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PubMed1976

[Idiopathic pulmonary hemosiderosis. Apropos of 1 case].

Idiopathic pulmonary hemosiderosis gives rise to anemia, due to repeated intra-alveolar hemorrhage, the reabsorption of which leads to hemosiderin deposits in the lung parenchyma. The authors report a case in a young woman aged 24 years whose illness started with anemia, then two months later, with hemoptysis and a broncho-pulmonary syndrome with a low grade fever. On the 6th month, there occurred a hazy infiltrate of both lung bases which was fleeting, mobile and recurrent. In the light of this triad of anemia, hemoptysis and infiltrates, the diagnosis of idiopathic pulmonary hemosiderosis was made and confirmed by three examinations:--Lung biopsy: siderophages were found in the sub-mucosa,--Radio-isotope examination, using Fe 59 which revealed iron deposits in the lung,--A surgical lung biopsy which showed a congestive area and a fibrous area. The congestive area was the site of recent hemorrhage, the alveolar limits were filled with siderophages. The fibrous area was the site of chronic repair of older hemorrhage. It was mutilating. The course was complicated by massive bleeding which led to acute recovering respiratory failure. The patient is at present stabilised by corticosteroids. Three hundred cases of idiopathic pulmonary hemosiderosis have been reported in the world literature. Although the main characteristic is intra-alveolar hemorrhage, its course has not yet been determined. It seems however, to be due to an immunologic process as shown by the relationship between this curious disease and Goodpasture's syndrome.

Adult↗
PubMed1988

[Idiopathic pulmonary hemosiderosis and rheumatoid arthritis. Apropos of a case].

A 38-year-old woman was known to have had a histologically proven "idiopathic" pulmonary hemosiderosis for 7 years; the authors report the onset in this patient of polyarthralgias with articular swelling and positivity of rheumatoid factor, all features consistent with the diagnosis of rheumatoid arthritis, whose beginning was certainly hidden by steroid therapy. This case, as some others previously published, outlines the possibility of the association of pulmonary hemosiderosis and rheumatoid arthritis: is this a casual association, or may pulmonary hemosiderosis be a rare manifestation of rheumatoid arthritis?

Adult↗
PubMed1978

Idiopathic pulmonary hemosiderosis: two cases in a family.

Two patients, a mother and her son, had idiopathic pulmonary hemosiderosis. In the son, the onset was acute and he died of massive hemoptysis. The mother's disorder developed less acutely and the condition improved after temporary respiratory support and massive corticosteroid therapy. This is the first reported instance of idiopathic pulmonary hemosiderosis occurring in more than one member of the same family. The diagnosis of idiopathic pulmonary hemosiderosis depends on compatible clinical and pathologic data and on exclusion of secondary causes of intrapulmonary hemorrhage.

Adult↗
PubMedDate not supplied

[Clinical and pathogenetic observation in a case of pulmonary hemosiderosis].

Pulmonary hemosiderosis is a rare disease of unknown aetiology, whose clinical, pathogenetic and prognostic aspects are still open to discussion. The authors report a case of pulmonary hemosiderosis in a 2 years and 3 months old girl. Peculiar features of this case include antibody deficiency (which may contribute to the pathogenesis of the disease) and severe and protracted melena. Fatal outcome, despite several therapeutic trials, confirms the poor prognosis of pulmonary hemosiderosis.

Albuterol↗
PubMed1997

Hepatic hemosiderosis in common marmosets, Callithrix jacchus: effect of diet on incidence and severity.

We examined the effect of dietary iron concentration on the incidence of hepatic hemosiderosis in common marmosets (Callithrix jacchus) and assessed the impact of hemosiderosis on animal health. Thirteen young adult common marmosets were fed nutritionally balanced natural-ingredient diets formulated to contain either 100 or 500 ppm of iron. Six were fed the low-iron and seven received the high-iron diet. Baseline blood values and liver iron content were determined for each animal. Animals were weighted monthly, blood work (hematologic analysis, serum iron concentration, total iron-binding capacity, percent of transferrin saturation) was performed semi-annually, and liver biopsies for iron analysis were obtained after marmosets had consumed the test diets for 13 months or at necropsy. Midway in study, the high-iron diet was reformulated to contain 350 ppm of iron because of the death of a male which had consumed that diet for 7 months. Four of seven marmosets fed the high-iron diet died during the first year of the study, compared with one death in the low-iron cohort. The mean increase in liver iron content of the marmosets fed the high-iron diet was 6,371 micrograms/g, dry weight analysis. In contrast the low-iron cohort had a mean decrease of 621.5 micrograms/g. These results indicate that liver iron content can be affected by dietary iron intake. The increased mortality in the marmosets fed the high-iron diet also suggests that hepatic hemosiderosis can be detrimental to marmoset health.

