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At least 667 records · Page 37Linked to original sources
PubMed1996

[Asymptomatic choledochal cyst].

HISTORY AND FINDINGS: A 45-year-old woman sustained an ankle fracture in an accident. At examination she was found to have marked pallor of skin and mucosae. There was no hint for melaena or haematemesis. INVESTIGATIONS: Biochemical tests showed marked iron deficiency anaemia (haemoglobin 7.5 g/dl) and raised serum bilirubin and C-reactive protein levels (1.94 mg/dl and 85.2 mg/l, respectively). Abdominal sonography revealed a cystic space-occupying mass (8 x 4.5 cm) projecting onto the gallbladder, interpreted as a choledochal cyst of unknown origins without bleeding. After treatment of the ankle fracture an endoscopic retrograde cholangiopancreatography was performed. This showed a large cyst of the choledochal duct into which the cystic and choledochal ducts entered, without evidence of tumour or haematoma. There was also a 1 cm prepapillary common choledochal and Wirsung duct. TREATMENT AND COURSE: With these findings, the diagnosis of a congenital choledochal cyst (type Ia of Todani) could be made. After healing of the ankle fracture the cyst was removed and a Roux Y-anastomosis created. The cystic tissue was benign. At follow-up 6 months later the patient was symptom-free and no longer anaemic. CONCLUSIONS: Congenital choledochal cysts are very rare in Europeans. The symptom-free course with anaemia and no manifestation until adulthood is also very unusual.

Anastomosis, Roux-en-Y↗
PubMed1988

[Diagnosis and therapy of dumping syndrome following Nissen fundoplication with reference to pathogenetic aspects].

Between 1982 and 1987 27 Nissen's fundoplications were carried out in our institution. Postoperatively 7 infants showed a typical dumping syndrome. The symptoms were irritability, pallor, sweating, tachycardia, lethargy, diarrhoea and vomiting. In all cases an absolute refusal of feeding was observed. The diagnosis was confirmed by a typical early postprandial hyperglycaemia with hyperinsulinaemia leading to a reactive hypoglycaemia. Additionally, we were able to demonstrate an increased HbA1c as an expression of recurrent hyperglycaemias in 3 infants. In 6 infants the dumping syndrome was of short duration and the symptoms disappeared after application of a so-called dumping diet. In this diet the easily resorbable carbohydrates are replaced by uncooked starch. But in one case we were forced to use continuous enteral nutrition because of persistence of the symptoms 1 year after the Nissen fundoplication. Complete refusal of feeding is an early symptom of the dumping syndrome. If this symptom is observed after a Nissen's fundoplication, a dumping syndrome must be excluded.

Blood Glucose↗
PubMedDate not supplied

[Spontaneous subdural hematoma in a 18-day-old male newborn infant with severe hemophilia A].

Most intracranial bleedings in hemophiliacs occur in patients more than 6 months of age. In the neonatal period, this complication is rare and almost always observed in the first week of life. Based on a review of the literature, intracranial hemorrhage is an exceedingly rare occurrence in infants with hemophilia aged 2 weeks-6 months. We report on a male infant with hemophilia A who was referred to our hospital on day 18 because of pallor and jaundice. The neurological examination was normal. A cerebral ultrasound showed a left sided subdural hematoma with a shift of the midline structures to the right. Packed red blood cells (10 ml/kg) and factor VIII replacement (250 IU) were rapidly instituted and a craniotomy with evacuation of the hematoma was performed. The postoperative course was uneventful. On discharge, the neurological examination was considered normal.

Echoencephalography↗
PubMedDate not supplied

[Neurovegetative symptoms in infants with sleep-related respiratory disorders].

