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At least 163 records · Page 9Linked to original sources
PubMed1989

Inflammatory siderosis of the nervous system in rats.

Large intravenous doses of a relatively nontoxic iron polymaltose complex were taken up by liver and spleen and did not enter the central nervous system (CNS) of normal rats. When the injections were given during development of the inflammatory lesions of experimental allergic encephalomyelitis (EAE), many iron-laden macrophages entered vessels, perivascular cuffs and neural parenchyma. Iron polymaltose injected before the EAE lesions started to develop, or during the healing phase, did not enter the lesions. This model of CNS siderosis may be useful for studies on long-term effects of iron and for neuroimaging by nuclear magnetic resonance.

Animals↗
PubMed1981

Siderosis from a retained intraocular stone.

A penetrating intraocular stone caused a retinal detachment that was repaired successfully. The patient returned 18 months later with siderosis bulbi. The patient was followed by serial neurosensory tests for the next three years. The electro-oculogram (EOG) showed the greatest abnormality, while the electroretinogram (ERG) and dark adaptation, although initially affected, showed no further deterioration. Surgical procedures on this eye included linear extraction of the siderotic lens, anterior vitrectomy, and irrigation of a hyphema. Fluorescein angiogram revealed a siderotic deposit on the retina. Progressive visual field loss prompted removal of the stone foreign body by an eye-wall resection technique. Five years later vision was 20/30. While dark adaptation, EOG, and ERG remained stable, the visual fields showed progressive constriction. Fluorescein angiogram revealed pigment epithelial defects, cystoid macular edema, reduced peripheral circulation, and progressive clearing of the retinal iron deposits.

Adult↗
PubMed1998

Neonatal intrahepatic cholestasis with hepatic siderosis and steatosis.

Neonatal intrahepatic cholestasis is a heterogeneous disease of undetermined cause. There is an unreported subset of idiopathic neonatal intrahepatic cholestasis with an unusual histological combination of hepatic siderosis and macrovesicular steatosis. The patients were a 34-day-old female and a 39-day-old male with normal birth weights. Their mothers had received oral iron supplement 4-6 weeks before delivery. The patients had obstructive jaundice noticed at the well-baby clinic at 1 month of life. They had high levels of serum galactose and tyrosine, hyperferritinemia. Urinary organic acid and bile acid analyses were negative, and galactose-1-phosphate uridyltransferase activity in red cells was normal. Liver biopsies showed diffuse iron deposits and macrovesicular fat. By substituting formula milk with lactose-free milk, the patients responded, and had normal biochemical tests within 5 months of life. Follow-up biopsies, at the age of 12 months, showed mild residual fibrosis without iron or fat deposits. They are both well at 3 and 6 years of age, respectively, without biochemical liver dysfunction and neurologic impairment. Prenatal iron-overload might contribute to the pathogenesis of the disease, but further studies are needed to confirm the assumption.

Cholestasis, Intrahepatic↗
PubMed1980

Generalised siderosis from an iris foreign body.

A case is presented of generalised siderosis resulting from a foreign body lodged in the iris. The diagnosis was made 10 years after the initial injury, when the patient presented with another, quite unrelated, eye injury. The metal particle was removed after tests revealed that ocular function was impaired with raised intra ocular pressure, severe field loss and an abnormal electroretinogram (E.R.G.).

Adult↗
PubMedDate not supplied

Transferrin glycans: a possible link between alcoholism and hepatic siderosis.

The hepatic uptake of 59Fe from diferric rat and rabbit asialotransferrins and from human transferrin lacking two sialyl residues was investigated in rats in experiments lasting for 1 hr. The 59Fe attached to either of these preparations disappeared from the plasma more rapidly than the 59Fe introduced with the unmodified respective parent proteins. Most of the 59Fe activity that had disappeared from the circulation could be recovered with the liver. Studies with double-labeled (125I, 59Fe) preparations showed that the enhanced 59Fe clearance was not associated with increased catabolism of the modified transferrins. Prolonged, heavy alcohol consumption, as shown by others, results in the appearance of sialic acid-deficient transferrin (two residues missing) in human serum. We suggest that the increased capacity of transferrin deficient in sialic acid to selectively deposit iron in the hepatocyte may be of significance for the development of the hepatic siderosis observed in alcoholism.

Alcoholism↗
PubMed1985

Experimental ocular siderosis after extrabulbar administration of iron.

