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 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many reports of diabetic ophthalmoplegia have been published from the clinical points of view. However, there have been only three autopsied cases in which the ocular nerves were investigated histopathologically. A 72-year-old housewife was diagnosed to have glycosuria at the age of 67, but no medical treatment was done. She admitted to the hospital, because of acute onset of right eyelid drooping and diplopia for previous four days. She showed complete eyelid ptosis, moderate dilatation of right pupil, loss of light reaction, and extraocular muscle palsy except abduction on the right. Blood pressure was normal. A glucose tolerance test was diabetic and HbA1c was moderately increased. Her diabetes was fairly well-controlled with a diet therapy and injection of lente insulin. Two and a half months after admission, the course of illness became regressive. Seven months later, external ophthalmoplegia was disappeared and only slight anisocoria was seen. She readmitted to the hospital one year and eleven months later, because of anorexia and emaciation. She died of adenocarcinoma of the stomach without chemotherapy. The duration from onset of ocular symptoms to death was two years and one month. At postmortem examination, stomach cancer infiltrated extensively to the abdominal and pelvic viscera, but no metastasis to the nervous system or intraorbital tissues was found. There were mild to moderate atherosclerotic changes in the small-and middle-sized arteries of the kidneys, pancreas and adrenal glands corresponding to her age. Moderate atherosclerosis was found in all of the major arteries including Willis ring, siphon of the right internal carotid artery and Vertebro-basilar one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic ophthalmoplegia--a clinico-pathological study of the first case in Japan]. 269 31

Echocardiographic data are reported for 84 diabetes mellitus patients with reference to their age, severity and clinical pattern of diabetes and its treatment. There was left-ventricular hypertrophy, reduced end-diastolic volume and reduced stroke volume, particularly so in moderate and severe diabetes mellitus. In young insulin-treated patients (11%) with labile glycemia, an obvious mitral prolapse and, perhaps, also aortic valve prolapse were detected. This category of patients would frequently exhibit heart rate and conductivity disorders, such as second-degree sino-auricular block and frequent supraventricular extrasystoles.
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PMID:[Study of the functional status of the heart in diabetes mellitus based on echocardiographic data]. 273 17

In 204 adult, white diabetics the palpebral fissure was measured and related to the state of metabolic control of the diabetes. A control group was formed of 204 persons matched by age and sex. The average palpebral fissure in the control group was 9.9 mm: there was a slight, but not significant, difference between the age groups and the sexes. In diabetics who were not insulin dependent the average width of the palpebral fissure was found to be 9.4 mm; in severe chronic deregulation of the diabetes, however, an average palpebral fissure of 8.0 mm was found, a significant narrowing. In insulin-dependent diabetics the average width of the palpebral fissure was 8.3 mm. This significant narrowing also increased if there was severe chronic deregulation of the diabetes. The average palpebral fissure associated with proliferative retinopathy in insulin-dependent type 1 diabetics was 6.0 mm (nearly 4 X standard deviation). This ptosis in diabetes is very probably due to chronic tissue hypoxia, to which the levator palpebrae muscle is probably extra sensitive, and in which thickening of the basal membrane of the capillaries may be one of the most important factors.
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PMID:Narrowing of the palpebral fissure in diabetes. 666 9

The destruction of N-methyl-D-aspartate (NMDA) receptor-bearing neurons by insulin-induced hypoglycemia has long been known to be due to excessively released aspartate and glutamate. In this study, the effects of NMDA-bearing neuron destruction by insulin-induced hypoglycemia on the development of morphine (M) physical dependence, which was found related to functional states of NMDA receptors, were investigated. NMDA receptor antagonists CGP 39551 and MK-801 were used to see whether they could change intensity of precipitated abstinence syndrome by preventing destruction. Therefore, two groups of fasting rats injected IP with physiological saline, and another two groups given IP 10 mg/kg CGP 39551 and 0.5 mg/kg MK-801 received 15 IU/kg crystalline zinc insulin IP. After 2 h, the rats were orally given 2 x 4 ml of 5% glucose solution. On the third day, two pellets containing 75 mg base M were SC implanted to all rats. On the sixth day, they were IP given 2 mg/kg naloxone (NL). Then jumps, wet-dog shakes, and defecation were counted while diarrhea and ptosis were rated for 15 min. The rats given insulin manifested significantly more intense NL-precipitated abstinence syndrome than controls. The rats administered CGP 39551 showed a less intense physical dependence than those injected with only insulin. But, the intensity was still significantly higher than controls. In the rats that received MK-801, the abstinence syndrome was more or less equal to that in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphine physical dependence intensification by hypoglycemia: NMDA receptor involvement. 793 7

