Delayed increased intraocular pressure after Nd:YAG laser posterior capsulotomy in a patient treated with apraclonidine.
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Aged↗
Biomedical subjects
R Nesher
Publications and source records attributed to R Nesher.
Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects.
To determine whether long-term reduction of intraocular pressure leads to a corresponding preservation of the pattern electroretinogram (PERG), PERGs were studied in 21 patients with ocular hypertension who had received unilateral timolol therapy for a minimum of 6 years. The mean difference in intraocular pressure (IOP) between the placebo-treated and the timolol-treated eyes (over 6 years) was 2.4 mm Hg. Steady-state PERGs (16.0 rps) were obtained simultaneously in both eyes of each patient, with four check sizes (0.25, 0.5, 1.0 and 2.0 degrees). Significant (p less than 0.05) steady-state PERG deficits (i.e., amplitude more than two standard deviations below the mean value of age-matched controls) were observed in 16 eyes of 12 patients (10 placebo-treated and 6 timolol-treated eyes). The mean PERG amplitude did not differ significantly between the placebo-treated and timolol-treated eyes. However, a significant correlation (r = -0.423) in the IOP differences between the placebo-treated and timolol-treated eyes and the corresponding PERG amplitude differences was noted in three of the four test conditions (i.e. 0.25, 0.5, and 1.0 degrees). These results suggest that reducing IOP may preserve ganglion cell function in some patients with ocular hypertension.
Aged↗
A glucose reduction challenge in the differential diagnosis of fasting hypoglycemia: a two-center study.
Investigation of patients with suspected or proven hypoglycemia is often a time-consuming and expensive process. We describe a glucose reduction challenge test which may be useful as an out-patient screening procedure. Insulin is infused for 3 h at 40 mU/kg.h. Plasma glucose was monitored at the bedside during the test, and blood samples were collected for measurement of C-peptide. Responses were examined in 17 normal controls, and 6 patients with insulinomas. In normal subjects, mean plasma glucose fell to a plateau value of 3.2 +/- 0.2 mmol/L (57 +/- 2.6 mg/dL) and remained at that level with few symptoms. In contrast, five of six patients with insulinomas developed severe hypoglycemia, with plasma glucose levels between 1.9 (34 mg/dL) and 2.2 mmol/L (39 mg/dL). Plasma C-peptide concentrations were suppressed to 0.08 pmol/mL or less in normal subjects, but in insulinoma patients remained at 0.32-1.6 pmol/mL i.e. outside the normal range, and diagnostic of nonsuppressible insulin secretion. These data demonstrate that moderate reduction of serum glucose maintained for a prolonged period results in marked suppression of plasma C-peptide, permitting improved discrimination between normal subjects and patients with insulinomas. This glucose reduction challenge can, therefore, be used as a test of glucose-regulating ability, where failure (hypoglycemia) per se represents a measurable abnormality. C-Peptide measurements will determine whether the cause of hypoglycemia is due to hyperinsulinemia.
Adult↗
Failure of apraclonidine to prevent delayed IOP elevation after Nd:YAG laser posterior capsulotomy.
An elderly pseudophakic man with advanced open-angle glaucoma underwent Nd:YAG laser posterior capsulotomy. Pigment deposits were also removed from the anterior lens surface with laser applications. In spite of pre- and post-laser treatment with topical apraclonidine (Iopidine) and normal IOP 1 hour postoperatively, the patient presented the next day with visual acuity of 20/300, corneal edema, pain, and IOP of 60 mm Hg. Prompt treatment reduced the pressure and normal visual acuity was achieved. While apraclonidine prevents early post-laser elevation of IOP in most cases, some pressure elevations may be delayed or persist longer than the duration of action of the drug. Examination of patients with advanced glaucomatous optic nerve damage is recommended the day after anterior segment laser surgery, even when apraclonidine is used at the time of laser surgery and IOP is normal 1 to 2 hours postoperatively.
Adrenergic alpha-Agonists↗
Glaucomatous visual field damage. Luminance and color-contrast sensitivities.
