Gene/Protein Disease Symptom Drug Enzyme Compound
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 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 9-year-old girl and an 11-year-old boy had ptosis, progressive external ophthalmoplegia, pigmentary retinopathy, and sensorineural hearing loss. The girl had diabetes mellitus and the boy had hypoparathyroidism. Both children also developed recurrent vomiting and cerebral infarcts with lactic acidosis. Muscle biopsy specimens showed ragged-red fibers and Southern analysis demonstrated a distinct heteroplasmic deletion of muscle mitochondrial DNA in each patient but no evidence of the point mutation in the transfer RNALeu(UUR) gene recently identified in mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). These 2 children had combined features of Kearns-Sayre syndrome and MELAS, suggesting that mitochondrial DNA deletions occasionally can have pleomorphic clinical expression.
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PMID:Deletion of mitochondrial DNA in patients with combined features of Kearns-Sayre and MELAS syndromes. 189 71

Disorders of ocular motility usually present with double vision which may be accompanied by ptosis and pupillary changes. The differential diagnosis comprises supranuclear, nuclear and infranuclear palsies and diseases of the myoneural junction. Accurate assessment is important, since the aetiological possibilities include neurosurgical emergencies such as intracranial aneurysm and systemic problems such as diabetes mellitus.
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PMID:Disorders of ocular motility. 202 91

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 the last five years, 500 one-eyed patients have undergone cataract surgery at the authors' hospital. A Simcoe-type posterior chamber lens was implanted in 425 of the eyes. An eye was defined as an only eye if corrected vision in the fellow eye was 1/60 or less, or better vision in cases of amblyopia. The main causes of loss of function in partner eyes were macular degeneration, amblyopia, and glaucoma. The rate of intraoperative and postoperative complications was the same as in the entire patient collective, and in absolute terms actually lower. There were four cases of intraoperative rupture of the posterior capsule (in two of which it subsequently proved possible to fit a posterior chamber intraocular lens (PCIOL], and one case each of corneal decompensation and excessive hemorrhage into the anterior chamber. PCIOLs were subsequently also implanted in both these eyes. Early postoperative complications included several cases of iris prolapse, all of which were easily rectified, and intermittent phases of endothelial decompensation associated with cornea guttata. In view of the low overall rate of intraoperative and postoperative complications, the authors advocate implantation of a PCIOL in remaining eyes with visual function, except those with proliferative retinopathies (primarily diabetes mellitus), pre-existing retinal detachments (particularly in young men with myopia and a history of detachment in the fellow eye), and unregulated glaucoma.
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PMID:[Cataract operations on the remaining eye]. 322 54

An alcoholic man with uncontrolled diabetes mellitus had right conjunctivitis, facial numbness, and periorbital edema progressing to bilateral visual loss, and left ptosis in association with a large necrotic palatal ulcer due to zygomycosis. The infection progressed to bilateral retinal vein engorgement; left-sided ophthalmoplegia, fixed dilated pupil, and absent corneal reflex; and right-sided ophthalmoplegia, ptosis, and facial nerve paralysis. Work-up revealed disease of both ethmoid sinuses and the right maxillary sinus, with bilateral thromboses of the cavernous sinuses. An aggressive combined therapeutic attack (three Caldwell-Luc procedures, exploration of orbit walls, control of diabetes, systemic and local amphotericin therapy) led to survival with a three-year follow-up thus far.
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PMID:Survival in cerebro-rhino-orbital zygomycosis and cavernous sinus thrombosis with combined therapy. 370 11

This review summarizes those neurological diseases which are accompanied by a drooping of the upper lid, due to weakness of the m. levator palpebrae or m. tarsalis respectively. After connatal ptosis with or without involvement of other bulbar muscles the different types of muscular dystrophies are mentioned. Myositis, disturbances of potassium regulation and myasthenia gravis are other causes of ptosis. Diseases involving the oculomotor nerve (aneurysm, upper herniation, cavernous sinus thrombosis, orbital cavity processes, superior orbital fissure syndrome) may lead to associated ptosis. Metabolic disturbances, such as diabetes mellitus, Wernicke's encephalopathy and botulism may be accompanied by ptosis. Infectious diseases such as polyneuritis, meningitis or encephalitis can lead to ptosis. Sympatholytic ptosis is due to diseases of the central or peripheral course of the sympathetic nerve from the diencephalon via the cervical medulla, the neck, internal carotid artery to the superior orbital fissure. This type of ptosis is usually accompanied by miosis and often by sweating loss on the same side.
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PMID:[Ptosis in the differential diagnosis of neurologic diseases]. 640 79

