Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral administration of 50 mg tartrazine to 122 patients with a variety of allergic disorders caused the following reactions: general weakness, heatwaves, palpitations, blurred vision, rhinorrhoea, feeling of suffocation, pruritus and urticaria. There was activation of the fibrinolytic pathway as shown by reduction of plasminogen with high pre-kallikrein and low kallikrein values. Reduction in complement activity (CH50) was seen in three out of sixteen reactions.
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PMID:The danger of "yellow dyes" (tartrazine) to allergic subjects. 62 44

In 1972, Neault and his co-workers reported seven cases of uveitis associated with intracranial reticulum cell sarcoma. Recently we have experienced a similar case for the first time in Japan. A 32-year-old woman registered on March 10, 1971, complaining of blurred vision in the left eye for about two weeks. By ophthalmic examination, left posterior uveitis was diagnosed but the etiology was unknown. Treatment with corticosteroids was begun, but her left eye continued to fail in spite of the treatment. In August, 1971, she complained of weakness of left arm and leg, and in October, she suffered from severe headache and vomiting. At that time, uveitis appeared in the right eye too. Neurological findings and carotid angiogram indicated a right cerebral lesion. On November 5, 1971, a right frontoparietal craniotomy was performed but no tumor was found. Since then her neurological and eye symptoms had been progressively worse. The patient died on July 12, 1972. Postmortem examination revealed the tumor infiltrating in the bilateral diencephalon, left internal capsule, left lenticular nucleus, left temporal lobe, midbrain, pons, left dentate nucleus, optic chiasma and intracranial portion of the optic nerves. But no tumor was found at any other parts of the body. Histologically the tumor was a reticulum cell sarcoma. The eyeballs were not examined histologically, but the uveitis in this case was thought to be closely related to the intracranial reticulum cell sarcoma. If the uveitis is resistant to the treatment, we must consider a possibility of reticulum cell sarcoma of the brain.
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PMID:[A case of primary reticulum cell sarcoma of the brain with uveitis (author's transl)]. 76 82

Cystic changes are rare in meningioma. The authors reported two cases of the cystic meningioma. 1) The first case was 56-year-old female, whose complaints were motor weakness and hypesthesia on the right side. At the operation, a hen egg-sized tumor with a large cyst was removed totally from the left frontoparietal mid-convexity. Multiple cystic cavities were contained in the tumor. Histologically the tumor was compatible with meningocytic meningioma with angiomatous component and showed numerous myxomatous degeneration and swollen vessel-walls. 2) The second case was 17-year-girl complaining of headache, blurred vision, right hemiparesis and episodes of Jacksonian seizure. At the operation, a goose egg-sized tumor in the left parietal lobe was removed and the tumor contained a large cyst. Histologically the tumor was a malignant meningioma, associating with relatively fresh necroses adjacent the cyst. 3) The pathogenesis of the cystic changes in meningioma was discussed.
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PMID:[Cystic meningioma--report of two cases (author's transl)]. 98 75

The allocation of some symptoms of acute hypoglycaemia to autonomic and neuroglycopenic groups has proved problematical, with possible misinterpretation of studies which depend upon the use of diverse symptom questionnaires. Two hundred and ninety-five randomly selected insulin-treated diabetic patients were asked to report the symptoms which they usually experienced and believed to be caused by hypoglycaemia. Sweating, trembling, inability to concentrate, weakness, hunger and blurred vision were the most frequently reported symptoms. To classify symptoms of hypoglycaemia objectively, Factor Analysis was used to identify related symptoms which grouped together. This resulted in five groups or clusters of symptoms, four of which could be denominated as groups with a presumed common aetiology, and were labelled: 'neuroglycopenic', 'general malaise', 'autonomic', 'motor dysfunction', and 'sensory dysfunction'. The groups of symptoms derived by Factor Analysis were assessed in relation to partial or absent symptomatic awareness of hypoglycaemia based on historical evidence from the 295 insulin-treated diabetic patients. Neuroglycopenic symptoms were reported more commonly by the patients who had reported partial awareness of hypoglycaemia (number of symptoms 2.6 +/- 1.8 (mean +/- SD] than by the patients who had reported normal hypoglycaemia awareness (1.4 +/- 1.5 symptoms) (p less than 0.05). By contrast autonomic symptoms were reported less frequently by the patients who had reported absent hypoglycaemia awareness (1.3 +/- 1.4 symptoms) than by those with normal awareness (2.2 +/- 1.4 symptoms) (p less than 0.05), which was similar to the number of autonomic symptoms reported by the patients who had partial hypoglycaemia awareness (2.1 +/- 1.3 symptoms).
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PMID:Classification of symptoms of hypoglycaemia in insulin-treated diabetic patients using factor analysis: relationship to hypoglycaemia unawareness. 155 13

