Cases reported "Siderosis"

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1/112. siderosis bulbi resulting from an intralenticular foreign body.

    PURPOSE: To report a case of siderosis bulbi that resulted from a small intralenticular foreign body. METHOD: Case report. RESULTS: A 36-year-old man with normal visual acuity and a peripheral intralenticular iron foreign body in the left eye was treated conservatively. Nine weeks after the injury, he had ocular signs of siderosis bulbi, with changes in the electroretinogram. A clear lens aspiration with removal of the foreign body was performed. After removal of the iron foreign body, no progression or regression of the ocular signs of siderosis bulbi has occurred, and the electroretinogram has not changed over a 2-year period. CONCLUSIONS: Even in the presence of good vision, a patient with an intralenticular ferrous foreign body should be followed closely, and the foreign body should be removed before irreversible siderosis bulbi occurs. ( info)

2/112. Ferumoxide-enhanced MRI of sideronecrosis superimposed on genetic hemochromatosis.

    Genetic hemochromatosis is an autosomal recessive disorder characterized by excessive iron absorption from the gut, resulting in increased total body iron stores, multisystem organ dysfunction, and an increased risk of hepatocellular carcinoma. The magnetic susceptibility effects of excess hepatocellular iron generally cause diffuse hepatic signal loss on T2- or T2*-weighted MR images. Although hepatic iron deposition is usually diffuse, focal areas of iron sparing can occur, and, when present, superimposed neoplasm is a consideration. We describe a patient with cirrhosis, hemochromatosis, and multiple small benign relatively hyperintense iron-poor foci consisting of piecemeal sideronecrosis. ( info)

3/112. Corneal iron ring after hyperopic laser-assisted in situ keratomileusis.

    PURPOSE: To report a new corneal iron ring after hyperopic laser-assisted in situ keratomileusis (LASIK). methods: Three patients underwent hyperopic LASIK for the correction of hyperopia in both eyes. Spherical equivalent refraction of the patients ranged from 3.37 to 6.50 diopters. LASIK procedure was performed using automated corneal shaper and 193-nm argon fluoride excimer laser. RESULTS: Both eyes of the patients were noted to have a corneal iron ring located at the paracentral area at 6-7 months after surgery. The localization of iron ring corresponded with outside border of central steep zone. Twelve-month examination showed there was no change in color, shape, and density of corneal iron ring. CONCLUSIONS: Corneal topographic changes induced by hyperopic LASIK may cause corneal iron ring to develop. ( info)

4/112. Pseudo-Fleischer ring after hyperopic laser in situ keratomileusis.

    A 37-year-old woman had bilateral hyperopic laser in situ keratomileusis (LASIK). Six months postoperatively, an epithelial pigmentation ring pattern was identified on both corneas. The appearance of the ring pattern was similar to the iron deposits of the Fleischer ring of keratoconus. While corneal iron deposits in various patterns have been reported after other forms of ocular therapeutic and refractive surgery, this is the first report of the association between hyperopic LASIK and a corneal iron line, which we have called the "pseudo-Fleischer ring." ( info)

5/112. Superficial siderosis of the CNS associated with multiple cavernous malformations.

    Superficial siderosis of the CNS due to chronic, recurrent subarachnoid hemorrhage is an uncommon and potentially debilitating disorder. The classic clinical manifestation is progressive bilateral sensorineural hearing loss (SNHL), although ataxia and pyramidal signs also are observed frequently. Cavernous malformations rarely present with subarachnoid hemorrhage. We describe an unusual case of a young patient who presented with progressive, bilateral SNHL who was found to have superficial CNS siderosis associated with multiple cavernous malformations. ( info)

6/112. 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. ( info)

7/112. Erosive injury to the upper gastrointestinal tract in patients receiving iron medication: an underrecognized entity.

