PTT (ra = -0.25). Univariate analyses of survival showed that a prolonged value of PT (P = 0.00167) and higher values of F (P = 0.00143) and DD (P = 0.0005) were associated with a poor prognosis. A few, weak relationships between well-known prognostic variables and coagulation abnormalities were also found. Because of the weakness of this correlation pattern, coagulation factors emerged in all the Cox's regression analyses as important predictors of survival, regardless of the number and type of cofactors used. A prethrombotic state (depicted by a prolongation of PT and increase of DD) is confirmed in this study as an aggravating condition in lung cancer. Studies attempting to reverse possible haemostatic abnormalities with the use of anticoagulants are justified by the present data.
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PMID:Haemostatic abnormalities in lung cancer: prognostic implications. 964 Feb 38

Optimal management of dyspnea in terminal cancer patients requires an understanding of the responsible pathophysiological mechanisms. This prospective study assessed visual analogue scales (VAS) of shortness of breath (SOB) and anxiety, bedside spirometry, maximum inspiratory pressure (MIP), chest radiography, arterial blood gases, hemoglobin, and electrocardiogram, if indicated, in 100 terminally ill cancer patients. Forty-nine percent of the patients had lung cancer. The median VAS scores for SOB and anxiety were 53 mm and 29 mm, respectively. Spirometry was abnormal in 93% of patients, with 5% having obstructive, 41% restrictive, and 47% mixed patterns. The median MIP was 16 cm H2O. Sixty-five percent of the patients had parenchymal or pleural involvement on chest radiograph. Twenty-nine percent had evidence of cardiac ischemia, recent or current myocardial infarction or atrial fibrillation. Patients had a median of five different abnormalities that could have contributed to their shortness of breath. Only anxiety (p = 0.001), a history of smoking (p = 0.02), and pCO2 levels were statistically significantly correlated with SOB VAS scores. The potentially correctable causes of dyspnea included hypoxia (40%), anemia (20%), and bronchospasm (52%). The finding of very low MIPs suggests severe respiratory muscle weakness may contribute significantly to dyspnea in this patient population. Further studies are needed to confirm this finding and characterize the underlying pathophysiology.
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PMID:Dyspnea in the advanced cancer patient. 1058 52

The Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that is often associated with lung cancer which shares a common antigenic protein with the motor nerve terminal. The myasthenic weakness is caused by an antibody-induced reduction in the release of acetylcholine from the nerve terminal. This study was undertaken to determine the target of LEMS antibodies and specify the voltage-gated calcium channel (VGCC) through which calcium influxes following the presynaptic membrane depolarization. Among the 5 types of VGCC, we found that the P/Q-type was highly recognized by LEMS antibodies. Using synthetic peptides or recombinant proteins as antigens for testing LEMS patients' sera or inducing an animal model of LEMS, we specified the S5-S6 linker regions in 3 of 4 domains constituting the alpha1 subunit of P/Q-type VGCC as immunodominant sites. Synaptotagmin, one of the functionally VGCC-associated proteins and a protein functioning as a calcium sensor for exocytosis of synaptic vesicles, was also found to be a pathogenic immunogen of LEMS when the recombinant protein for antibody assay and the synthetic peptide for the induction of animal model were used as antigens. The present study forms a united front against cancer and cancer-related myasthenic syndrome.
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PMID:An autoimmune channelopathy associated with cancer: Lambert-Eaton myasthenic syndrome. 1022 62

The intensity of complains, short survival and great number of patients makes many oncologists to apply chemotherapy in advanced non-small cell lung cancer/NSCLC/. The achieved median duration of life after chemotherapy was 6 to 12 month. From the other hand non small cell lung cancer chemotherapy is a big burden even to healthy persons. It can worsen the quality of life. That was the reason we evaluated the quality of life after chemotherapy in advanced non small cell lung cancer patients. Taking into account, that the evaluation of quality of life, used in most diseases is useless in advanced NSCLC patients, for appreciation the quality of life in these cases the lung cancer symptoms scale/LCSS/was adopted. In 110 non small cell lung cancer patients in stage IIIB and IV, who received combined chemotherapy by Le Chevalier/Vindesine, Cisplatin, Cyclophosphamide, Lomustin/or by Rosell/Mitomycin, Cyclophosphamide, Cisplatin/the quality of life was evaluated. In 20-persons control group all patients received the symptomatic treatment. In observed group of 110 patients, tumor regressions after 4 courses of chemotherapy allowed to resect cancer in 14 cases, to apply radiotherapy in 42 and to continue chemiotherapy in 23 persons. In every person from above mentioned group the quality of life was evaluated on the basis of intensity of cancer symptoms, accordingly to LCSS. The intensity of cancer symptoms was compared before and after treatment. There were compared; the innensity of complains, weakness, appetite, malnutrition, and hematological, neurological, performans state as well as respiratory sufficiency, infections, cardiac disorders and pain. Apart it, the side effects of applied therapy were assessed in 5 degree scale. The level of hemoglobin, the number of leucocytes, thrombocytes, bilirubine and transaminases in peripheral blood, hematurie, proteinurie, bleedings, appetite, nausea, vomitings, diarrhea, mucosal lesions, infections, skin lesions, cardiac lesions, neurological lesions, respiratory disorders, allergy, alopecia. It was established that, chemotherapy in the most patients improved the performance status and minimized cancer symptoms especially, after good response to treatment. After anticancer therapy more frequently severe infections and cardiac disorders, independently to results of treatment were seen. In non-responders, the cancer symptoms were intensified by side effects of antineoplastic-therapy. In this group of patients the severe side effects of therapy more frequently were seen.
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PMID:[The quality of life after chemotherapy in advanced non-small cell lung cancer patients]. 1034 48

Superior sulcus tumor refers to any primary lung cancer presenting with constant pain in the nerve distribution of the eighth cervical, first and second thoracic nerve roots and Horner's syndrome caused by invasion of the stellate ganglion. The pain is steady, severe, and unrelenting, involving the shoulder, the vertebral margin of the scapula and ulnar distribution of the arm to the elbow and finally to the ulnar surface of the forearm, and the small and ring fingers of the hand (Pancoast-Tobias syndrome). Weakness and atrophy of the hand muscles can also occur as the lesions spreads to involve the first and second ribs and vertebrae. Radiologically, there is a small shadow at the extreme apex of the lung with rib and possible vertebral body invasion. Pulmonary symptoms are less frequent because of the peripheral location of the lesions. Since Shaw and Paulson approached superior sulcus tumors in 1961 by using preoperative radiation-therapy (30 to 45 Gy in four weeks including the primary tumor, mediastinum and supraclavicular region) followed by surgical resection, this radiosurgical approach shortly became the standard treatment yielding better disease control and survival than that offered by other treatment modalities. It has now become evident that en bloc resection of the chest wall, involved adjacent structures as well as lobectomy must be considered the standard surgical approach for superior sulcus tumors combined with external radiation (preoperative, postoperative, or both). The goal of the operation is the complete and en bloc resection of the upper lobe in continuity with the invaded ribs, transverse processes, subclavian vessels, T1 nerve root, upper dorsal sympathetic chain and prevertebral muscles.
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PMID:Surgical management of superior sulcus tumors. 1055 56


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