The authors studied the penetration of iron administered extrabulbarly into the ocular tissues of rabbits. It was found that iron passes from the orbit into the eyeball and accumulates in considerable quantities in the sclera, choroid, retina, ciliary body, and even in the vitreous and corneal epithelium. However, light microscopy failed to show any damage to the ocular tissues. The mechanism by which iron penetrates into the eyeball is discussed, and comparison is made between changes in the tissues, which characterise siderosis produced by an intrabulbar iron foreign body, and those in which an extrabulbar foreign body is involved.

Animals↗
PubMed1969

Aetiology of extrahepatic epithelial iron deposits in siderosis in Bantu.

Twenty-seven specimens of human tissue, obtained by operation, were tested to evaluate the theory that iron uptake by tissues from serum is greater when transferrin is nearly completely saturated than when the degree of saturation is normal. Samples of each tissue were incubated in autologous serum so prepared that in one instance the transferrin was 50% saturated and in the second 90% saturated with iron containing (59)Fe. In all samples the uptake of iron was greater from the transferrin which was 90% saturated. The uptake by tissues of epithelial origin was significantly greater than that by non-epithelial tissues. Considerable variation in uptake was noted between samples of the same tissue from different individuals. The role of iron stores in the tissue and folic acid deficiency are discussed. It is concluded that the degree of transferrin saturation is important in determining iron uptake by tissues, especially in those of epithelial origin, and that such uptake may be modified by tissue stores and folic acid deficiency. It is felt that these factors are probably responsible for the extrahepatic parenchymal deposits of iron sometimes found in Bantu subjects with siderosis.

Epithelium↗
PubMed2004

The importance of suspecting superficial siderosis of the central nervous system in clinical practice.

Once the central nervous system surface is greatly encrusted with haemosiderin, even removing the source of bleeding will have little effect on the progression of clinical deterioration. Superficial siderosis of the central nervous system is rare and insidious, but magnetic resonance imaging has turned a previously late, mainly autoptical diagnosis into an easy, specific, in vivo, and possibly early one. Avoiding long diagnostic delay will be very important in those cases susceptible of causal treatment.

Aged↗
PubMedDate not supplied

Superficial siderosis of the central nervous system. A case report on examination by ECoG and DPOAE.

This is a case of superficial siderosis of the central nervous system (SSCN). The diagnosis of SSCN was based on the result of T2-weighted magnetic resonance imaging and on suggestive clinical manifestations. The pure-tone audiogram showed bilateral progressive sensorineural hearing loss with a poor speech discrimination score and Jerger type IV. The remarkable elevation of the detective threshold of cochlear microphonics on electrocochleography was found and distortion product otoacoustic emission (DPOAE) showed no response: These electrophysiologic examinations, including electrocochleography and DPOAE, revealed that the progressive sensorineural hearing loss in this case was caused by both retrocochlear and cochlear damages.

Central Nervous System Diseases↗
PubMedDate not supplied

Superficial siderosis of the central nervous system: a 70-year-old man with ataxia, depression and visual deficits.

BACKGROUND: Superficial siderosis of the central nervous system (SSNS) is caused by cerebral, cerebellar and spinal cord tissue deposition of hemosiderin, often related to repeated episodes of subarachnoid hemorrhage. Typical symptoms include ataxia, sensorineural deafness and dementia. METHODS AND RESULTS: An elderly patient with SSNS presenting with ataxia, depression and severe visual impairment was admitted to the Unit of Geriatrics of the University Hospital of Perugia, Italy. Late diagnosis and the association of symptoms with SSNS prevented the possible surgical treatment of the disease. CONCLUSIONS: Recognition of uncommon clinical variants may facilitate early diagnosis of SSNS and improve therapeutic results.

Aged↗
PubMed1992

Superficial siderosis of the central nervous system: neuroradiological evaluation of two cases.

We present 2 cases of superficial siderosis of the central nervous system secondary to chronic subarachnoid bleeding. The diagnosis was made with MR and cerebrospinal fluid (CSF) examination. MR showed, in T2-weighted images, superficial hypointensity of the cervical cord, brainstem, cerebellum, and basal cisterns due to hemosiderin deposits. CSF was xanthochromic, with increased protein content. In 1 of the 2 cases also the CT examination was positive, showing a hyperdense rim around the brainstem. A complete neuroradiological evaluation (MR, CT, angiography and myelography) did not permit to detect the source of the bleeding.