Using a modified Humphrey perimeter, we evaluated 16 eyes with primary open-angle glaucoma and visual field loss (defects 0.5-3.0 log units in depth), and 14 normal eyes. Each eye was tested twice in random order with conventional luminance-increment static perimetry and with the perimeter modified to produce a high-luminance yellow adapting background and a blue test stimulus. The background was a broad-spectrum light of 500 nm and above (yellow), while the stimulus was a broad-spectrum light of 500 nm and below (blue). Paired comparisons were made between conventional and blue/yellow sensitivities for every point examined (1184 points in 16 diseased eyes and 1036 points in 14 normal eyes). Defect depths were determined by using the age-corrected norms distributed in the Humphrey Statpac software. In glaucomatous eyes, blue/yellow sensitivity showed greater impairment than did conventional perimetric sensitivity, in which defect depths were less than 1.0 log unit. However, for defects greater than 1.0 log unit in depth, conventional perimetric sensitivity and blue/yellow sensitivity showed equivalent degrees of damage. Receiver operating characteristic (ROC) analysis was used to compare the ability of blue/yellow and of conventional perimetry in distinguishing between glaucomatous and normal eyes. Results indicated that although blue/yellow color-contrast perimetry may be more sensitive for the detection of incipient glaucomatous damage, in the manifest stages of visual field damage blue/yellow color-contrast perimetry is no more sensitive than is conventional (luminance-increment) perimetry for defining the extent of glaucomatous visual field defects.
Adult↗
Laser trabeculoplasty in glaucoma. Ten-year evaluation.
Argon laser trabeculoplasty was evaluated in 134 eyes of 94 patients with glaucoma, over a follow-up period of three to ten years. Success was defined by the patient having intraocular pressures (IOPs) below 20 mm Hg under the prelaser medical regimen, or taking less medication, and having no evidence of progressive field loss. The overall success rate by three years was 70%; it decreased to 55% after six years and remained at this level thereafter. Altogether, there were 26 eyes that had controlled glaucoma for six to ten years. The favorable factors for success were age over 60 years (82%), pseudoexfoliation glaucoma (75%), and lower baseline IOPs (69.3%). Argon laser trabeculoplasty was found to be a useful means of treatment in low tension glaucoma.
Adult↗
Reduced early and late phase insulin response to glucose in isolated spiny mouse (Acomys cahirinus) islets: a defective link between glycolysis and adenylate cyclase.
The spiny mouse (Acomys cahirinus) exhibits low insulin responsiveness to glucose with a nearly absent early phase release. The alternative fuel-secretagogue glyceraldehyde (10 mmol/l) produced a maximal early insulin response in rat islets but failed to affect early response in Acomys; however, it potentiated the late insulin response in both species alike. Glucagon (1.5 mumol/l) potentiated the early insulin response to intermediate (8.3 mmol/l) glucose in rat and Acomys islets by two- and four-fold, respectively. Glucose doubled cyclic AMP levels in rat islets but no significant response was noted in Acomys islets. Isobutylmethylxanthine (0.1 mmol/l) and forskolin (25 mumol/l) caused a significant rise in islet cyclic AMP levels in both types of islets; however, neither agent restored the glucose stimulation of cyclic AMP in spiny mouse islets. Forskolin and isobutylmethylxanthine potentiated early and late phase insulin release in both species; however, neither augmented the early response in the Acomys to the degree observed in rat islets. Thus: (1) A deficient link exists in Acomys between glycolysis and subsequent signals. (2) These islets contain a glucose-insensitive adenylate cyclase. (3) The early insulin response may be potentiated by direct activation of adenylate cyclase. (4) The glucose effects on early and late phase insulin release are probably mediated by distinct pathways. (5) In the spiny mouse the signals mediating the early response are deranged to a greater extent than those activating the late phase insulin release.
1-Methyl-3-isobutylxanthine↗
Persistent hyperinsulinaemic hypoglycaemia of infancy: long-term treatment with the somatostatin analogue Sandostatin.
Six infants with severe, persistent hyperinsulinaemic hypoglycaemia were treated with the long-acting somatostatin analogue SMS 201-995 (Sandostatin, Sandoz, Basle, Switzerland). Effective control of hypoglycaemia without the need for parenteral glucose was achieved in five of the six cases with doses ranging from 10 to 40 micrograms/kg day given either by four s.c. injections per day, or by continuous subcutaneous infusion (CSI). One has been well controlled on SMS 10 micrograms/kg day for 17 months as an out-patient without requiring surgery, while the five others underwent sub-total pancreatectomy after receiving short courses of the drug. In two patients where hypoglycaemia persisted after sub-total pancreatectomy SMS was effective in inhibiting insulin secretion and preventing hypoglycaemia. Plasma somatomedin concentrations and linear growth were not suppressed in any patient. It is concluded that Sandostatin is useful in the pre and post-operative management of most infants with this syndrome. In selected cases this analogue of somatostatin may also be a long-term treatment option in place of pancreatectomy.
Blood Glucose↗
Beta-cell memory to insulin secretagogues: characterization of the time-dependent inhibitory control system in the isolated rat pancreas.