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.
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PMID:Acute pyridostigmine overdose: a report of nine cases. 175 42

This report describes a rare complication after the resection of a tumor of the posterior fossa, the "one-and-a-half" syndrome. The one-and-a-half syndrome is a disturbance of horizontal eye movements in which patients have lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other direction. The patient was a 54-year-old woman who developed headaches, diplopia, and blurred vision over 6 months. Computed tomographic scans and magnetic resonance imaging demonstrated an enhancing, mixed density, midline mass of the cerebellum. After a resection of the mass, an anaplastic astrocytoma, the patient complained of more severe diplopia and facial weakness. An examination disclosed a left one-and-a-half syndrome, left peripheral facial paralysis, dysarthria, dysphagia, mild left hemiparesis, dysmetria of the left upper limb, and truncal ataxia. The brain stem showed no abnormalities on postoperative computed tomographic scans. After 4 months of follow-up, the one-and-a-half syndrome had not improved, even though other signs had improved or resolved. This syndrome is caused by damage to structures within the pontine tegmentum: the medial longitudinal fasciculus, the ipsilateral paramedian pontine reticular formation, or the ipsilateral abducens nucleus. Multiple sclerosis and brain stem infarction are the most common causes of the one-and-a-half syndrome. Less frequently, it is caused by primary and metastatic tumors of the brain stem and cerebellum. Rarely, the one-and-a-half syndrome can develop postoperatively after the removal of tumors of the posterior fossa. The mechanism of pontine tegmental injury remains unknown.
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PMID:"One-and-a-half" syndrome after a resection of a midline cerebellar astrocytoma: case report and discussion of the literature. 196 11

Midodrine, a peripheral alpha-adrenergic agonist, finds use in the clinical management of patients with orthostatic hypotension or hypotension secondary to other clinical conditions or drug therapies. Midodrine is almost completely absorbed after oral administration and undergoes enzymatic hydrolysis to form its pharmacologically active metabolite, de-glymidodrine. In patients with refractory orthostatic hypotension oral midodrine increases standing blood pressure and improves symptoms of orthostatism, such as weakness, syncope, blurred vision and fatigue, without any associated cardiac stimulation. Comparative studies have shown midodrine to be clinically at least as effective as other sympathomimetic agents (norfenefrine, etilefrine, dimetofrine and ephedrine) and dihydroergotamine in this regard. Additionally, midodrine appears to cause less frequent and severe adverse effects associated with alpha-receptor agonism such as piloerection and urinary hesitancy. The most commonly experienced adverse effects--piloerector reactions, gastrointestinal disorders, and cardiovascular complaints--are generally mild and can be controlled by reducing the dosage of midodrine. Thus, midodrine is at least as useful as other currently available options in the management of orthostatic or secondary hypotension, and represents a stepping stone towards optimal therapy.
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PMID:Midodrine. A review of its pharmacological properties and therapeutic use in orthostatic hypotension and secondary hypotensive disorders. 248 Aug 81

Neuromyelitis optica also named Devic's disease is an acute combined optic neuritis and transverse myelitis. It is thought to be a variant of multiple sclerosis, but its clinical presentation probably has only one attack without further recurrence and exacerbation. We present a 12-year-old girl who suffered from sudden onset of lower extremeties weakness, sensory loss and blurred vision after a prodromal URI symptom. CSF examination showed mild pleocytosis, elevated immunoglobulins, mild elevation of protein concentration. No oligoclonal band was detected. Serum virology showed high titer of anti-EB virus antibody. Visual evoke potential showed prolong of latency and decreased amplitude of both eyes. After prednisolone treatment, her visual accuity began to improve on the 7th hospital day and motor function improved on the 11th hospital day. Two years later, she has normal visual accuity, normal motor function and shows no evidence of disease recurrence.
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PMID:Neuromyelitis optica (Devic's disease) report of one case. 256 81

One hundred adults with a chief complaint of chronic fatigue were evaluated in an outpatient setting to determine a possible association with somatization disorder. Somatization disorder was diagnosed in 15 patients. Eight functional somatic symptoms were reported more frequently by these patients: pain in extremities, joint paint, chest pain, other pain, shortness of breath, blurred vision, muscle weakness, and sexual indifference (p less than 0.001). Current mood disorders, anxiety disorders, and psychoactive substance use disorders were less common in patients with somatization disorders than in patients without this diagnosis (p less than 0.01).
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PMID:Somatization disorder in patients with chronic fatigue. 279 31


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