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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study was to examine the effects on cataractogenesis of daily sc administration of the Ca2+ antagonist drug verapamil to diabetic rats. Streptozotocin-induced diabetic rats were given verapamil half-way through the 8-week experimental period or during the full 8 weeks of diabetes. Verapamil administration had no effect on the high blood glucose values, low circulating insulin levels, or elevated triglyceride and cholesterol concentrations in the diabetic rats. Untreated diabetic rats had a 90% incidence of cataracts. Four weeks of verapamil administration reduced this incidence to 41%, and a full 8 weeks of drug treatment further lowered the incidence to 20%. Diltiazem, another Ca2+ antagonist, lowered the incidence of cataracts in the diabetic rats to a similar extent. Verapamil administration to the diabetic animals also partially protected against the presence of retinal microangiopathy in the diabetic animals. Lenticular hydration and lipid accumulation were only indirectly related to cataractogenesis in the diabetic rats and its protection by verapamil treatment. Lenticular electrolyte imbalance, particularly Ca2+, in the diabetic animals was closely correlated with cataract formation, and verapamil significantly reduced the alterations in these ion concentrations. The present results demonstrate the efficacy of verapamil as a protective agent against cataractogenesis and some retinal damage in diabetic animals. Most importantly, this occurs in the absence of any change in the glycemic status of the diabetic animals. The findings strongly support a role for lenticular Ca2+ imbalance in cataract development in diabetes and provide initial evidence to suggest its clinical use in the diabetic population at risk for blindness.
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PMID:Cataract formation is prevented by administration of verapamil to diabetic rats. 275 74

A 5-year observation over 510 patients with initial senile cataract allowed to attribute to a group of risk relatives of the patients with senile cataract; persons who had suffered endocrine diseases; those with cardiovascular pathology; those who had suffered viral infections, rheumatism, renal and hepatic diseases; such workers, as drivers, founders, smiths, stockers, agricultural workers, teachers, lawyers. After 35 years of age, the patients of the group of risk should be yearly examined by the ophthalmologist. In case of general diseases, the main disease and disturbed turn-over should be treated. For local treatment and prevention of progression of senile cataracts the most effective are drops of catachrome, methyluracil with insulin. As to general treatment, it is recommended to use angioprotectors, methyluracil, tissue therapy.
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PMID:[Patterns of the development and progression of age-related cataracts in Voroshilovgrad Province (based on office visit data)]. 279 83

This discussion reviews drugs that affect the eye, including antihyperglycemic agents; corticosteroids; antirheumatic drugs (quinolines, indomethacin, and allopurinol); psychiatric drugs (phenothiazine, thioridazine, and chlorpromazine); drugs used in cardiology (practolol, amiodarone, and digitalis gylcosides); drugs implicated in optic neuritis and atrophy, drugs with an anticholinergic action; oral contraceptives (OCs); and topical drugs and systemic effects. Refractive changes, either myopic or hypermetropic, can occur as a result of hyperglycemia, and variation in vision is sometimes a presenting symptom in diabetes mellitus. If it causes a change in the refraction, treatment of hyperglycemia almost always produces a temporary hypermetropia. A return to the original refractive state often takes weeks, sometimes months. There is some evidence that patients adequately treated with insulin improve more rapidly than those taking oral medication. Such patients always should be referred for opthalmological evaluation as other factors might be responsible, but it might not be possible to order the appropriate spectacle correction for some time. The most important ocular side effect of the systemic adiministration of corticosteroids is the formation of a posterior subcapsular cataract. Glaucoma also can result from corticosteroids, most often when they are applied topically. Corticosteroids have been implicated in the production of benign intracranial hypertension, which is paradoxical because they also are used in its treatment. The most important side effect of drugs such as chloroquine and hydroxychloroquine is an almost always irreversible maculopathy with resultant loss of central vision. Corneal and retinal changes similar to those caused by the quinolines have been reported with indomethacin, but there is some question about a cause and effect relationship. The National Registry of Drug Induced Ocular Side Effects in the US published 30 case histories of cataract suspected to be induced by allopurinol; numerous additional cases have been reported to the registry since. Phenothiazine, with an estimated 3% incidence of side effects, appears to be safer than other antipsychotic drugs, but the rate of ocular effects increases with the duration of therapy. Thioridazine and chlorpromazine are known to cause lens deposits and pigmentary retinopathy. There is a significantly high prevalence of thrombophlebitis and pseudotumor cerebri among women who use OCs and thrombotic retinal vascular disease, such as retinal vein occulsion, might be linked with them. It also is probable that, because of altered hydration of the cornea, there is a decreased tolerance to contact lenses.
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PMID:Drugs affecting the eye. 286 12

