Cases reported "hemosiderosis"

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1/199. hyperpigmentation caused by hyperthyroidism: differences from the pigmentation of Addison's disease.

    Two cases of hyperthyroidism with hyperpigmentation are presented. In both cases, hyperpigmentation was seen on the lower extremities, most strikingly on the shins, backs of the feet and the nail bed. histology of the pigmented skin showed basal melanosis and heavy deposition of haemosiderin around dermal capillaries and sweat glands. Treatment with mercazol in both cases resulted in no significant waning of pigmentation. Distribution of hyperpigmentation, haemosiderin deposition and poor response to the treatment may be characteristic features of the pigmentation caused by hyperthyroidism, and may represent differences from the pigmentation seen in Addison's disease. ( info)

2/199. Microvesicular steatosis, hemosiderosis and rapid development of liver cirrhosis in a patient with Pearson's syndrome.

    BACKGROUND/AIMS: Pearson's marrow-pancreas syndrome consists of refractory sideroblastic anemia with vacuolization of marrow precursors and exocrine pancreas dysfunction. patients with this disease usually have large deletions of the mitochondrial genome. We report a patient with Pearson's syndrome who had predominantly hepatic manifestations such as microvesicular steatosis, hemosiderosis and rapidly developing cirrhosis. methods: Analysis of the mitochondrial and nuclear genomes, determination of enzyme activities and of the hepatic iron content were performed using standard techniques of molecular biology and biochemistry. RESULTS: The patient had typical ringed sideroblasts in a bone marrow smear and a 7436-bp deletion of the mitochondrial genome in all tissues investigated, compatible with Pearson's syndrome. He died within 3 months after birth due to liver failure. Histopathological analysis of the liver revealed complete cirrhosis with signs of chronic cholestasis, microvesicular steatosis and massive hemosiderosis. In addition, the patient was heterozygous for the C282Y and H63D mutations of the hemochromatosis gene. CONCLUSIONS: Pearson's syndrome should be added to the list of neonatal diseases which can cause microvesicular steatosis, hepatic accumulation of iron and liver cirrhosis. ( info)

3/199. Isolation of stachybotrys from the lung of a child with pulmonary hemosiderosis.

    Recently, stachybotrys atra, a toxigenic fungus, has been implicated as a potential cause of pulmonary hemorrhage/hemosiderosis in infants living in water-damaged homes. Although epidemiologic evidence supports this association, neither the organism nor its toxic products has ever been recovered from humans. We report the first case in which stachybotrys was isolated from the bronchoalveolar lavage fluid of a child with pulmonary hemorrhage. stachybotrys was also recovered from his water-damaged home. The patient recovered completely after his immediate removal from the environment and subsequent cleaning of his home. This case provides further evidence that this fungus is capable of causing pulmonary hemorrhage in children. ( info)

4/199. cerebrospinal fluid oligoclonal IgG bands in patients with spinal arteriovenous malformation and structural central nervous system lesions.

    OBJECTIVE: To investigate the incidence and characteristics of patients with structural central nervous system (CNS) lesions and cerebrospinal fluid oligoclonal IgG bands. DESIGN: A retrospective study. METHOD: The medical records of patients with cerebrospinal fluid oligoclonal IgG bands were evaluated for the presence of structural CNS lesions, their location and cause, and for clinical characteristics. SETTING: cerebrospinal fluid oligoclonal IgG bands were examined in the Neuroimmunology Laboratory, Hadassah University Hospital, Jerusalem, israel. patients: Two hundred seventy of 570 patients with positive cerebrospinal fluid oligoclonal IgG bands were available for analysis. Twenty patients had structural CNS lesions. RESULTS: Twenty (7.5%) of the 270 patients had structural CNS lesions: 3 patients had spinal arteriovenous malformation; 5 patients had tumors; 9 patients had compressive cervical myelopathy. Traumatic leukomalacia, arnold-chiari malformation type 1, and CNS hemosiderosis were present in 1 patient each. In 2 patients (1 patient with recurrent meningioma and 1 patient with posttraumatic encephalomalacia) the presence of a structural CNS lesion was followed by the development of multiple sclerosis. In all 3 patients with spinal arteriovenous malformation, oligoclonal IgG identification prolonged the time to diagnosis and therapy, which varied from a few weeks to 3 years. CONCLUSIONS: Structural CNS lesions, responsible for the neurological disorder, were present in 20 patients (7.5%) with cerebrospinal fluid oligoclonal IgG bands. The mechanism underlying oligoclonal IgG presence in spinal arteriovenous malformation and the coexistence of multiple sclerosis and structural CNS lesions is unknown, but may be related to recurrent tissue damage with repeated presentation of CNS antigens to the immune system. ( info)

5/199. chloroquine in idiopathic pulmonary hemosiderosis. A case report.

