Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BLAG--benign lymphocytic angiitis and granulomatosis is a granulomatosis disease which histologically presents a dense infiltrate of lympnoid cells that disturbes the normal alveolar architecture. Faint granuloma formation occur within the lympnoid infiltrate. A 32 years female patient was admitted for dry cough, exertional dispnea, low fever during last 11 month. Histological diagnosis was BLAG. The treatment was a combination of cyclophosphamide and prednisone. Follow up information after 9 month of treatment show a generally favorable evolution (clinical and radiological).
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PMID:[Pulmonary benign lymphocytic angiitis and granulomatosis--a benign lymphoproliferative condition]. 1269 70

A 5-year-old cross-bred dog was examined with an 8-week history of coughing and a 3-week history of collapsing during exercise. Thoracic radiography revealed moderate right-sided cardiomegaly and a partially mineralized area over the dorsocranial heart base. Echocardiography demonstrated moderate eccentric and concentric right ventricular hypertrophy and a hypoechoic mass in the main pulmonary artery. The owners declined further investigations and the dog died at home 4 days later. Postmortem revealed a primary pulmonary artery chondrosarcoma. This is the first case report of a pulmonary artery chondrosarcoma in a dog and presents another differential diagnosis of syncope in the dog.
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PMID:Primary chondrosarcoma in the pulmonary artery of a dog. 1281 75

The aim of this study was to explore and compare initial treatment effects of captopril (Tensiomin) and sodium dimercaptosulphonate (DMPS) on a relatively large series of Wilson's disease inpatients. Two important markers of anticopper efficacy: serum sulphydryl and 24 h urinary copper levels in the patients were evaluated before and after treatment. The patients were randomly subdivided into 4 groups to allow statistical analysis (ANOVA) of the values recorded. The protocol was an open-label study of all the patients treated for 8 weeks (i.e., all the patients except those in the no-drug group), and a further six-month follow-up (post hospitalization) of the 14 patients administered captopril. Several copper-related variables were studied to evaluate the effect of the drugs on copper, and several biochemical and clinical variables were studied to evaluate potential toxic effects. Captopril was found to have a significant anticopper effect and did not markedly raise serum sulphydryl levels within this limited patient sample; the anticopper efficacy of captopril was, however, found to be markedly lower than that of DMPS; DMPS was found to raise the patients' serum sulphydryl and urinary copper levels. Evaluation of data from individual patients revealed evidence of a toxic side effect in only 1 patient, treated with DMPS, who exhibited transiently raised serum alanine aminotransferases, while no serious adverse events, upstanding syncope, irritating cough and leukopenia induced by captopril were noted. The results obtained in this four-group sample suggest that captopril might be a mild anticopper agent for Wilson's disease, possibly relieving the hepatic portal hypertension, but that DMPS has a greater field of anticopper efficiency than captopril. The authors also discuss recent experience of the overall treatment in China.
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PMID:Anticopper efficacy of captopril and sodium dimercaptosulphonate in patients with Wilson's disease. 1470 96

Bosentan is a nonpeptide, specific, competitive, dual antagonist at both endothelin receptor subtypes (ET(A) and ET(B)). Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Improvement in exercise capacity from baseline was significantly greater with bosentan than with placebo in two phase III trials in patients with WHO functional class III or IV pulmonary arterial hypertension (primary or associated with connective tissue disease) despite treatment with vasodilators, diuretics, anticoagulants, cardiac glycosides, or supplemental oxygen. The beneficial effects of bosentan on exercise capacity were maintained for at least 20 weeks. Compared with placebo, bosentan led to a significantly greater improvement from pretreatment values in secondary efficacy endpoints such as the Borg dyspnea index, WHO functional class, and cardiopulmonary hemodynamic parameters (cardiac index, pulmonary vascular resistance, pulmonary artery pressure, pulmonary capillary wedge pressure, mean right atrial pressure). Bosentan significantly reduced the incidence, and delayed the onset, of clinical worsening of pulmonary arterial hypertension compared with placebo. In published clinical trials, adverse events that occurred with similar or greater frequency with bosentan 125 mg twice daily than with placebo included headache, syncope, flushing and abnormal hepatic function. Those that occurred less frequently with bosentan 125 mg twice daily than with placebo included dizziness, worsening of symptoms of pulmonary arterial hypertension, cough and dyspnea.
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PMID:Bosentan. 1472 63

We report serial spinal MRI T2 findings in a patient with acute autonomic and sensory neuropathy (AASN). A 20-year-old woman was admitted to our hospital with progressive sensory disturbance in her extremities and orthostatic syncope after her symptoms of upper respiratory infection. Neurological examination demonstrated reduced tendon reflexes, hypalgesia, paresthesia, reduced position sensation in distal dominant extremities (predominant in lower legs) and wide variety of autonomic dysfunction (severe orthostatic hypotension, anhidrosis, urinary disturbance, coughing attack, constipation and appetite loss). She was diagnosed as having AASN. Although high dose intravenous immunoglobulin therapy successfully prevented the symptom progression, her sensory disturbance and autonomic dysfunction were prolonged and showed only slow improvement. Spinal MRI on acute phase was normal. On chronic phase (11 month after the onset), spinal MRI T2 weighted images demonstrated high intensity lesion in the posterior column successive from upper cervical to lower thoracic spinal cord. Those abnormal findings were attenuated in concordance with her symptom improvement and finally disappeared when she became to walk stably without assist.
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PMID:[Reversible MRI findings of posterior column of the spinal cord in a patient with acute autonomic and sensory neuropathy]. 1519 58

