Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The afferent loop syndromes result from obstruction to the afferent jejunal loop. Acute ALS results from complete obstruction, usually occurs early after surgery and runs a devastatingly lethal course unless promptly treated by reoperation. In chronic ALS the obstruction is intermittent and produces a clinical syndrome from which a diagnostic histroy can usually be obtained. Although the exact incidence is unknown, it is certainly not rare, especially in antecolic Billroth II gastrectomies. Treatment consists of doing away with the afferent loop. In gastroenterostomy alone takedown of the anastomosis with a Weinberg pyloroplasty is the treatment of choice. The safest and simplest treatment for patients whose original operation was Billroth II gastrectomy is conversion to a Roux-en-Y procedure. In all cases vagotomy should be added unless previously performed. No medical treatment is available and patients with no other contraindication should have revisional surgery if symptoms are clinically significant. Both acute and chronic afferent loop syndromes should be completely prevented by appropriate choice of the initial operative procedure. The vagotomized stomach should be drained by pyloroplasty, not gastrojejunostomy. Vagotomy and antrectomy should be reconstructed with a Billroth I gastroduodenostomy. The Braun enteroanastomosis should be utilized after subtotal gastrectomy for carcinoma. The wider application of parietal cell vagotomy for duodenal ulcer deserves close observation and further consideration.
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PMID:The afferent loop syndrome. 95 82

Neuropsychiatric and psychosomatic disorders occurring the exocrine pancreatic diseases are not rare, nevertheless didn't it seem to be very interesting in research and there exists no summarizing work of this disorders. Therefore we tried to give a comprehensive representation of those neuropsychiatric problems which are connected with the function of this organ. At first we give a description of psychopathology and pathogenesis of the functional pancreatic psychosis. The problematic of the reciprocal relationship of nervous system and pancreatitis, alcoholism and pancreatitis are demonstrated as well as the psychic disorders occurring the pancreas insufficiency, cystes of pancreas and congenital pancreatic diseases. Psychosomatic and mental disorders of pancreas carcinoma and mucoviscidosis are shown in detail. The question of the interrelation between pancreatic function and amyotrophic lateral sclerosis or parathyreotic diseases are discussed just as themes of neuropsychiatric pharmacotherapie and pancreatic function and mental disorders in pancreatic treatment.
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PMID:[Neuropsychiatric disorders of the diseases of exocrine pancreas (author's transl)]. 105 12

A 75-year-old woman had breast carcinoma, an IgA paraprotein and autopsy-proven amyotrophic lateral sclerosis. Autopsy tissues showed immune-reactive IgA within surviving motor neurons and deposits of IgA and C3 within renal glomeruli. By indirect immunofluorescence, the patient's serum contained high-titer IgA that bound to axons and to the perikarya of nerve cells in central and peripheral nervous system. The IgA paraprotein reacted with the 200 kDa, high molecular weight subunit of neurofilament protein (NFH) in Western blots of purified neurofilaments. It also reacted with dephosphorylated NFH and with NFH expressed as a fusion protein in E. coli, suggesting that the autoantibody recognized a peptide epitope. The IgA crossreacted with a surface antigen of cultured human neuroblastoma cells but mouse monoclonal antibodies to NFH did not. Absorption of the patient's serum with neurofilaments eliminated IgA binding to neuroblastoma cells, indicating that the same antibodies bound to both determinants. The IgA paraprotein seems to be an autoantibody with specificity for neurofilament protein and a cell surface component of neuronal cells; the antibody may have been important in the pathogenesis of neuronal degeneration.
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PMID:A monoclonal IgA in a patient with amyotrophic lateral sclerosis reacts with neurofilaments and surface antigen on neuroblastoma cells. 236 86

Serum autoantibodies found by radioimmunoassay in 27 of 52 patients with the Lambert-Eaton myasthenic syndrome (LES) bound specifically to a soluble omega-conotoxin binding component of a voltage-gated Ca2+ channel (VGCC) complex extracted from small cell lung carcinoma (SCC). These antibodies were not found in 43 control patients with other neurologic diseases, including myasthenia gravis, peripheral neuropathies, and amyotrophic lateral sclerosis, or in 9 patients with endocrine autoimmunity, but they were found in 2 of 21 control patients with SCC without a history of LES, 1 of whom had severe autonomic neuropathy. Seropositivity was more frequent in patients with LES who had evidence of a primary lung cancer (76%) than in those with other neoplasms or without evidence of cancer (30%). Antigens extracted from SCC tumor lines derived from patients with and without LES and from a human neuroblastoma line yielded results that were highly correlated. A control extract of colonic carcinoma (derived from a patient with LES) yielded negative results. The data implicate a tumor-associated VGCC as the autoimmunizing stimulus in a subset of patients with LES and provide the first direct evidence that the VGCC complex in SCC is a target for some LES antibodies. The serologic test described should be a useful aid in diagnosing LES.
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PMID:Autoantibodies bind solubilized calcium channel-omega-conotoxin complexes from small cell lung carcinoma: a diagnostic aid for Lambert-Eaton myasthenic syndrome. 255 95

Non metastatic neurological concomitants of tumors are well known. They include an amyotrophic lateral sclerosis (ALS)-like syndrome in association with various tumors. The association with prostatic carcinoma is very rare. The case reported here seems to confirm the outcome of epidemiological research: the association is fortuitous.
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PMID:Carcinoma of the prostate and motor neuron disease. 399 56