Most secretagogues, in addition to their acute stimulatory effect on insulin release, modify the responsiveness of the islet to subsequent stimulations. According to the nature and duration of the stimulus, the generated islet memory may either amplify [time-dependent potentiation, (TDP)] or diminish [time-dependent inhibition (TDI)] the responsiveness of the beta-cell. This work characterizes the kinetic parameters of TDI in the isolated rat pancreas. When subjected to a low dose (8.3 mmol/liter) glucose stimulus, maximal TDI was observed after 5 min of priming, while at a higher dose (16.7 mmol/liter) shorter exposures were sufficient. Longer periods of stimulation (10-40 min) resulted in the predominance of TDP, thus amplifying the release rate. TDI was not affected by previous generation of TDP; 40-min priming with 16.7 mmol/liter glucose markedly augmented the subsequent insulin responses to a pair of 6.9 mmol/liter stimuli, but the response to the second stimulus was inhibited, as in unprimed pancreas. Stimulation with arginine (5.0 mmol/liter) in the presence of basal (3.3 mmol/liter) glucose activated TDI only, and hence revealed monophasic insulin release. Tolbutamide (100 micrograms/ml), glucagon (5 micrograms/ml), and isobutylmethylxanthine (0.1 mmol/liter) also demonstrated TDI when given as a pair of 10-min stimuli; they all elicited monophasic insulin responses during prolonged stimulation. Arginine was chosen for detailed characterization of TDI because of its potency. Using identical concentrations of arginine for the generation and expression of TDI, a similar degree of inhibition (60-80%) was observed at all doses tested (0.5-5.0 mmol/liter). However, there existed competition between TDI and the acute secretory signal. Thus, TDI generated by 1.0 mmol/liter arginine had a minimal effect on insulin release induced by 2.0-5.0 mmol/liter amino acid, while it was fully inhibitory of the response to 1.0 mmol/liter arginine. Similarly, inhibition of the insulin response to 5.0 mmol/liter arginine was dependent on the dose (0.5-5.0 mmol/liter) of the priming pulse of arginine. The generation of TDI was unaffected by the insulin release rate during priming, since synergistic augmentation (combined arginine-glucose or arginine-isobutylmethylxanthine stimulation) or partial inhibition (arginine plus epinephrine) of the response had no effect on the subsequent expression of TDI. It is concluded that TDI and TDP are two distinct regulatory systems that independently control the rate of insulin release, most probably operating through different mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)
1-Methyl-3-isobutylxanthine↗
[Age-related macular degeneration after retinal detachment surgery].
We studied a group of 157 patients who had retinal detachment surgery in one eye with successful anatomical reattachment and a fellow eye without a retinal detachment. In a group of 7 out of 8 patients who had a retinal detachment that included the macula and who underwent surgery, we found that the development of macular degenerative changes was much less pronounced in the operated eye than in the fellow, control eye. In a group of 3 patients who had retinal detachment without macular involvement, the appearance of macular degenerative changes appeared to be rather symmetric in the operated and in the fellow eye. The presence of a circling buckle did not appear to have an influence on the ARMD changes. It appears that the presence of a macular detachment is a factor in modifying the natural history of age-related macular degeneration. The diminution of signs of ARMD could be related to a degree of atrophy in the retinal pigment epithelium occurring after a retinal detachment with the macula off.
Aged↗
Pulmonary barotrauma including orbital emphysema following inhalation of toxic gas.
Severe pulmonary barotrauma occurred following smoke and toxic gas inhalation in a 20-year-old male. He developed pneumothorax, pneumomediastinum, and extensive facial subcutaneous emphysema which intensified during treatment with positive pressure ventilation. Following the appearance of diplopia and exotropia, orbital emphysema was demonstrated radiologically. The diplopia and exotropia were manifestations of mechanical interference in extra-ocular muscle function by the intra-orbital air, an unusual expression of pulmonary barotrauma.
Adult↗
Immediate and time-dependent effects of glucose on insulin release: differential calcium requirements.