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

In connection with 4 new cases of Kearns syndrome (multisystem form of mitochondrial CPEO), the condition was found to be present in slight to oligosymptomatic form in all 4 families. The marker symptom in subclinical patients was nearly always ptosis (sometimes very slight) and occasionally diabetes. In the literature other endocrine disorders, retinal anomalies, deafness, growth disturbances, etc., have been noted as subclinical symptoms in former generations. Heredity appears to be autosomal dominant in these 4 families, with very variable expressivity. The possibility that one gene is responsible for the disease seems to be plausible, but the marked variation in expressivity suggests a modifying influence of other alleles; in this sense, therefore, one may speak of multifactor inheritance. Supporting facts could also be found in the literature, where there was autosomal dominant heredity of the disease-carrying gene, but for its complete expression 'amplifying' factors (alleles) were needed. The pleiotropia of the disease-carrying gene is explained by a mitochondrial disorder of various organs. On the basis of the heredity, therefore, Kearns syndrome is not a syndrome but a disease. The most serious, most progressive and most extensive (multisystem) variant of Kearns disease is the infantile form, known as the 'Kearns-Sayre syndrome. When the expressivity of the disease is less extensive it usually occurs later in life and is less progressive: the adult form of Kearns disease.
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PMID:Kearns syndrome: a heterogeneous group of disorders with CPEO, or a nosological entity? 706 93

94 maternal deaths and 1546 fetal and neonatal deaths were registered among 28,706 births at the CHU Averroes in Casablanca between 1978-80. 45% of women who deliver at the clinic are very poor and only 10% are relatively well off. Obstetrical antecedents were noted in 27% of the fetal deaths. 70% of the maternal deaths occurred in women aged 20-34. 32 maternal deaths occurred among 16,232 women with 1-2 children, 30 among 6514 women with 3-5 children, and 32 among 5960 women with 6-14 children. 11,027 of the 28,706 were primaparas. Perinatal mortality was 4.46% among primaparas, 8.24% among grand multiparas, and 4.1% among secondiparas. In 58 of the 94 cases of maternal mortality the woman was hospitalized after attempting delivery at home or in a village clinic. Among women with 1 or 2 children, hemorrhage was the cause of death in 8 cases, infection in 7 cases, eclampsia in 3 cases, thromboembolism in 2 cases, uterine inversion in 2 cases, pulmonary tuberculosis in 1 case, embolism in 5 cases, and other causes 1 case each. Among women with 3-5 children hemorrhage was the cause of death in 10 cases, septicemia in 3 cases, uterine rupture in 3 cases, eclampsia in 3 cases, uterine inversion in 2 cases, viral hepatitis in 2 cases, emboli in 2 cases, and other reasons 1 case each. Among grand multiparas hemorrhage was the cause of death in 11 cases, uterine rupture in 12 cases, peritonitis in 2 cases, eclampsia in 2 cases, emboli in 2 cases, and other causes 1 case each. 19 of the maternal deaths were judged to have been avoidable with better management. Prematurity and birth weight of 1000-2500 g associated or not with other pathology were found in 714 of 1546 perinatal deaths. Of 390 cases of death in utero with retention and maceration, 68 were caused by reno-vascular syndromes, 76 by maternal infections, 33 by maternal syphilis, 26 by fetal malformation, 18 by maternal diabetes, 10 by Rh incompatability, and 159 by indeterminate causes. In 795 cases of intrapartum mortality without maceration, 114 were caused by retroplacental hematomas, 61 by placenta previa, 74 by uterine rupture, 119 by prolapse of the cord, 51 by fetal malformation, 45 by dystochia, 53 by twin pregnancies, 104 by fetal distress, 44 by obstetrical trauma, 55 by prematurity, and 75 by undetermined causes. In 361 cases of early neonatal mortality, 88 were caused by renovascular syndromes, 24 by diabetes, 13 by Rh incompatibility, 34 by placenta previa, 94 by prematurity, 28 by fetal malformation, 35 by fetal infections, 31 by fetal distress, and 14 by obstetrical trauma. The rates of maternal and perinatal mortality are very high compared to those of European countries.
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PMID:[Maternal mortality and perinatal mortality]. 720 85


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