The relationship of survival to systemic and ocular factors in diabetic persons was studied using data collected as part of the Wisconsin Epidemiologic Study of Diabetic Retinopathy. Six years after the baseline examination, 9.5% of 996 insulin-taking people who were younger than age 30 years when their diabetes was diagnosed (younger onset) had died. Of 1370 people whose diabetes was diagnosed after age 30 years (older onset), 35.3% had died. After adjusting for age and sex, longer duration of diabetes, presence of proteinuria, a history of cardiovascular disease, higher blood pressure, diuretic use, a history of smoking, poorer visual acuity, and more severe retinopathy were significantly associated with decreased survival in both groups. Glaucoma was associated with decreased survival in the younger onset group and cataract in the older onset group. These findings suggest that some ocular complications are important risk indicators for death. Their presence in diabetic patients suggests the need for frequent examinations to detect systemic complications and to intervene to minimize their effect.
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PMID:Relation of ocular and systemic factors to survival in diabetes. 291 72

The permeability of the blood aqueous and blood retinal barrier, the lens transmission, and the lens autofluorescence were measured by fluorophotometry in 7 diabetic youngsters treated by conventional therapy (mean age, 10.9 +/- 4.4 years), 9 diabetic youngsters treated by continuous s.c. insulin infusion (mean age, 12.3 +/- 5.0 years), and 13 healthy controls (mean age, 12.4 +/- 5.1 years). The mean permeability value for the blood retinal barrier of the diabetic juveniles did not differ significantly from that of the controls (P greater than 0.4), and no correlation with metabolic control (HbAlc) or duration of diabetes was found (P greater than 0.1). No differences in lens transmission larger than 4% were found. The mean value of lens autofluorescence corrected for normal age-dependency was found to correlate with the metabolic control: an increase of mean HbAlc by 1% resulted in an extra increase of autofluorescence by 11% (P = 0.002). This result suggests that good metabolic control can suppress excess lens autofluorescence, a precursor of cataract.
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PMID:Blood-retinal and blood-aqueous barrier permeability, lens autofluorescence and transmission in insulin-dependent diabetic youngsters. 292 Sep 5

Endocrine abnormalities in myotonic dystrophy (MyD) reflect some of the multi-systemic involvement resulting from this disorder. One of these, abnormal insulin secretion, is considered to be caused by receptor dysfunction. Bone abnormalities, cataract and calcium transport defect suggest the abnormal calcium metabolism in MyD. The calcium metabolism is chiefly regulated by parathyroid hormone (PTH). An interest in the similarity between MyD and pseudohypoparathyroidism, which is a disorder of PTH receptor dysfunction, encouraged the authors to evaluate renal PTH receptor function from the responses of urinary adenosine 3',5'-monophosphate (cAMP) and phosphate excretion after administration of human PTH(1-34). The responses of cAMP were high in 3 cases, low in one case, but normal in the 4 other cases. The phosphaturic responses were elevated in 3 cases, reduced in 3 cases, and normal in 2 other cases. Since these abnormal responses closely mimic those in hypoparathyroidism, there may also be renal PTH receptor dysfunction in some cases of MyD. The results of the present study suggest another peptide hormone receptor defect, similar to insulin, which supports the hypothesis of generalised receptor dysfunction in MyD.
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PMID:Evaluation of renal parathyroid hormone receptor function in myotonic dystrophy. 299 4