Glucose regulates insulin release in a complex manner; apart from its acute secretory action it induces time-dependent effects which modulate subsequent islet responses. The Ca2+ sensitivities of the diverse secretory events generated by glucose were investigated in the perfused rat pancreas. First- and second-phase insulin responses to 16.7 mmol/l glucose were obliterated in the presence of 5 mmol/l EgTA; threshold Ca2+ concentrations for significant responses were 0.25 mmol/l for second-phase, and 'O' (no Ca2+ added, approx 20 mumol/l) for first-phase release (both around 10% of control). The apparent Km of the Ca2+ dependencies were 0.6 mmol/l for first-phase, and 1.25 mmol/l for second-phase release. Time-dependent potentiation was demonstrated by subjecting the pancreas to two 40-min 16.7 mmol/l glucose stimuli separated by a 30-min rest period; this amplified the first-phase response to the second stimulus 2.5 +/- 0.9-fold. Also the generation of potentiation was Ca2+ dependent, with characteristics similar to those of the acute second-phase insulin response (apparent Km approximately 1.0 mmol/l Ca2+). In contrast, the amplified first-phase response to the second glucose pulse retained its high sensitivity to Ca2+, thus resembling the unprimed first-phase. The inhibitory message of glucose was demonstrated by applying two sequential 5-min pulses of 8.3 mmol/l glucose: the insulin response to the second stimulus was reduced by 43 +/- 9%. Addition of EgTA to the first glucose pulse had no effect on the inhibition of the second insulin response. Thus: 1. Despite its high sensitivity to Ca2+, also first-phase release is fully dependent on extracellular Ca2+.2.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Improved beta-cell function after intensive insulin treatment in severe non-insulin-dependent diabetes.
In Type II, non-insulin-dependent diabetes, insulin secretion is often reduced to the point where oral hypoglycaemic agents fail to control the plasma glucose level. We studied 12 patients (age 41-66 years; 4 lean, 8 obese) with Type II diabetes mellitus for 1-25 years who were uncontrolled despite maximal dose glibenclamide and metformin. After withdrawal of medication, blood glucose control was determined by measuring glucose before and 2 h after each meal for 48 h, and beta-cell function by insulin or C-peptide response to glucagon and to iv glucose. Following these tests, intensive insulin treatment (CSII) was initiated, and near-euglycaemia (mean of 7 daily glucose determinations less than 7.7 mmol/l) was maintained for 16.6 +/- 1.5 days, at which time the tests were repeated. Mean daily insulin requirement was 61 +/- 9 IU (0.81 +/- 0.09 IU/kg). Glucose control was improved after cessation of CSII (mean glucose 12.7 +/- 0.6 mmol/l after vs 20 +/- 1.5 mmol/l before, P less than 0.005). Maximum incremental C-peptide response improved both to glucagon (214 +/- 32 after vs 134 +/- 48 pmol/l before, P = 0.05) and to glucose iv bolus injection (284 +/- 53 vs 113 +/- 32 pmol/l, P less than 0.05). Peak insulin response, measured after iv glucose infusion, also tended to be higher in the post-CSII test (42 +/- 18 vs 22 +/- 5.6 mU/l). Basal and stimulated proinsulin concentrations were high relative to C-peptide levels during the pre-treatment period, but returned to normal after CSII.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Pattern reversal electroretinogram (PRERG) abnormalities in ocular hypertension: correlation with glaucoma risk factors.
The indices employed commonly for the diagnosis of glaucoma (tonometry, ophthalmoscopy and perimetry) do not always identify which patients with ocular hypertension (OHT) will develop primary open-angle glaucoma (POAG) before irreversible visual field loss is manifest (1). The human pattern reversal electroretinogram (PRERG) is a bioelectric response reflecting neural activity of the proximal retina. PRERG amplitude reductions have been observed in POAG and other diseases affecting the optic nerve and retinal ganglion cells. This study was designed to determine whether OHT patients exhibit PRERG amplitude reductions and whether PRERG results are correlated with routinely evaluated clinical parameters. Steady-state PRERG (16 rps) were elicited by high contrast (76%), phase alternating checkerboard patterns (15-20 min checks) from one eye of 130 patients with ocular hypertension and 47 age matched visual normals (AMVNs). A significant (p less than 0.05) reduction in PRERG amplitude was noted for the OHT patients and 11.5% of those patients exhibited PRERG amplitudes more than 2.0 standard deviations below the AMVN mean. PRERG amplitude was found to be positively correlated with diastolic blood pressure (DBP) and negatively correlated with age, but no correlation between PRERG amplitude and either IOP, C/D ratio, or systolic blood pressure was evident. The lack of correlation between PRERG amplitude and the commonly used clinical indices may suggest a complementary role for this neurophysiologic test in determining which OHT patients will develop glaucoma.
Analysis of Variance↗
Dissociation of visual deficits in ocular hypertension.