    Severe gastrointestinal necrosis and strictures after an iron overdose are well described. However, mucosal injury in patients receiving therapeutic iron has received only scant recognition despite its wide use. We studied the clinical and histologic features of 36 upper gastrointestinal tract biopsies from 33 patients (24 gastric, 9 esophageal, 1 gastroesophageal junction, and 2 duodenal) containing characteristic brown crystalline iron material, and evaluated the amount and tissue distribution of the iron. In addition, we investigated the prevalence of iron-associated mucosal injury in upper gastrointestinal endoscopic examinations. The majority of the biopsies (32 of 36, 89%) contained luminal crystalline iron adjacent to the surface epithelium or admixed with luminal fibrinoinflammatory exudate. Thirty biopsies (83%) showed crystalline iron deposition in the lamina propria, either covered by an intact epithelium, subjacent to small superficial erosions, or admixed with granulation tissue. Three biopsies (8%) demonstrated iron-containing thrombi in mucosal blood vessels. Erosive or ulcerative mucosal injury was present in 30 of 36 biopsies (83%). The amount of iron accumulation in cases with mucosal injury was greater than in cases without mucosal injury (mean grades, 2.4 vs. 1.3 on a 1 to 3 scale; p = 0.002). iron medication was confirmed in 25 of 33 patients (76%) 22 patients were receiving ferrous sulfate. Approximately half of the patients (17 of 33, 51%) also had underlying infectious, mechanical, toxic, or systemic medical conditions that could have initiated or exacerbated tissue injury. Crystalline iron deposition was found in 0.9% of upper gastrointestinal endoscopic examinations (12 of 1,300), and iron medication-associated erosive mucosal injury was present in 0.7% (9 of 1,300). These results indicate that crystalline iron deposition in the upper gastrointestinal tract is not uncommon. It can induce or exacerbate a distinctive histologic pattern of erosive mucosal injury, especially in patients with associated upper gastrointestinal disorders. Recognition of this pattern by pathologists and its communication to clinicians may aid in optimizing therapy. ( info)

8/112. Transthyretin amyloidosis and superficial siderosis of the CNS.

    OBJECTIVE: To describe a previously unreported clinical and radiologic presentation of hereditary transthyretin (TTR)-related amyloidosis. BACKGROUND: Unexplained cerebellar ataxia, pyramidal syndrome, and hearing loss are observed in some patients with TTR-related amyloidoses. methods: We performed clinical, radiologic, and pathologic examinations of three family members with TTR-related (Ala36Pro) amyloidosis. RESULTS: The patient was a 69-year-old woman with vitreal amyloid deposits, progressive sensorineural deafness, cerebellar ataxia, pyramidal syndrome, and recurrent transient neurologic symptoms. Cranial MRI showed symmetric thin rims of low signal intensity in T2- and T2*-weighted images in the cortex of the sylvian fissures, of the cerebellar hemispheres and vermis, and in the quadrigeminal plate consistent with superficial siderosis of the CNS. Her older daughter had vitreal amyloid deposits, acute brown-sequard syndrome at C4, acute sensorineural deafness, and recurrent transient neurologic symptoms. Cranial MRI at age 48 revealed a rim of low signal intensity in T2- and T2*-weighted images in the superior vermis folia and the right sylvian cortex. In addition, two small hemosiderin deposits were seen in the left parietal cortex. Lumbar puncture yielded colorless CSF with increased ferritin content and was followed by fourth ventricle hemorrhage. Cranial MRI 11 months later showed progression of brain hemosiderin deposits. The younger daughter had vitreal deposits, sensorimotor polyneuropathy, and acute sensorineural hearing but no evidence of siderosis on cranial MRI. She died at age 43 years of posterior fossa subarachnoid hemorrhage, and the neuropathologic examination showed amyloid deposition in the leptomeningeal spaces and vessels. CONCLUSION: Transthyretin-related amyloidosis may cause superficial siderosis of the CNS through subarachnoid bleeding related to meningovascular amyloid deposition. ( info)

9/112. Superficial siderosis of the central nervous system and anticoagulant therapy: a case report.

    Superficial siderosis of the central nervous system is a rare condition characterized by deposition of haemosiderin in the leptomeninges and in the subpial layers of the brain and spinal cord. With the widespread use of magnetic resonance imaging, an increasing number of cases of superficial siderosis are being discovered, secondary forms being more frequent than idiopathic ones. We report a 78-year-old man in oral anticoagulant therapy, who presented neurosensory hearing loss, gait ataxia and spastic paraparesis. magnetic resonance imaging suggested the diagnosis of superficial siderosis of the central nervous system, without an evident bleeding source. ( info)

10/112. Surgical resection of a cerebral arteriovenous malformation for treatment of superficial siderosis: case report.

    BACKGROUND: To our knowledge, there are only two reported cases of cerebral arteriovenous malformation associated with superficial siderosis. In both cases, the patients were asymptomatic and were discovered on retrospective review of magnetic resonance imaging. CASE DESCRIPTION: We describe a case of superficial siderosis in a 47-year-old male with a remote history of closed head injury that presented with progressive hearing loss, cerebellar ataxia, and urinary incontinence. Lumbar puncture was indicative of active subarachnoid bleeding. cerebral angiography revealed a small vascular malformation that was resected.RESULTS: Pathological examination confirmed the diagnosis of the arteriovenous malformation. Six months after surgery the patient is neurologically stable with no further progression of clinical signs or symptoms. CONCLUSIONS: We report the first case of surgical resection of an intracranial arteriovenous malformation for the treatment of superficial siderosis. We emphasize the necessity of a detailed evaluation when superficial siderosis is suspected to localize and resect potential bleeding sources, because the disease is progressive and often irreversible. ( info)
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