A relationship between neurovegetative symptoms and an increased risk of sudden infant death (SID) has been frequently described. Such symptoms are vomiting because of gastroesophageal reflux, breathing disorders while nutritive sucking, excessive sweating during sleep, prolonged apneas and apneas with associated symptoms, further unexplained episodes of cyanosis, pallor and loss of muscle tone. An acute decompensation of the cardiorespiratory autonomic system during sleep is currently discussed to be one of the causes of SID. Polysomnographic investigations are used to diagnose sleep related cardiorespiratory autonomic dysfunction. In this study, infants up to the age of 5 months were examined using polysomnography throughout their entire nocturnal sleep. The findings from 79 infants with neurovegetative symptoms were compared with the results from 163 healthy control children. Indications of an impaired respiratory regulation during sleep were shown to be significantly more frequent in infants with neurovegetative symptoms. In particular the occurrence of periodic breathing with a high frequency of periodic apnea plus a large number of acute decreases in oxygen saturation could be shown in infants with neurovegetative symptoms. The findings were most pronounced during the first 1.5 months after birth. The results of this investigations lead to the conclusion that, in the case of young infants with breathing abnormalities, neurovegetative symptoms can frequently be observed. The occurrence of such symptoms should therefore be a reason for a polysomnographic examination.

Autonomic Nervous System↗
PubMed1992

[Autoregulation in the choroid].

The cerebral perfusion is continuously and highly sensitively dependent on arterial pCO2. Does the ocular perfusion behave in a similar manner? To answer this question, the authors measured the following parameters before and after the inhalation of 10% CO2: a) the increase of capillary pCO2, using a transcutaneous sensor, and b) the redness (pallor) of the retinal tissue, an expression of its hemoglobin content, was measured at two retinal locations with the Ocular Photometer (OPM). Initial results from young test-volunteers and patients with documented carotis stenoses show that the choroid is able to maintain constant its blood-volume even under changing loads.

Adult↗
PubMed1988

[Autoregulation of the papillary vessels and their behavior as affected by halothane].

Halothane lowers the peripheral vascular resistance and blocks autoregulation in the cerebral vessels. Proceeding from the assumption that the papillary vessels behave in like manner, the authors examined increases in papillary pallor under artificial IOP elevation in anesthetized patients with and without Halothane, using the photopapillometer. This provocation test was conducted in 14 patients, first on one eye under normal (N2O/O2) anesthesia, then on the fellow eye after steady state had been attained with subsequently administered Halothane. By quantifying ocular circulatory conditions, the demonstration of the lowering of peripheral vascular resistance in the papillary vessels under Halothane was convincing; the blockage of autoregulation was less obvious. To explain these results the authors suggest that the two effects are gradual and mutually influential.

Adult↗
PubMed1985

[Myambutol (ethambutol)-induced retinoneuritis].

A retinoneuritis due to ethambutol (Myambutol) occurs with Myambutol doses of over 20 mg/kg per day after 3 weeks to 15 months. Visual acuity can deteriorate within the following 6 months even after immediate discontinuation of treatment with Myambutol. It may recover 2 months (though in some cases only 16 months) after the onset of the deterioration; in cases of optic atrophy a more severe loss of vision usually remains. If there was loss of vision to 1/10 or less there was in most cases no change in the visual acuity. On the other hand, a primary loss of vision to only 0.3 or 0.4 usually ended with recovery of full vision. The occasionally observed clinical picture of a reddish optic disk, retinal hemorrhages, a very fine granular pigment alteration of the macular region, and loss of vision for more than a year without optic disk pallor suggests a toxic retinitis or retinoneuritis rather than neuritis. This is confirmed by electrophysiological observations.

Adult↗
PubMed1982

[Migratory embolism of the retinal artery (author's transl)].

The clinical history of a man suffering from recurrent embolisms of the retinal artery is presented, extending over 11 years from the time when the patient was 57. The initial finding was a retinal artery embolism whose course was photographically recorded for an hour, until the emboli disappeared at the periphery. Three days and between three-and-a-half and six-and-a-half years later there were recurrences of the embolism. The patient's visual acuity dropped from 0.5 after the first, photographically recorded embolism, to 0.05-0.1 after the last. The gravity of the event is documented by the visual field losses in the lower half and the pronounced pallor of the disk.

Aged↗
PubMed1982

[Symptomatology of a primary intraorbital meningioma of the optic nerve].

Report on an 18-year-old man with a histologically confirmed intraorbital meningioma (transitional type) of the right optic nerve. The symptoms were slowly progressive loss of vision with central scotoma and pallor of the disk, without proptosis or disturbance of eye motility. Computer tomography performed preoperatively did not permit the differential diagnosis of glioma.

Adolescent↗
PubMed1994

[Acute ischemia of an arm as an unusual manifestation of ergotism].

