Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A follow up study three years after exposure to methyl isocyanate in 93% of exposed survivors and "control" residents in 10 Bhopali communities showed an excess of eye irritation, eyelid infection, cataract, and a decrease in visual acuity among the exposed people. Breathlessness was twice as common in the heavily exposed clusters as those with lower exposure, a trend that could not be explained by different age or smoking patterns (OR 2.05, 95% CI 1.36-3.08). Case referent analysis of outpatient attendances at Bhopal Eye Hospital, considering patients with severe refractive errors and astigmatism as "controls," showed a 40% increased risk of trachoma, 36% increased risk of other lid infections, and 45% increased risk of irritant symptoms among previously exposed people. "Bhopal eye syndrome" may thus include full resolution of the initial interpalpebral superficial erosion, a subsequent increased risk of eye infections, hyperresponsive phenomena (irritation, watering, and phlyctens), and possibly cataracts. It remains to be confirmed whether this reflects a more generalised disease as a consequence of previous exposure to methyl isocyanate or whether it is only the eye that is affected.
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PMID:Delayed eye and other consequences from exposure to methyl isocyanate: 93% follow up of exposed and unexposed cohorts in Bhopal. 239 36

A 36-year-old man was stung by a wasp OD. He became delirious and had dyspnea, ocular pain, and severely decreased visual acuity OD. A broken stinger was found in the central deep cornea. Additional ocular findings were keratitis, iritis, cataract, secondary glaucoma, and unrecordable electroretinographic responses.
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PMID:Wasp sting-induced retinal damage. 848 60

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

Even in the twenty-first century, welding is still a common and a highly skilled occupation. The hazardous agents associated with welding processes are acetylene, carbon monoxide, oxides of nitrogen, ozone, phosgene, tungsten, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, silver, tin, and zinc. All welding processes involve the potential hazards for inhalation exposures that may lead to acute or chronic respiratory diseases. According to literature described earlier it has been suggested that welding fumes cause the lung function impairment, obstructive and restrictive lung disease, cough, dyspnea, rhinitis, asthma, pneumonitis, pneumoconiosis, carcinoma of the lungs. In addition, welding workers suffer from eye irritation, photokeratitis, cataract, skin irritation, erythema, pterygium, non-melanocytic skin cancer, malignant melanoma, reduced sperm count, motility and infertility. Most of the studies have been attempted previously to evaluate the effects of welding fumes. However, no collectively effort illuminating the general effects of welding fumes on different organs or systems or both in human has not been published. Therefore, the aim of this review is to gather the potential toxic effects of welding fumes documented by individual efforts and provide informations to community on hazards of welding.
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PMID:Health hazards of welding fumes. 1464 49

Dexamethasone-cyclophosphamide pulse (DCP) is the prefered mode of therapy in pemphigus in India because it is relatively free from the side effects seen with heavy doses of daily oral steroids. One hundred forty-six pemphigus patients treated with DCP were observed for side effects of this regimen. One hundred forty mg of dexamethasone was administered IV in 200 ml of 5% dextrose over a period of 60-90 minutes on 3 consecutive days. Five hundred mg of cyclophosphamide was added on first day of the pulse and 50 mg given orally daily in the intervening period. DCP was repeated every 4 weeks and continued for 6 months after subsidence of the disease (no new lesions). Flushing over the face was the most common event recorded during the adiministration in 78 subjects followed by palpitations in 11, hiccups in 9, and numbness of feet in 6. Fourteen patients had polyurea, and 3 developed skin rash. Shivering, shooting pains along thighs, breathlessness, seizure and unilateral limb edema were observed in one patient each. Generalized weakness/malaise was the most troublesome delayed side effect in 81 (55.4%) patients; it lasted for 8-15 days after the pulse. Thirty-six (24.6%) had inadequate sleep syndrome, 23 (15.7%) had headache, 21 (14.3%) complained of arthralgias, 19 (13%) experienced alteration in taste, and 13 (9%) had diffuse hair loss. 28 females developed menstrual disturbances, and 14 (9.5%) had blurring of vision (glaucoma in 3 and posterior subcapsular cataract in 1). Thirteen of eighteen diabetics had an increase in blood sugar requiring higher doses of insulin. Five NIDDM patients needed insulin. Four (2.7%) developed hypertension. Pulse therapy is not absolutely free from side effects. Hypertension and diabetes occur less frequently as compared to conventional steroid therapy. Generalized weakness, flushing, headache and taste alteration occur exclusively with pulse therapy.
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PMID:Immediate and delayed complications of dexamethasone cyclophosphamide pulse (DCP) therapy. 1468 52

Cicatricial Pemphigoid is a subepithelial bullous dermatosis which essentially involves the mucous membranes with cicatricial evolution We report the case of a 66-year old patient hospitalized with erosive gingivitis associated with dysphagia, dyspnea and blurred vision. Dermatologic examination showed erosive lesions involving the palate and the pharynx. Ophthalmologic examination showed symblepharons, ectropion and bilateral cataract. Gingival biopsy revealed a necrotic detachment of the buccal epithelium. Direct immunofluorescence showed linear IgA deposit at the dermo-epidermal junction. Indirect immunofluorescence test was negative. The diagnosis of cicatricial pemphigoid was confirmed. Esophagogastroduodenoscopy objectified double stenosis of the esophagus. Nasopharyngeal and bronchial endoscopy showed ulceration of the epiglottis, hypopharynx, pharynx and bronchial tree. The patient was treated with Solumedrol bolus corresponding to 0.5mg/kg/day prednisone associated with 100mg/day disulone. The patient showed a favorable early clinical outcome complicated because of the aggravation of dysphagia and esophageal stenosis after 2 months. Our case study is singular due to the occurrence of a cicatricial pemphigoid in a male patient with a serious clinical picture due to lesions extending to conjunctival, oral, nasal, esophageal and bronchial mucous membranes associated with direct immunofluorescence only showing IgA deposit.
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PMID:[A particular type of cicatricial Pemphigoid with unique IgA deposit]. 2853 59

A 78 year-old man, who received levofloxacin eye drops as a perioperative prophylactic antibacterial agent for cataract surgery, developed pyrexia and dyspnea, followed by respiratory failure. He was diagnosed as drug-induced lung injury due to levofloxacin, and the symptoms improved after the administration of corticosteroids and discontinuation of levofloxacin eye drops. The incidence of levofloxacin-induced lung injury is rare for its frequent prescription. Moreover, eye drops of it has never been reported to cause lung injury. We should be aware of eye drops as a causative dosage forms of drug-induced lung injury.
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PMID:A case of drug induced lung injury caused by levofloxacin eye drops. 2997 47