    This report describes an 11-year-old boy with idiopathic pulmonary hemosiderosis. His only presenting symptom was severe anemia due to iron deficiency. Idiopathic pulmonary hemosiderosis was diagnosed nine years after the onset of symptoms. During this period many invasive and non-contributory investigations were performed. This report describes the patient's diagnostic problems, clinical features and dramatic improvement with chloroquine (250 mg/day) after failing to respond to megadose methylprednisolone (30 mg/kg). One year later, chloroquine was discontinued. The patient has remained in remission since March 1994. chloroquine should be used for this life-threatening condition since it is less toxic than other immunosuppressive drugs. ( info)

6/199. Idiopathic pulmonary hemosiderosis with cystic lesions: a rare presentation.

    This report describes a case of a 49-year-old man with cough, recurrent hemoptysis, and dyspnea during 18 months, presenting with radiological findings of alveolar infiltrate and cystic lesions in left upper lobe. Laboratory studies revealed normocytic hypochromic anemia and normal coagulation tests. c-reactive protein and mucoproteins were negative. serum protein electrophoresis and complement, urinalysis, serum creatinine, creatinine clearance, and 24-hour urine protein were normal. Tests for antineutrophil cytoplasmic antibodies and anti-glomerular-basement membrane antibodies were negative. Tests for connective tissue diseases were all negative. Histological findings were consistent with those of idiopathic pulmonary hemosiderosis. Radiological findings are discussed. ( info)

7/199. Pulmonary hemosiderosis with juvenile rheumatoid arthritis: a case report.

    Pulmonary hemosiderosis may rarely be associated with juvenile rheumatoid arthritis or can develop during the course of the disease. We present a three-year-old boy with severe iron deficiency anemia (without any pulmonary symptoms) and arthralgia at the time of diagnosis. Two years after the initial diagnosis he developed pulmonary hemosiderosis and pauciarticular type of juvenile rheumatoid arthritis which progressed to seronegative polyarticular juvenile rheumatoid arthritis. He responded very well to prednisolone and was maintained well on low-dose alternate-day prednisolone and naproxen sodium treatment. This is the only case of association of these two diseases in our experience in both the Pediatric rheumatology and Pediatric Respiratory Diseases Departments. ( info)

8/199. Juvenile hemochromatosis associated with B-thalassemia treated by phlebotomy and recombinant human erythropoietin.

    Juvenile hemochromatosis is a rare genetic disorder that causes iron overload. Clinical complications, which include liver cirrhosis, heart failure, hypogonadotropic hypogonadism and diabetes, appear earlier and are more severe than in HFE-related hemochromatosis. This disorder, therefore, requires an aggressive therapeutic approach to achieve iron depletion. We report here the case of a young Italian female with juvenile hemochromatosis who was unable to tolerate frequent phlebotomy because of coexistent ss-thalassemia trait. The patient was successfully iron-depleted by combining phlebotomy with recombinant human erythropoietin. ( info)

9/199. Pulmonary haemosiderosis in Saudi children: report of two cases and review of the literature.

    Two children with idiopathic pulmonary haemosiderosis are reported. These are the first cases of this disease from saudi arabia and highlight the diagnostic problem caused by their presentation as cases of iron deficiency anaemia. The aetiopathogenesis, clinical presentation, diagnosis and management are discussed. The attention of paediatricians is drawn to this relatively rare cause of iron deficiency anaemia. ( info)

10/199. Segmental wall motion abnormalities in an individual with idiopathic pulmonary hemosiderosis.

    Idiopathic pulmonary hemosiderosis (IPH) is a rare condition characterized by diffuse pulmonary hemorrhage of unknown etiology. Cardiac involvement in the form of myocarditis and right ventricular hypertrophy have been reported to occur in association with IPH, although findings on echocardiography have not been described. Herein is presented a case of an adult with IPH and echocardiographic abnormalities. ( info)
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