Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of oro-pharyngeal and oesophageal ulcerative disease in a AIDS patient. The patient complained of severe oral pain and dysphagia. Systemic manifestations as fever and fatigue were also present. Repeated microbiological exams were negative and therapy with either antibiotics or antiviral agents or corticosteroids or colchicine was unsuccessful. Thus, we started thalidomide: 200 mg/day X 21 days, followed by 100 mg/day X 25 days. A dramatic reduction of symptoms was observed within 15 days from the onset of treatment. The healing of ulcers was evident already one month after the start of therapy. No relevant side effects were reported. Among those patients with AIDS at low risk of side effects, thalidomide may represent a successful therapeutic presidium for severe ulcerative disease of the gastrointestinal tract.
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PMID:[Not Available]. 1497 87

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63

In three patients, a woman aged 87 years who presented with signs indicating a myocardial infarction, a man aged 31 suffering from postprandial epigastric pain that suddenly worsened, and a woman aged 60 years with longstanding postprandial pain and recent fatigue due to anaemia, a para-oesophageal hernia was diagnosed. Para-oesophageal herniation is an uncommon disorder accounting for approximately 5% of all hernias at the oesophageal hiatus. They are distinguished from the more common sliding hiatal hernia by a relative preservation of the intra-abdominal fixation of the gastro-oesophageal junction. These patients show that the clinical presentation of para-oesophageal rolling hernias is different from that of sliding hernias. Pathological reflux may occur; though symptoms associated with a relative obstruction of the stomach within the hernia sac, such as dysphagia, are more common. Rare non-specific symptoms such as anaemia and loss of weight are also seen. Adequate therapy differs from that of a sliding hernia and should be individualized: surgical correction is indicated in a healthy patient with a symptomatic para-oesophageal hernia, such as in the last patient. However, when the hernia is incidentally diagnosed or when comorbidity is present, such as in the first patient, a wait-and-see policy is recommended. Only in case of a threatening incarceration, such as in the second patient, is an emergency operation indicated.
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PMID:[The para-esophageal hernia: a rare hiatal hernia requiring a specific approach]. 1522 26

We report the case of a 72-year-old lady who presented with fatigue and bruising. Initial investigations were compatible with iron deficiency anaemia and idiopathic thrombocytopenic purpura (ITP). The anaemia and recent heartburn symptoms led to endoscopy, which revealed an extensive oesophageal squamous cell carcinoma. The tumour was inoperable due to local extension and the patient was not deemed fit enough for aggressive chemotherapy. A course of radical local radiotherapy was given. The patient's ITP, which had initially been responsive to high-dose intravenous immunoglobulin, subsequently became refractory to all therapeutic modalities. The patient developed significant dysphagia but therapeutic options were limited due to her severe thrombocytopenia. The patient eventually died from a combination of gastrointestinal and intrapulmonary haemorrhage. This case is of interest for two reasons. First, the development of refractory ITP appeared to mirror the progression of the carcinoma, and to our knowledge this is the first case of ITP associated with oesophageal carcinoma. Second, despite recent endoscopic advances in palliating oesophageal tumours, this case highlights the difficulties that can still occur.
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PMID:Oesophageal carcinoma and refractory idiopathic thrombocytopenic purpura: a challenging combination. 1525 82

Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.
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PMID:Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis. 1568 93

A 72-year-old man presented with a 6-month history of dysphagia, fatigue, 60-lb weight loss, and central nervous system (CNS) deficits. Diffusion-weighted magnetic resonance imaging (MRI) of the brain showed mildly elevated nonrestricted apparent diffusion coefficients in the middle cerebellar peduncles, and magnetic resonance spectroscopy (MRS) showed decreased N-acetylaspartate and creatine with increased choline. Diffusion-weighted MRI and MRS offer noninvasive methods to help evaluate in vivo physiologic changes of CNS involvement in Whipple disease.
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PMID:Proton magnetic resonance spectroscopy and diffusion-weighted imaging of central nervous system whipple disease. 1589 98