The activity of the polyol pathway--a non insulin-dependent metabolic pathway of glucose--is increased in diabetic patients. Polyol accumulation is involved, by a myoinositol-dependent mechanism, in the pathogenesis of some degenerative complications of diabetes. Thus, sorbitol accumulation in the eye lens and in nerves seems to be an important factor in the development of cataract and in the slowing down of nerve conduction. Recent studies suggest that the polyol pathway may play a role in early structural abnormalities of retinal and renal microangiopathy. Synthetic aldose reductase inhibitors could be used for a physiopathogenic treatment of these complications, but the first trials in diabetic neuropathy proved disappointing. Further studies, prolonged and well controlled, are necessary to pronounce on the future of this new category of drugs.
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PMID:[Role of the polyol pathway in the occurrence of degenerative complications of diabetes]. 301 8

The natural history of brittle diabetes is unknown. We have followed up 13 patients with disabling brittle diabetes unresponsive to continuous subcutaneous insulin infusion (CSII) for 3-6 yr. All were young, C-peptide deficient females. One patient has died (of hypoglycaemia). In the others, disruption of life has generally lessened, but only one patient is currently considered metabolically stable. Insulin treatment regimens have included long-term intravenous insulin infusions and intraperitoneal insulin, but all but four have now reverted to subcutaneous injections. Eleven patients intermittently required greater than 200 U/day of insulin and two have needed greater than 1,000 U/day. Insulin dosages have fallen significantly during follow-up (from 6.8 +/- 3.1 to 1.4 +/- 0.3 U/kg/day). Diabetic complications, initially present in only 2 cases (1 cataract, 1 proliferative retinopathy), have now developed in 5 others (2 background retinopathy, 1 proliferative retinopathy, 1 mixed peripheral neuropathy and 1 intermittent proteinuria). Psychosocial disturbance and non-compliance were common. We conclude that brittleness generally seems to improve, which probably explains the scarcity of older brittle patients. However, these patients are at considerable risk from diabetes, its complications and its treatment.
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PMID:The natural history of brittle diabetes. 304 51

Evidence linking the enzyme aldose reductase (alditol:NADP+ oxidoreductase, EC 1.1.1.21) to the pathogenesis of several diabetic complications is rapidly mounting. The results of several animal studies combined with preliminary reports of ongoing clinical trials indicate that inhibition of aldose reductase produces a beneficial effect against such diabetic complications as neuropathy, cataract, corneal epitheliopathy, retinopathy, microangiopathy, and possibly nephropathy. The observations that aldose reductase inhibitors appear to provide a new direct mode of treatment for the control of diabetic complications--a method independent of the insulin-related control of blood glucose levels--has spurred interest in the development of more potent and selective inhibitors. That goal can be more easily realized through an understanding of how these inhibitors interact with the aldose reductase protein. This requires insight into the steric and electronic requirements of both the inhibitors and the enzyme site where they bind (inhibitor site). Through the use of computer molecular modeling, molecular orbital calculations, known structure-activity relationships (SAR), protein modification reagents, and irreversible inhibitors, specific structural, and electronic similarities among the apparently structurally diverse aldose reductase inhibitors (ARIs) have been observed. In turn, these studies have led us to postulate the pharmacophor requirements of the ARI site.
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PMID:The aldose reductase inhibitor site. 308 1

We reviewed a series of 137 cataract extractions with intraocular lenses (IOLs) in patients with diabetes, mellitus between 1977 and 1983. All patients were followed for an average of 36 months to determine if they subsequently showed progression of diabetic retinopathy. Divided into groups according to the type of procedure and IOL received, they were compared for age, sex, duration of diabetes, treatment required for the diabetes, intraoperative complications, and follow-up period. Patients who had intracapsular cataract extractions with anterior chamber IOLs were three times as likely to show proliferative retinopathy as those who had extracapsular cataract extractions with posterior chamber IOLs. Insulin-dependent patients were three to four times more likely to show progression to proliferation than noninsulin dependent patients. We conclude that, while some procedures are riskier for the diabetic eye, extracapsular lens extraction with implantation of a posterior chamber lens does not imply an increased risk of development of proliferative retinopathy.
J Cataract Refract Surg 1988 Nov
PMID:Effect of cataract surgery and intraocular lenses on diabetic retinopathy. 323 May 18


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