Neurally mediated reflex syncope (sometimes referred to as neurocardiogenic syncope), encompasses a group of disorders of which the best known and most frequently occurring forms are the vasovagal (or common) faint, and carotid sinus syndrome. Postmicturition syncope, defecation syncope, cough syncope, and other situational reflex faints are also included among these conditions. With the exception of carotid sinus syndrome in which cardiac pacing is effective, treatment of most neurally mediated reflex faints is shifting from reliance on various drugs to greater emphasis on education and nonpharmacologic therapy. Initial management should include counseling of patients regarding recognition of early warning symptoms, and avoidance of precipitating factors. Volume expansion with salt tablets or electrolyte-containing beverages and patient education on how to perform isometric arm contractions and/or leg crossing in order to abort impending syncope are also important. Thereafter, tilt-training has demonstrated benefit in several clinical studies. When symptoms remain despite the above-noted interventions, pharmacologic therapy with midodrine or a nonselective b-blocker can be considered. In the case of most neurally mediated reflex faints, permanent cardiac pacing should be reserved only for those older patients with significant bradycardia or asystole at time of syncope when all other interventions have failed.
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PMID:New approaches to the treatment and prevention of neurally mediated reflex (neurocardiogenic) syncope. 1530 96

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

Cough induced syncope belongs to the heterogenous group of situational syncopes. The mechanism of tussive syncope is demonstrated by presenting an illustrative case. A 79 year old male with underlying COPD was evaluated because of repeated cough related syncopal episodes. The nature of fainting was elucidated by haemodynamic monitoring of an induced cough attack. As documented by continuous blood pressure and middle cerebral artery blood flow velocity recordings, fainting was the result of the equalization of arterial and central venous pressures, with concomitant decrease in cerebral blood flow. Analogies and differences between haemodynamic responses induced by cough and Valsalva straining are highlighted. The typical lack of prodromal symptoms in cough syncope are well explained by the rapidly developing cerebral hypoperfusion.
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PMID:[Mechanism of cough syncope]. 1538 60

"Neurally-mediated (reflex) syncope" refers to a reflex response that, when triggered, gives rise to vasodilation and/or bradycardia; however, the contribution of each of these two factors to systemic hypotension and cerebral hypoperfusion may differ considerably. The initial evaluation may lead to a certain diagnosis in the case of classical vasovagal syncope and of situational syncope. Classical vasovagal syncope is diagnosed if precipitating events such as fear, severe pain, emotional distress, instrumentation or prolonged standing, are associated with typical prodromal symptoms. Situational syncope is diagnosed if syncope occurs during or immediately after urination, defecation, cough or swallowing. In the absence of a certain diagnosis, absence of cardiac disease, long history of syncope, syncope after sudden unexpected unpleasant sight, sound or smell, prolonged standing at attention or crowded, warm places, nausea and vomiting, post-prandial and post-exercise state suggest a neurally-mediated cause which needs to be confirmed by specific tests. Among them, the most useful are carotid sinus massage and tilt testing. In general, education and reassurance are the sufficient initial treatment. Additional treatment may be necessary in high-risk or high-frequency settings. Treatment is not necessary in patients who have sustained a single syncope and are not having syncope in a high-risk setting. It is valuable to assess the relative contribution of cardioinhibition and vasodepression before embarking on treatment as there are different therapeutic strategies for the two aspects. Even if evidence of utility of such an assessment exists only for the carotid sinus massage, it is recommended to extend this assessment also by means of tilt testing or implantable loop recorder. Tilt training and isometric leg and arm counterpressure maneuvers are indicated in patients with recurrent vasovagal syncope. Cardiac pacing is indicated in patients with cardioinhibitory or mixed carotid sinus syndrome and in patients with cardioinhibitory vasovagal syncope with a frequency > 5 attacks per year or severe physical injury or accident and age > 40 years. The evidence fails to support the efficacy of any drug.
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PMID:Neurally-mediated syncope. 1587 16

Autosomal dominant hereditary sensory neuropathy (HSN I) is a clinically and genetically heterogeneous group of disorders, and in some families it is due to mutations in the serine palmitoyltransferase (SPTLC1) gene. We have characterized two families with HSN I associated with cough and gastro-oesophageal reflux (GOR). From a large Australian family, 27 individuals and from a smaller family, 11 individuals provided clinical information and blood for genetic analysis. Affected individuals had an adult onset of paroxysmal cough, GOR and distal sensory loss. Cough could be triggered by noxious odours or by pressure in the external auditory canal (Arnold's ear-cough reflex). Other features included throat clearing, hoarse voice, cough syncope and sensorineural hearing loss. Neurophysiological and pathological studies demonstrated a sensory axonal neuropathy. Gastric emptying studies were normal, and autonomic function and sweat tests were either normal or showed distal hypohidrosis. Cough was likely to be due to a combination of denervation hypersensitivity of the upper airways and oesophagus, and prominent GOR. Most affected individuals were shown on 24 h ambulatory oesophageal pH monitoring to have multiple episodes of GOR, closely temporally associated with coughing. Hoarse voice was probably attributable to acid-induced laryngeal damage, and there was no evidence of vocal cord palsy. No other cause for cough was found on most respiratory or otorhinological studies. Linkage to chromosome 3p22-p24 has been found in both families, with no evidence of linkage to loci for known HSN I, autosomal dominant hereditary motor and sensory neuropathy, hereditary GOR or triple A syndrome. These families represent a genetically novel variant of HSN I, with a distinctive cough owing to involvement of the upper aerodigestive tract.
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PMID:Autosomal dominant hereditary sensory neuropathy with chronic cough and gastro-oesophageal reflux: clinical features in two families linked to chromosome 3p22-p24. 1631 Dec 70


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