A 35-year-old woman with features of Kearns-Sayre syndrome consisting of progressive ptosis, ophthalmoparesis, mitochondrial myopathy, and pigmentary retinopathy also had autoimmune polyglandular syndrome type 11 (Addison's disease, autoimmune insulin-dependent diabetes mellitus, Hashimoto's thyroiditis, and primary ovarian failure). There was no history of similarly affected relatives. Analysis of muscle mitochondrial DNA (mtDNA) revealed a 2,532-bp deletion of the type seen in Kearns-Sayre syndrome as well as a heteroplasmic A3243G mutation in the tRNA-Leu(UUR) gene of the type seen in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). The patient's blood and her mother's blood harbored the A3243G mutation but not the deletion, and the maternal grandmother's blood had neither mutation. In muscle, the species of mtDNA harboring the deletion was exclusively associated with the species harboring the A3243G mutation, suggesting that the point mutation predisposed to the large-scale deletion. The mtDNA species with both mutations accounted for 88% of total muscle mtDNA. Other and as yet unrecognized point mutations in mtDNA might also be associated with, and possible causally related to, large-scale mtDNA deletions.
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PMID:MELAS- and Kearns-Sayre-type co-mutation [corrected] with myopathy and autoimmune polyendocrinopathy. 865 48

A 75-year-old woman presented with fever and right temporal, periorbital and facial pain for 7 days. Physical examination revealed an ipsilateral paresis of the superior division of the oculomotor nerve with mild exophthalmos. She also had hyperglycemia. CT scan of the paranasal sinuses showed acute sinusitis. Rhinoscopy demonstrated black necrotic tissue in the nasal septum. KOH preparation of tissue biopsy specimen revealed large, non septate hyphae with right angle branching, diagnostic of rhinocerebral mucormycosis. She was treated with amphotericin B, surgical debridement and insulin therapy. Surgical tissue specimen also confirmed mucormycosis. She improved after treatment, but 4 months later, ptosis and upward palsy still persisted.
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PMID:Superior branch palsy of the oculomotor nerve caused by rhinocerebral mucormycosis. 1156 Feb 25

The author contends that neither behavioral nor psychological factors are responsible for obesity or overweight, but that physiological and nutritional factors are. Obesity and overweight are relevant to natural family planning because they contribute to various problems of the female reproductive system. Body fat stores estrogen, and excess body fat increases estrogen levels which creates various problems. For example, elevated estrogen levels may contribute to endometrium build-up, resulting in heavy, prolonged bleeding during menstruation or in midcycle. They may kick off a reaction, causing suppressed ovulation, premenstrual spotting, and menstrual cramps. Other possible effects of high estrogen levels are fibroid tumors, breast cancer, endometrial cancer, ovarian cancer, and amenorrhea. The consistent pressure of excess body fat on the uterus can result in uterine prolapse. Overweight may also be a symptom of a reproductive problem, e.g., ovarian failure. Hypoglycemia, including reactive hypoglycemia, caused by a diet high in sugar and white flour, plays a key role in overweight. Excessive insulin secretion in reactive hypoglycemic cases maintains high glucose levels, and the body stores the excess glucose in fat cells. Thus, a diet low in sugary foods and high in fiber-rich complex carbohydrates is the most successful way to lose weight. However, vitamins and minerals needed to maintain blood sugar levels must supplement this diet to be successful. These vitamins and minerals include the B vitamins, magnesium, and, perhaps, chromium. Iodine, vitamins A and E, zinc, and selenium help the thyroid gland operate optimally, so as to avoid excess blood sugar levels. Vitamin E, lecithin, and evening primrose oil assist the body in using fat better. Regular exercise is also important to burn excess fat. Aspartame (Nutrasweet) exacerbates hypoglycemia and is usually found in refined foods and non-foods.
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PMID:An empathetic look at overweight. 1231 98

We examined the role of efferent neural signaling in regulation of net hepatic glucose uptake (NHGU) in two groups of conscious dogs with hollow perfusable coils around their vagus nerves, using tracer and arteriovenous difference techniques. Somatostatin, intraportal insulin and glucagon at fourfold basal and basal rates, and intraportal glucose at 3.8 mg.kg(-1).min(-1) were infused continuously. From 0 to 90 min [period 1 (P1)], the coils were perfused with a 37 degrees C solution. During period 2 [P2; 90-150 min in group 1 (n = 3); 90-180 min in group 2 (n = 6)], the coils were perfused with -15 degrees C solution to eliminate vagal signaling, and the coils were subsequently perfused with 37 degrees C solution during period 3 (P3). In addition, group 2 received an intraportal infusion of norepinephrine at 16 ng.kg(-1).min(-1) during P2. The effectiveness of vagal suppression was demonstrated by the increase in heart rate during P2 (111 +/- 17, 167 +/- 16, and 105 +/- 13 beats/min in group 1 and 71 +/- 6, 200 +/- 11, and 76 +/- 6 beats/min in group 2 during P1-P3, respectively) and by prolapse of the third eyelid during P2. Arterial plasma glucose, insulin, and glucagon concentrations; hepatic blood flow; and hepatic glucose load did not change significantly during P1-P3. NHGU during P1-P3 was 2.7 +/- 0.4, 4.1 +/- 0.6, and 4.0 +/- 1.2 mg.kg(-1).min(-1) in group 1 and 5.0 +/- 0.9, 5.6 +/- 0.7, and 6.1 +/- 0.9 mg.kg(-1).min(-1) in group 2 (not significant among periods). Interruption of vagal signaling with or without intraportal infusion of norepinephrine to augment sympathetic tone did not suppress NHGU during portal glucose delivery, suggesting the portal signal stimulates NHGU independently of vagal efferent flow.
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PMID:Vagal cooling and concomitant portal norepinephrine infusion do not reduce net hepatic glucose uptake in conscious dogs. 1516 5