A 27-year-old woman developed acute pain, pallor and feeling of cold in her left arm. She had been a smoker of 15-20 cigarettes daily since the age of 15 years, but had not previously had any serious illness. In addition to contraceptives she had had been taking one to several suppositories containing caffeine and ergotamine tartrate (2 mg) daily against migraine. Angiological examination 5 days after onset of symptoms discovered a weak brachial pulse low in the left upper arm, while ulnar and radial pulses were absent. All other pulses were normally palpable. Colour duplex sonography demonstrated occlusion of the brachial artery which angiographically was due to a 5 cm severe narrowing without thrombus, blood flowing distally via collaterals. No improvement was achieved by local injection of 100,000 IU urokinase, 0.5 mg nitroglycerin, 20 mg tolazoline and a 3-hour infusion of alprostadil. On infusion of 560 ml hydroxyethylstarch over 8 hours, 400 mg naftidrofuryl, therapeutic doses of heparin and abstinence from ergotamine (since admission) the vessel diameter increased by 50% within 23 hours and after a further 24 hours to almost 100% of the comparable arterial segment of the right arm while merely on heparin infusion.

Acute Disease↗
PubMed1995

Epidemic optic neuropathy in Cuba--clinical characterization and risk factors.

BACKGROUND: From 1991 to 1993, epidemic optic and peripheral neuropathy affected more than 50,000 people in Cuba. The number of new cases decreased after the initiation of vitamin supplementation in the population. In September 1993, Cuban and U.S. investigators conducted a study to characterize and identify risk factors for the optic form of the syndrome. METHODS: We conducted ophthalmologic and neurologic examinations, assessed exposure to potential toxins, administered a semiquantitative food-frequency questionnaire, and assessed serum measures of nutritional status in 123 patients with severe optic neuropathy, matched for sex and age to randomly chosen normal subjects. RESULTS: In the case patients, prominent clinical features were subacute loss of visual acuity with field defects, diminished color vision, optic-nerve pallor, and decreased sensitivity to vibration and temperature in the legs. Tobacco use, particularly cigar smoking, was associated with an increased risk of optic neuropathy. The risk was reduced among subjects with higher dietary intakes of methionine, vitamin B12, riboflavin, and niacin and higher serum concentrations of antioxidant carotenoids. The risk was also reduced among subjects who raised chickens at home or had relatives living overseas--factors that may be indirect measures of increased food availability. CONCLUSIONS: The epidemic of optic and peripheral neuropathy in Cuba between 1991 and 1993 appears to be linked to reduced nutrient intake caused by the country's deteriorating economic situation and the high prevalence of tobacco use.

Adolescent↗
PubMed1988

Long-term brachial artery catheterization: ischemic complications.

The brachial artery is not used for long-term catheterization and routine hemodynamic monitoring because a high incidence of ischemic complications is anticipated. However, in a review of 157 patients who had 225 percutaneous transbrachial hepatic artery catheters placed for infusion of chemotherapeutic agents, catheters remained in situ from 1 day to 14 months (median 68 days). One hundred seventy-three catheters (77%) were removed electively and 52 catheters (23%) were removed because of complications. Diminution or loss of the radial pulses occurred on insertion of 88 catheters (39.1%) and 16 of these (8%) were removed after 24 hours because ischemic symptoms developed. Subsequently, 25 other catheters (11.1%) were removed because of complications such as paresthesia, eight (3.5%); brachial artery thrombosis, four (1.7%); microembolization, three (1.3%); claudication, two (0.8%); and pseudoaneurysm, one (0.4%). Seven catheters (3.1%) were removed because of a combination of pallor, diminished pulses, and muscle weakness. Hemorrhage from the arteriotomy site necessitated the removal of 11 other catheters (4.9%). Amputation, ischemic ulceration, major neuromuscular sequelae, and peripheral embolization to the head or lower limbs did not occur. This study suggests that long-term brachial artery catheterization is associated with a low incidence of permanent ischemic complications.

Antineoplastic Agents↗
PubMed2002

Severe iron deficiency anemia in transgenic mice expressing liver hepcidin.

