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)

Extracapsular parathyroid haemorrhage is a rare but ominous occurrence, which may cause cervico-mediastinal haematoma and a severe calcaemia imbalance. We identified only 23 cases reported in the literature and these were always secondary to adenoma, hyperplasia or cysts, and never to carcinoma. We describe a case of a 56-year-old man who was admitted to our Institute because of the sudden development of an anterior neck swelling, together with dysphagia, dyspnoea and hoarseness. Physical examination revealed a large ecchymosis extending from the anterior neck to the upper chest, while the early symptoms had disappeared. Laboratory studies, ultrasonography and 99mtTC-Sestamibi scintiscan demonstrated the presence of primary parathyroidism due to a right inferior parathyroid neoplasm. At operation, the parathyroid was excised en bloc with the right thyroid lobe because they were joined together by an extensive fibrous reaction. Histological examination showed a well-differentiated parathyroid carcinoma with evidence of recent haemorrhage. To the best of our knowledge this is the first case of extracapsular haemorrhage due to a parathyroid carcinoma. In summary, although parathyroid haemorrhage is a rare condition, it should always be suspected when a painful mass or diffuse swelling suddenly occurs in the anterior neck, with or without ecchymosis, especially when serum calcium and phosphorus are abnormal.
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PMID:[Cervico-mediastinal hematoma secondary to extracapsular hemorrhage of parathyroid carcinoma. Clinical case and review of the literature]. 1287 80

The usual clinical manifestations of a parathyroid adenoma are due, in most of the cases, to hypercalcemia. The development of a spontaneous cervical or cervicomediastinal haematoma is a rare form of presentation. In case of a spontaneous cervical haematoma associated with dysphagia: measurement of serum calcium, phosphate and parathyroid hormone allows the diagnosis of haematoma due to extracapsular haemorrhage from a parathyroid adenoma. We report herein 2 cases.
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PMID:[Spontaneous cervical haematoma due to extracapsular haemorrhage of a parathyroid adenoma: a report of 2 cases]. 1455 11

Sixty patients (age 73 +/- 14 years; 22 women, 38 men) with dysphagia (67% neurological diseases, 33% tumors) were followed up for 1 year after placement of a percutaneous endoscopic gastrostomy (PEG). Before PEG placement and at six appointments thereafter, the patients' nutritional status was measured using bioelectric impedance analysis (BIA) and hematological nutritional parameters. A validated questionnaire was used to assess quality of life (the Gastrointestinal Quality of Life Index, GIQLI). The overall mortality rate was 65%, and mortality during the hospitalization period was 22%. Depending on the duration of the dysphagia, marked nutritional deficits were observed at the start of the study (deficiencies in albumin in 49% of the patients, calcium in 15%, magnesium in 18%, retinol in 78%, alpha-tocopherol in 16%, folic acid in 16%, vitamin B12 in 8%, vitamin D in 40%, and zinc in 46%). With the exception of vitamin E, all parameters returned to normal during the follow-up period. At the start of the study, BIA indicated nutritional deficiency in 90% of the patients, with no overall improvement being observed during the follow-up period. The GIQLI scores, on average, reached a figure of 61% of an unrestricted quality of life. In conclusion, long-term nutrition via the PEG tube maintained the patients' quality of life. For BIA most patients were malnourished during the follow-up period, but nevertheless PEG feeding was enough to compensate for gross nutritional deficiencies. Not infrequently, the indication for PEG placement is established too late.
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PMID:Nutritional status and quality of life in patients with percutaneous endoscopic gastrostomy (PEG) in practice: prospective one-year follow-up. 1462 55

Achalasia is a condition of unknown etiology. It represents a motor disorder of the esophagus characterized by absent or incomplete relaxation of the lower esophageal sphincter upon swallowing and by non-propulsive swallow-induced contraction waves or amotility of the esophageal body. Dysphagia and regurgitation of ingesta are the most frequent symptoms. Medical treatment, i.e. by calcium-channel blockers and nitric oxide donors, may be tried in patients with mild dysphagia or in elderly patients but rarely yields adequate symptom relief. Mechanical dilatation of the achalasic sphincter may be performed as an initial treatment option. Intrasphincteric injections of botulinum toxin seemed to be a promising alternative, but it has become obvious that, in most cases, repeated applications of the toxin are required to maintain patients symptom-free. Myotomy of the achalasic sphincter with or without fundoplication to prevent gastroesophageal reflux, is employed mainly in patients in whom dilatations have failed, but since the introduction of minimally invasive surgery, myotomy has become the primary treatment at many centers. This article aims to provide an overview of the development of the conservative and surgical treatment of achalasia.
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PMID:[Treatment of achalasia]. 1523 54

Although hypocalcemia is a common postoperative complication of patients who have undergone a total laryngectomy with total thyroidectomy for treatment of laryngeal cancer or cancer of adjacent organs and hypocalcemia can produce the symptom of dysphagia, there has never been a report that hypocalcemia is the cause of dysphagia in these patients. The authors reported two cases who had hypocalcemia after total laryngectomy with total thyroidectomy and presented with sudden and severe dysphagia. However, the symptom of dysphagia was dramatically improved after calcium replacement therapy.
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PMID:Dysphagia after total laryngectomy resulting from hypocalcemia: case report. 1527 57