Central Nervous System Diseases↗
PubMed1989

Siderosis bulbi induced by intraocular lens implantation.

A 43-year-old man had a silent intraocular foreign body at the ciliary body that was composed of iron. Siderosis bulbi was observed after an extracapsular cataract extraction with intraocular lens implantation was performed. The mechanical forces applied during the surgery might have been responsible for liberating the ferrous ion into the globe.

Adult↗
PubMed1992

Superficial siderosis of the central nervous system: a neglected cause of sensorineural hearing loss.

Superficial siderosis of the central nervous system is a rare, often unrecognized condition in which there is a deposition of intracellular and extracellular hemosiderin in the leptomeninges, subpial tissue, spinal cord, and cranial nerves as a result of chronic bleeding in the subarachnoid space. On the basis of our cases and a review of the literature, the majority of patients manifest sensorineural hearing loss in addition to cerebellar dysfunction, pyramidal tract signs, and progressive mental deterioration. Recent imaging techniques--particularly CT and MRI--can define the presence of iron deposition, confirming the diagnosis ante mortem. From post mortem specimens, histologic sections demonstrate severe damage to the eighth nerve, with microglial metabolism of iron. Cases will be presented to illustrate these points.

Adult↗
PubMed1999

Evidence for preganglionic pupillary involvement in superficial siderosis.

A 36-year-old man presented with spinal myoclonus, ataxia, hearing loss, and unilateral pupillary dilation. MRI demonstrated hemosiderin deposition along the superficial surfaces of the brain, brainstem, cerebellum, and spine. The pupillary changes were localized to the preganglionic oculomotor nerve. In contrast to vasculopathic oculomotor nerve palsies, superficial siderosis may cause selective involvement of the superficially located pupillary fibers.

Adult↗
PubMed2004

Delayed central nervous system superficial siderosis following brachial plexus avulsion injury. Report of three cases.

Chronic subarachnoid hemorrhage may cause deposition of hemosiderin on the leptomeninges and subpial layers of the neuraxis, leading to superficial siderosis (SS). The symptoms and signs of SS are progressive and fatal. Exploration of potential sites responsible for intrathecal bleeding and subsequent hemosiderin deposition may prevent disease progression. A source of hemorrhage including dural pathological entities, tumors, and vascular lesions has been previously identified in as many as 50% of patients with SS. In this report, the authors present three patients in whom central nervous system SS developed decades after brachial plexus avulsion injury. They believe that the traumatic dural diverticula in these cases may be a potential source of bleeding. A better understanding of the pathophysiology of SS is important to develop more suitable therapies.

Adult↗
PubMed2000

Hemochromatosis gene mutations in chronic hepatitis C patients with and without liver siderosis.

Chronic hepatitis C is often associated with liver iron overload, which may affect the long-term prognosis and the response to antiviral treatment. The occurrence of hemochromatosis (HFE) mutations were studied to determine whether may contribute to the liver iron overload of chronic hepatitis C patients. The prevalence of two HFE mutations (C282Y and H63D) in 120 chronic hepatitis C patients was determined and the findings were correlated with clinical, histological and virological features. Hepatic iron was determined semiquantitatively by a histochemical hepatic iron index, defined as the ratio of a histochemical staining score to the patient's age, after correction for heterogeneous lobular iron distribution. Serum hepatitis C virus (HCV) RNA was measured by bDNA assay and typed by restriction fragment length polymorphism. Liver HCV RNA was measured by a semi-quantitative strand-specific reverse transcription-polymerase chain reaction (RT-PCR). Excess liver iron was stained in the liver of 36 patients (30%). Siderotic patients had the same geographic origin, serum and liver HCV RNA levels and H63D and C282Y mutations frequency as non-siderotic patients. However, siderotic patients were older (P = 0.015), more frequently males (P = 0.02), less frequently infected with HCV genotype 3 (P = 0.037) and had a higher liver fibrosis score (P = 0.008). The liver iron content did not correlate with the serum or liver HCV RNA titers. Ten of the 36 patients with liver siderosis had neither a history of excess alcohol intake, multiple transfusions, or HFE mutations. In conclusion, the pathogenesis of the liver iron overload in chronic hepatitis C patients cannot be fully explained by the occurrence of HFE mutations. The exact mechanism of iron accumulation in these patients therefore remains unexplained.

Adult↗