We recently reported the hemochromatosis-like phenotype observed in our Usf2 knockout mice. In these mice, as in murine models of hemochromatosis and patients with hereditary hemochromatosis, iron accumulates in parenchymal cells (in particular, liver and pancreas), whereas the reticuloendothelial system is spared from this iron loading. We suggested that this phenotypic trait could be attributed to the absence, in the Usf2 knockout mice, of a secreted liver-specific peptide, hepcidin. We conjectured that the reverse situation, namely overexpression of hepcidin, might result in phenotypic traits of iron deficiency. This question was addressed by generating transgenic mice expressing hepcidin under the control of the liver-specific transthyretin promoter. We found that the majority of the transgenic mice were born with a pale skin and died within a few hours after birth. These transgenic animals had decreased body iron levels and presented severe microcytic hypochromic anemia. So far, three mosaic transgenic animals have survived. They were unequivocally identified by physical features, including reduced body size, pallor, hairless and crumpled skin. These pleiotropic effects were found to be associated with erythrocyte abnormalities, with marked anisocytosis, poikylocytosis and hypochromia, which are features characteristic of iron-deficiency anemia. These results strongly support the proposed role of hepcidin as a putative iron-regulatory hormone. The animal models devoid of hepcidin (the Usf2 knockout mice) or overexpressing the peptide (the transgenic mice presented in this paper) represent valuable tools for investigating iron homeostasis in vivo and for deciphering the molecular mechanisms of hepcidin action.

Anemia, Iron-Deficiency↗
PubMed1996

Arrested development of embryonic red cell precursors in mouse embryos lacking transcription factor GATA-1.

The X chromosome-linked transcription factor GATA-1 is expressed specifically in erythroid, mast, megakaryocyte, and eosinophil lineages, as well as in hematopoietic progenitors. Prior studies revealed that gene-disrupted GATA-1- embryonic stem cells give rise to adult (or definitive) erythroid precursors arrested at the proerythroblast stage in vitro and fail to contribute to adult red blood cells in chimeric mice but did not clarify a role in embryonic (or yolk sac derived) erythroid cells. To examine the consequences of GATA-1 loss on embryonic erythropoiesis in vivo, we inactivated the GATA-1 locus in embryonic stem cells by gene targeting and transmitted the mutated allele through the mouse germ line. Male GATA-1- embryos die between embryonic day 10.5 and 11.5 (E10.5-E11.5) of gestation. At E9.5, GATA-1- embryos exhibit extreme pallor yet contain embryonic erythroid cells arrested at an early proerythroblast-like stage of their development. Embryos stain weakly with benzidine reagent, and yolk sac cells express globin RNAs, indicating globin gene activation in the absence of GATA-1. Female heterozygotes (GATA-1+/-) are born pale due to random inactivation of the X chromosome bearing the normal allele. However, these mice recover during the neonatal period, presumably as a result of in vivo selection for progenitors able to express GATA-1. Our findings conclusively establish the essential role for GATA-1 in erythropoiesis within the context of the intact developing mouse and further demonstrate that the block to cellular maturation is similar in GATA-1- embryonic and definitive erythroid precursors. Moreover, the recovery of GATA-1+/- mice from anemia seen at birth provides evidence indicating a role for GATA-1 at the hematopoietic progenitor cell level.

Alleles↗
PubMed1999

Inhibition of nitric-oxide synthase 2 by aminoguanidine provides neuroprotection of retinal ganglion cells in a rat model of chronic glaucoma.

Glaucoma is an optic neuropathy with cupping of the optic disk, degeneration of retinal ganglion cells, and characteristic visual field loss. Because elevated intraocular pressure (IOP) is a major risk factor for progression of glaucoma, treatment has been based on lowering IOP. We previously demonstrated inducible nitric-oxide synthase (NOS-2) in the optic nerve heads from human glaucomatous eyes and from rat eyes with chronic, moderately elevated IOP. Using this rat model of unilateral glaucoma, we treated a group of animals for 6 months with aminoguanidine, a relatively specific inhibitor of NOS-2, and compared them with an untreated group. At 6 months, untreated animals had pallor and cupping of the optic disks in the eyes with elevated IOP. Eyes of aminoguanidine-treated animals with similar elevations of IOP appeared normal. We quantitated retinal ganglion cell loss by retrograde labeling with Fluoro-Gold. When compared with their contralateral control eyes with normal IOP, eyes with elevated IOP in the untreated group lost 36% of their retinal ganglion cells; the eyes with similarly elevated IOP in the aminoguanidine-treated group lost less than 10% of their retinal ganglion cells. Pharmacological neuroprotection by inhibition of NOS-2 may prove useful for the treatment of patients with glaucoma.