We describe a patient with paraneoplastic neurologic syndrome confirmed on postmortem examination. This 42-year-old man was admitted due to general fatigue, emaciation and acute-onset disorientation. Neurological examination revealed disorientation, moderate cognitive impairment, cerebellar ataxia, bilateral limitations and nystagmus in all directions during external ocular movement, swallowing disorder, bilateral Babinski sign, sensory disturbance in the distal parts of all extremities, and Romberg's sign. T-cell lymphoma was diagnosed following biopsy of the cervical lymph node. Neurological condition improved slightly after chemotherapy, but subsequently deteriorated. At about 6 years after the disease onset, brain magnetic resonance imaging (MRI) revealed atrophy of bilateral hippocampi and the upper vermis of the cerebellum. The patient died of pneumonia after a clinical course of about 6 years and 6 months. Pathologically, neuronal loss, reactive gliosis and perivascular lymphocytic infiltration were observed in the hippocampi, cerebellum, and inferior olivary nuclei. Lymphocytes around the vessels were positive for LCA and UCHL-1, but negative for CD8 and L26, and thus were considered to be T cells. No lymphoma cell was observed in the central nervous system or lymphatic organs. Based on the pathological findings, paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration and olivary pseudohypertrophy) associated with T-cell type malignant lymphoma was diagnosed. Only three other cases of paraneoplastic neurologic syndrome associated with T-cell lymphoma have been reported. In those cases, death occurred due to the deterioration of malignant lymphoma, whereas the present patient died about 6 years after the remission of malignant lymphoma. Prognosis may thus depend on the course of the malignant lymphoma. In the present patient, neurological symptoms deteriorated after remission of malignant lymphoma, and no pathological lesion were found in the lymphatic organs. Lesions in the central nervous system in paraneoplastic neurological syndromes may follow a course independent of the original malignant disease.
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PMID:[An autopsied case of paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration, and pseudohypertrophy in the inferior olivary nuclei) associated with T cell lymphoma]. 1618 Jul 7

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29

Self-reports of 32 symptoms and their treatments were obtained from patients of three palliative care programs that provide services to seriously ill HIV patients (>or=95% AIDS) in Alabama (n=47), Baltimore (n=91), and New York City (n=117). On average, patients reported 10.9 (SD=7.6) to 12.7 (SD=6.2) symptoms. Pain, lack of energy, and worrying were reported by a majority of patients at all sites, often with a high level of associated distress. For only four symptoms (pain, nausea, difficulty swallowing, and mouth sores) did half or more of patients at all sites experiencing the symptom also report treatment. Less than a third of patients experiencing 12 symptoms (five of six comprising a psychological subscale) reported treatment. Results show that despite the availability of more efficacious treatments, many HIV/AIDS patients continue to experience significant physical and psychological symptomatology. Many of those experiencing symptoms, however, do not perceive their symptoms as being treated.
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PMID:Patient reports of symptoms and their treatment at three palliative care projects servicing individuals with HIV/AIDS. 1631 Jun 15

A 66-year-old woman felt dysphagia gradually seven years after an operation of breast cancer. We diagnosed her with esophageal metastasis of the breast cancer, and carried out irradiation and outpatient chemotherapy. Because her general condition became worse after the treatment for about four years, we performed an operation of gastric fistula and tracheotomy to manage her nutrition and of an accidental swallowing. Although the patient and her family resisted a discharge from hospital due to the progressive nature of her illness and change in physical surroundings, she was eventually switched to take a homecare medical treatment with the support of a team care approach. The main purposes of the homecare treatment were to manage gastric fistula including the administration of anti-cancer drugs, cervicobrachial pain control and tracheal cannula exchange. Though she was mentally stable and got along well with the family during the home stay, she was hospitalized again two months after the homecare treatment because of aggravated symptoms and the family's fatigue. We respected the value of her quality of life and gave careful considerations to support her during the entire period of re-hospitalization. She gently died two months after re-hospitalization. We considered that this palliative home care could be realized with the palliative team care, nursing intervention visit and family support.
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PMID:[Palliative home care of a breast cancer patient with esophageal metastasis after the operation of gastric fistula and tracheotomy--a case study]. 1642 92


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