Recurrent corneal erosions (RCE) are common. They are characterised by repeated episodes of pain, difficulty in opening the eyes, watering, and photophobia resulting from poor epithelial adhesion. In the majority of patients with RCE, trauma is the initiating factor. Epithelial, stromal, and endothelial corneal dystrophies have all been described in association with RCE. Other causes that may lead to RCE include chemical and thermal injuries, previous herpetic keratitis, meibomian gland dysfunction, ocular rosacea, diabetes mellitus, Salzmann's nodular degeneration, band keratopathy, previous bacterial ulceration, kerato-conjunctivitis sicca, and epidermolysis bullosa. The conditions that are associated with RCE can be either primary or secondary depending on whether the basement membrane complex abnormality is intrinsic or acquired. Primary types tend to be bilateral, symmetrical and develop in multiple corneal locations. The pathogenetic mechanism of this disorder is related to poor adhesion of the corneal epithelium to the underlying stroma. Excessive matrix metalloproteinase (MMP) activity may play a role in the pathogenesis. Although the majority of patients will respond to simple measures such as padding and antibiotic ointment, RCE resistant to simple measures require approaches that are more elaborate. The common goal of these approaches is to encourage proper formation of adhesion complexes between the epithelium and the stroma. The use of long-term contact lenses, autologous serum eye drops, botulinum toxin, induced ptosis, oral MMP inhibitors, diamond burr polishing of Bowman's membrane have been reported with varying degree of success in treating RCE. Anterior stromal puncture with insulin needles or Neodymium : aluminium-yttrium-garnet may enhance the epithelial adhesion to the basement membrane by scar formation and success rates of up to 80% have been reported in the treatment of recalcitrant RCE. Excimer laser photo-therapeutic keratectomy (PTK) is now a well-established treatment modality for RCE and is being used both safely and effectively. Partial ablation of Bowman's layer with PTK gives a smooth surface for the newly generating epithelium to migrate and form adhesion complexes. The pathogenesis, clinical features, and management options of this common disorder are discussed in this review article.
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PMID:Pathogenesis, clinical features and management of recurrent corneal erosions. 1757 Oct 89

We report herein the case of a 28-year-old man presenting with hyperglycemic chorea-ballism (HCB) in addition to mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). He was admitted to a local hospital due to weight loss, general fatigue and thirst. The patient had diabetes mellitus, with a blood glucose level of 738 mg/dl and HbA1c of 19.8%. Although insulin therapy improved hyperglycemia, he noticed involuntary movements in the right upper and lower limbs, which subsequently extended to the left side. The patient was thus transferred to our hospital. He displayed short stature (154 cm) and emaciation, and a maternal family history of diabetes mellitus was elicited. He had no history of stroke-like episode, headache, vomiting and seizure. Neurological examination revealed low intelligence (IQ 57), mild sensorineural deafness, and chorea-ballism in the extremities and head without ptosis or eye movement disturbance. Brain computed tomography (CT) demonstrated areas of high density, while T1-weighted magnetic resonance imaging (MRI) revealed extreme hyperintensity and T2-weighted MRI showed hyperintensity in bilateral caudate nuclei, putamina and globi pallidus. HCB was diagnosed. In, CSF, lactate level was increased to 43.9 mg/dl (n, 4-16), pyruvate level was 1.65 mg/dl (n, 0.3-0.9) and total protein concentration was 59 mg/dl. Histological examination of a biopsy sample from the biceps brachii muscle demonstrated ragged-red fibers. An A3243G point mutation in the tRNA(Leu(UUR)) gene was detected, indicating the presence of MELAS. Involuntary movements improved on treatment with haloperidol up to 4.5 mg/day. HCB usually appears in elderly individuals, and cases less than 40-years-old are very rare. The mitochondrial dysfunction in MELAS may accelerate development of HCB.
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PMID:[A case of MELAS presenting juvenile-onset hyperglycemic chorea-ballism]. 1611 32


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