Animals↗
PubMed2000

Association of ocular pressure and optic disc cup volume with red blood cell sodium-potassium ATPase inhibition.

PURPOSE: To determine if there were significant differences between the number of red blood cell ouabain binding sites in normals and untreated ocular hypertensives plus one open-angle glaucoma patient. METHODS: We measured the binding of (3)H ouabain to erythrocyte membranes of 23 normals, 25 ocular hypertensives and one open-angle glaucoma. We also measured the levels of plasma cortisol and digoxin in these subjects. Characteristics of cupping of the optic disc and thickness of the retinal nerve fiber layer, as well as area of optic disc pallor of these subjects were measured by stereophotogrammetry and by computerized image analysis from single and stereo photographs. RESULTS: The number of (3)H ouabain binding sites was observed to be significantly less in the ocular hypertensives and one glaucoma compared to the normals (p = 0.0009). In multi-variate analyses, to determine what other factors affected this difference, there was a significant negative association with mean intraocular pressure (p = 0.003) (average of both eyes) and total cup volume (average of both eyes) (p = 0.005), diagnosis of ocular hypertension and glaucoma (p = 0.0005) and male gender (p = 0.019). There was a significant positive association with plasma cortisol levels (p = 0.048), and diastolic blood pressure (p = 0.037). CONCLUSIONS: The number of (3)H ouabain binding sites in red blood cells decreases significantly with increasing ocular pressure and increasing cup volume indicating the possible presence of an increased systemic endogenous digoxin-like inhibitor and/or difference in the isozymes of Na(+), K(+)-ATPase which may be associated with increased levels of plasma cortisol in ocular hypertensives and glaucomas.

Binding Sites↗
PubMed2003

Ophthalmic manifestations of congenital disorder of glycosylation type 1a.

PURPOSE: To present the ophthalmic manifestations of patients with congenital disorder of glycosylation type Ia (CDG-Ia) due to the frequent R141H/F119L PMM2 genotype. METHODS: Ophthalmic records of 23 patients (age: 10 months to 20 years) were evaluated. They had had at least one ophthalmic reexamination. RESULTS: Measurements of refractive error showed that 18 patients were myopic, two were hypermetropic, and three could not be measured. Serial measurements in 12 patients indicated a progression towards myopia of 0.80 diopters (D) per year. Congenital esotropia and delayed visual maturation (DVM) were consistent findings. Two children developed good visual acuity (VA), 16 had low vision, and five were legally blind. Pallor of the optic disc was noted in five patients. Electroretinography (ERG) performed in nine patients showed reduced rod responses, while cone responses were only slightly reduced. CONCLUSIONS: The present study illustrates the difficulties in examining severely disabled children. Consistent ophthalmic manifestations of CDG-Ia patients due to the R141H/F119L genotype were congenital esotropia, DVM, and a reduced rod response in ERG-examined patients. The vast majority of patients had reduced VA and developed myopia. We speculate that there is a relationship between the glycosylation defect in CDG-Ia and the development of myopia. We recommend that CDG-Ia patients be followed annually by an ophthalmologist.

Acyl Carrier Protein↗
PubMed2001

Unilateral congenital oculomotor nerve palsy, optic nerve hypoplasia and pituitary malformation: a preliminary report.

A newborn male presented with complete external third nerve palsy of his right eye immediately at birth. Pediatric examination and MRI of the skull revealed no abnormalities. At the age of six weeks, strabismus surgery was performed to facilitate amblyopia treatment. The muscles appeared small and fibrotic. At the age of ten weeks, a brow suspension of the upper lid and a second strabismus surgery were performed. The amblyopia treatment and patching, applied for half of the waking hours over a period of six weeks, were unsuccessful. At the age of six months, a relative pallor of the right optic nerve head became evident. At the age of three years, at a new examination because of growth deficiency, a second MRI revealed defects involving the pituitary region. We concluded that extraocular muscle abnormality or oculomotor nerve palsy was present together with optic nerve dysplasia and pituitary gland malformation.

Amblyopia↗