Both acquired color vision deficiencies and abnormal pattern electroretinograms (PERGs) are observed in patients with ocular hypertension (OHT) as well as in patients with glaucoma. In the present study we determined the prevalence of both of these functional deficits in a large group of OHT patients (N = 130). Color vision was tested with the desaturated D-15 and a color confusion score was used to quantitatively assess the magnitude of the color vision deficiency. Steady-state PERGs were evoked with rapidly alternating high contrast checkerboard patterns. Color vision deficits were detected in 23% of OHTs while 11.5% of the patients exhibited significant PERG amplitude reductions. Only 2.3% exhibited both abnormalities. The results suggest that although color vision deficiencies and PERG abnormalities are both evident in OHT, they are often dissociated findings.
Adult↗
Transient blindness following intracranial pressure changes in a hydrocephalic child with a V-P shunt.
A hydrocephalic child with a V-P shunt developed transient blindness following shunt revision. A year later, visual function deteriorated when shunt malfunction occurred. Following shunt revision, the child regained sight. The effects of intracranial hypertension and hypotension on the visual pathways are discussed.
Blindness↗
Insulin deficiency and insulin resistance in type 2 (non-insulin-dependent) diabetes: quantitative contributions of pancreatic and peripheral responses to glucose homeostasis.
A non-steady state dose-response study was designed to quantitate peripheral sensitivity to insulin and pancreatic responsiveness to glucose, and to assess their relative contribution to glucose intolerance in Type 2 diabetes (Type 2 DM, non-insulin-dependent). Eleven lean and eleven obese patients with mild diabetes (fasting plasma glucose, FPG, 10.3 +/- 1.0 and 9.4 +/- 0.6 mmol l-1, respectively) were examined; twenty-six lean and twelve weight-matched obese subjects served as controls. Pancreatic response was measured by sequential injection of 0.1, 0.3 and 0.9 g kg-1 glucose; peripheral sensitivity to insulin was determined from the rate of clearance (Kgluc) of 0.3 g glucose injected sequentially together with 25, 50 and 100 mU insulin kg-1 or with 0, 12.5 and 50 mU kg-1, under somatostatin infusion. The mean dose-response curve describing glucose-induced insulin release showed increased maximal capacity to secrete insulin in obese controls, while the responses of lean as well as obese Type 2 DM were reduced by more than 80%. The mean dose-response curves relating plasma exogenous insulin levels to Kgluc were similar in lean diabetics and lean controls. The curves of both obese controls and obese diabetics were shifted to the right, demonstrating similar insulin resistance. In four lean controls, sensitivity to insulin was tested also during a hyperglycemic clamp set at 10.3 +/- 0.6 mmol l-1. Hyperglycemia reduced the Kgluc at all insulin levels. Individual dose-response curves were transformed to single weighted numerical pancreatic responsiveness scores [PRS], and peripheral sensitivity scores [PSS].(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Biphasic insulin release as the expression of combined inhibitory and potentiating effects of glucose.
The dynamics of insulin release were investigated in vitro in order to determine the regulatory processes governing its biphasic shape. When subjected to a square wave glucose stimulation, the isolated perfused rat pancreas responded with typical biphasic insulin release. Both the duration of the nadir between the two phases and the slope of recovery of insulin release during second-phase secretion exhibited glucose dose dependency. Successive 40-min stimuli with glucose (8.3 and 16.7 mM), separated by a 20-min rest period, resulted in 2.6- 3.3-fold potentiation of the early phase insulin release rate, previously described as glucose-primed time-dependent potentiation (TDP) of insulin secretion. A linear relationship (r = 0.89, P less than 0.001) was observed between the degree of TDP and the slope of second-phase insulin release. Successive short stimuli with glucose (5-10 min long, 5-10 min apart; 6.9, 8.3, and 16.7 mM) resulted in the inhibition of the response to the second stimulus; this effect was termed time-dependent inhibition (TDI) of insulin release. Arginine also induced TDI; this was completely overcome by synergistic interaction with glucose (8.3 mM). The glucose-arginine interaction was utilized to demonstrate that the interphasic nadir of insulin release was the expression of TDI. Thus, introduction of an arginine stimulus during the nadir in glucose-induced insulin release abolished the silent phase, the secretion rate reaching the level expected for the combined glucose-arginine stimulus. However, the continued presence of TDI could be demonstrated by removal of the arginine stimulus, at which time, despite ongoing glucose stimulation, insulin secretion was markedly inhibited. These observations support the concept that the biphasic dynamics of insulin release is the net expression of three regulatory processes: 1) the acute stimulus-secretion coupling system, best observed as the immediate, first-phase response to a stimulus; 2) TDI of insulin release, a relatively rapid signal responsible for the silent period; and 3) TDP of insulin release, a slow rising signal responsible for recovery from the silent phase, building up the second-phase of secretion.
Animals↗