Post-traumatic stress-induced disorders are still the focus of interest and most recently discussions are under way whether stress-induced cortisol excess leads to atrophy of the brain. In investigation on carcinogenesis the first reports were published on the use of antisense-oligonucleotides during inhibition of the development of tumours by a humoral mechanism and on the gene-based neuroendocrine differentiation of the lungs, perhaps associated with the basis for the development of small cell carcinoma. The oncogenic action of superoxides has also humoral mediators. Interest in nitrogen oxide is focused on two areas: inflammations and hypertension. Intraluminal NO concentrations increase in asthma 2-10x, in cystitis 30-100x, in Crohn's disease 20-200x. Humoral mechanisms in asthma offer new drugs--inhibitors of the development or action of leucotrienes. The basal NO production is reduced in "essential" hypertension but it is not known whether it is the cause or consequence. IGF-I increases the formation of NO in the vascular wall and thus perhaps reduces vascular contractility. As far as IGF is concerned, it is obvious that if recombinant preparations will be available, they will be tested in amyotrophic lateral sclerosis, myotonic dystrophy, multiple sclerosis, catabolic conditions, osteoporosis, in renal failure and to promote wound healing. STH may also prove useful in cardiac failure, in particular in cardiac cachexia. That TRH has receptors in the gut is not surprising, it acts, however, even there via TSH. Thrombopoietin is being tested in clinical trials. Neocytolysis is a new phenomenon: when erythropoietin secretion declines new erythrocytes disappear and only old ones remain in the blood stream. Alpha-adducin is a renal tubular protein, regulating the sodium balance.
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PMID:[Endocrinology 1996-1997]. 965 Mar 40

Prostate-specific membrane antigen (PSMA) is a 100 kDa type II transmembrane protein with folate hydrolase and NAALAdase activity. PSMA is highly expressed in prostate cancer and the vasculature of most solid tumors, and is currently the target of a number of diagnostic and therapeutic strategies. PSMA is also expressed in the brain, and is involved in conversion of the major neurotransmitter NAAG (N-acetyl-aspartyl glutamate) to NAA and free glutamate, the levels of which are disrupted in several neurological disorders including multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease and schizophrenia. To facilitate analysis of the role of PSMA in carcinoma we have determined the structural organization of the gene. The gene consists of 19 exons spanning approximately 60 kb of genomic DNA. A 1244 nt portion of the 5' region of the PSMA gene was able to drive the firefly luciferase reporter gene in prostate but not breast-derived cell lines. We have mapped the gene encoding PSMA to 11p11-p12, however a gene homologous, but not identical, to PSMA exists on chromosome 11q14. Analysis of sequence differences between non-coding regions of the two genes suggests duplication and divergence occurred 22 million years ago.
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PMID:Mapping, genomic organization and promoter analysis of the human prostate-specific membrane antigen gene. 983 72

Autopsy of patients with sporadic amyotrophic lateral sclerosis (ALS) rarely provides clues to a genetic etiology. We studied a 66-year-old woman who developed progressive weakness, fasciculations and upper motor neuron signs 1 year after mastectomy and chemotherapy for a breast carcinoma. She died 14 months after the onset of neurological symptoms. Autopsy showed characteristic features of ALS but also with posterior column degeneration and conglomerate hyaline inclusions. These features suggested a mutation of SOD1 mutation although no other family members were affected. DNA analysis of autopsy tissue indicated an I113T SOD1 mutation.
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PMID:Sporadic amyotrophic lateral sclerosis and breast cancer: Hyaline conglomerate inclusions lead to identification of SOD1 mutation. 1642 67

We present a 72-year-old woman with progressive dysphagia, dysarthria and tongue palsy who was initially diagnosed with bulbar-onset amyotrophic lateral sclerosis (ALS). However, the absence of atrophy or fasciculations in the tongue, as in other voluntary muscles, and the lack of reproducible neurophysiological evidence of denervation, prompted a revision of the diagnostic work-up, which eventually led to the discovery of a carcinoma of the tongue. This case report describes a relatively rare type of oropharyngeal carcinoma that, in its early stage, resembled a bulbar-onset ALS. This differential diagnosis is unusual, and it was fostered by the persistent lack of atrophy of the tongue and the absence of spreading of signs and symptoms of motor neuron degeneration.
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PMID:Carcinoma of the tongue and bulbar-onset amyotrophic lateral sclerosis: unusual differential diagnosis. 1848 13

Bulbar weakness, including dysarthria, dysphagia, or progressive respiratory weakness, occurs as the presenting feature in approximately 25% of patients with amyotrophic lateral sclerosis (ALS). Misdiagnosis of ALS in patients with progressive bulbar symptoms is uncommon. This report describes a 73-year-old man who had a 10-month history of progressive hoarseness, dysphagia, and respiratory failure. The initial diagnosis was bulbar ALS. Computed tomography of his neck identified a postcricoid squamous cell carcinoma, which was causing bilateral vocal cord paralysis. To the author's knowledge, postcricoid carcinoma has not been previously described as mimicking ALS but should be considered in the differential diagnosis of bulbar ALS.
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PMID:Postcricoid pharyngeal carcinoma mimicking bulbar amyotrophic lateral sclerosis. 1907 5


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