Xeroderma pigmentosum group A (XPA) is a hereditary disorder characterized by cutaneous symptoms and progressive neurodegeneration. Since XPA patients exhibit peripheral neuropathy, neuronal deafness, rigidity, dysphagia, and laryngeal dystonia, it is indispensable for investigation of the neurodegeneration to analyze brainstem and basal ganglia lesions clinically and pathologically; we have previously shown the role of oxidative stress in the development of basal ganglia lesions. Here we immunohistochemically examined the expression of neurotransmitters, calcium-binding proteins, and neuropeptides in the brainstem, basal ganglia, and thalamus in 5 XPA autopsy cases. In the brainstem, immunoreactivity for tyrosine hydroxylase, tryptophan hydroxylase, and calbindin-D28K was severely reduced throughout the brainstem in all the XPA cases. Nevertheless, the expressions of parvalbumin, substance P, and methionine-enkephalin in the brainstem were comparatively preserved; the exception being reduced immunoreactivity for them in the cochlear and dorsal column nuclei in 3 cases. The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways. The expression of substance P and methionine-enkephalin, which are involved in the efferent pathways in the basal ganglia, in the globus pallidus and substantia nigra was spared. It is speculated that the selective damage to the dopamine system in the basal ganglia and the disturbed monoaminergic expression in the brainstem could be related to clinical abnormalities such as the rigidity, laryngeal dystonia, and several neurophysiological changes. Functional analysis of autopsy brains will facilitate clarification of the pathogenesis of the neurodegeneration in XPA.
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PMID:Brainstem and basal ganglia lesions in xeroderma pigmentosum group A. 1553 32

Tonsilloliths or tonsil stones are calcifications that form in the crypts of the palatal tonsils. These calculi are composed of calcium salts either alone or in combination with other mineral salts, and are usually of small size - though there have been occasional reports of large tonsilloliths or calculi in peritonsillar locations. We present the case of a 55-year-old woman with a one-year history of dysphagia and pharyngeal discomfort with a foreign body sensation, though the manifestations had recently intensified. Exploration of the oral cavity revealed a hard bulging submucosal mass in the region of the soft palate, at right anterior tonsillar pillar level. The mucosa overlying the lesion appeared erythematous. Computed tomography revealed a large, delimited and highly calcified oval image measuring 2.5 x 1.5 cm, which was subsequently surgically removed.
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PMID:Giant tonsillolith: report of a case. 1587 67

In a new family with X-linked congenital autophagic vacuolar myopathy (AVM), seven affected boys presented with congenital hypotonia, dyspnea, and dysphagia with delayed motor milestones. Muscle pathology revealed autophagic vacuoles with sarcolemmal features, multilayered basal lamina with marked sarcolemmal deposition of C5-9 membrane attack complex and calcium, histologically indistinguishable from childhood-onset X-linked myopathy with excessive autophagy (XMEA). Haplotype analysis suggests that this new AVM and XMEA may be allelic despite different clinical presentations.
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PMID:A new congenital form of X-linked autophagic vacuolar myopathy. 1621 76

Whereas the most powerful stimuli for bone formation is supposed to be a stretching of muscles, Frost HM classified the effect of muscle on bone mineral density (BMD) into various types: 1. age-related loss of bone mineral density (BMD) is partly due to loss of muscular wasting, 2. the increase of BMD in obesity is due to the increase in muscular power to support the increased body weight and 3. the decrease of BMD in chronic wasting disease is partly due to the decrease in muscular power. Likewise, the decrease in BMD in mandibular alveolar bones will be partly due to the decrease in the power of masticating muscles, if such exists. A case report of mitochondrial encephalo-myopathy associated with impaired function of cranial nerves involving trigeminus nerves and impaired function of masticating muscles and dysphagia. This patient showed decrease in alveolar BMD and atrophy of mandibular.
Clin Calcium 2006 Feb
PMID:[Muscular power of masticating muscles and mandibular osteoporosis]. 1646 28

Oesophageal spasm is a common empiric diagnosis clinically applied to patients with unexplained chest pain. In contrast it is an uncommon manometric abnormality found in patients presenting with chest pain and/or dysphagia and diagnosed by >or=20% simultaneous oesophageal contractions during standardized motility testing. Using Medline we searched for diagnostic criteria and treatment options for oesophageal spasm. While the aetiology of this condition is unclear, studies suggest the culprit being a defect in the nitric oxide pathway. Well-known radiographic patterns have low sensitivities and specificities to identify intermittent simultaneous contractions. Recognizing that simultaneous contractions may result from gastro-oesophageal reflux this diagnosis should be investigated or treated first. Studies have documented improvements with proton-pump inhibitors, nitrates, calcium-channel blockers and tricyclic antidepressants or serotonin reuptake inhibitors. Small case series reported benefits after botulinium toxin injections, dilatations and myotomies. Uncertainties persist regarding the optimal management of oesophageal spasm and recommendations are based on controlled studies with small numbers of patients or on case series. Acid suppression, muscle relaxants and visceral analgetics should be tried first. Botulinium toxin injections should be reserved for patients who do not respond. Pneumatic dilatations or myotomies represent rather heroic approaches for non-responding patients.
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PMID:Review article: oesophageal spasm - diagnosis and management. 1666 54


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