Animals↗
PubMed1998

[Pulmonary hemosiderosis and gastroesophageal reflux in an infant].

Pulmonary hemosiderosis (PH) has been described in association with a variety of immunological and non-immunological diseases. It is characterised by iron-deficiency anaemia, hemoptysis and diffuse pulmonary infiltrates based on recurrent intraalveolar hemorrhages. We present the case of a child with pulmonary hemosiderosis and a pathological gastroesophageal reflux activity. The child suffered from recurrent anaemic episodes the age of three months (hemoglobin level up to 5.4 g/dl). The symptoms decreased after removal of the gastroesophageal reflux and accompanying steroid therapy. There has been one relapse of pulmonary hemorrhage seven months later (hemoglobin level 6.1 g/dl). Since then the patient has been in good general condition and the steroid was slowly reduced. No more anaemic episodes occurred. We discuss a possible association of pathological gastroesophageal reflux activity in pulmonary hemosiderosis.

Bronchoalveolar Lavage Fluid↗
PubMed1996

Severe hemosiderosis post allogenic bone marrow transplantation.

Abnormal liver function persisting late after allogeneic BMT is usually attributed to chronic GvHD, viral hepatitis or drug toxicity. We describe a patient who had negative hepatitis serology, was on no hepatotoxic medication, had no evidence of GvHD but had abnormal liver function 15 months post MBT. She was diagnosed as having grade IV hemosiderosis of the liver. Her total red cell support had only been 52 units. We therefore postulate that in a proportion of patients receiving allogeneic BMT impaired intestinal iron absorption may be an important cause of hemosiderosis.

Bone Marrow Transplantation↗
PubMed2004

Celiac disease and pulmonary hemosiderosis in a patient with chronic granulomatous disease.

We report on a patient with the hitherto undescribed combination of chronic granulomatous disease, pulmonary hemosiderosis, and celiac disease. The hemosiderosis resolved with a gluten-free diet and glucocorticosteroid pulse therapy, but the restrictive lung function pattern remained unchanged. Lung function improved markedly by immunosuppression with daily glucocorticosteroid and azathioprine treatment.

Aconitine↗
PubMed2006

Quantification of siderophages in bronchoalveolar fluid in transfusional and primary pulmonary hemosiderosis.

Transfusional iron overload may occur in the lungs. We hypothesized that quantitating siderophages in the bronchoalveolar fluid (BALF) of heavily transfused patients may prove to be a useful tool in determining lung iron overload in transfusion-dependent patients. The study included six patients (7-20 years) with thalassemia major (TM) who had received multiple blood transfusions, one with hereditary spherocytosis (four blood transfusions) and one with sickle cell disease (never transfused); they were compared to three children with idiopathic pulmonary hemosiderosis (IPH) (2.5-7.0 years) as positive controls. Fiberoptic bronchoscopy with bronchoalveolar lavage was performed in seven patients under general anesthesia for elective surgery and the rest were bronchoscoped electively under sedation. Spirometry was also performed in eight patients. There was no significant difference between children with TM and IPH in siderophages as percentage of total count (95% CI -31.0 to 1.5, P = 0.068). There were positive relationships between both mean serum ferritin values during the preceding year and the total number of units of transfused blood, and percent siderophage count among multiply transfused patients (P = 0.010, P = 0.052, respectively); similar findings were noted for the Golde score (P = 0.001, P = 0.031, respectively). None of the patients showed lung function impairment. In conclusion, in this small study, we found that the BALF of multiply transfused patients with benign hematological disorders contain similar numbers of siderophages to that of patients with IPH; this is strongly suggestive of secondary pulmonary hemosiderosis. The correlation between the patients' serum ferritin, and the BALF siderophages suggests that the later may serve as a marker of pulmonary iron overload in patients requiring blood transfusion and appear to be more sensitive than standard pulmonary function tests.

Adolescent↗
PubMed1996

Hereditary ceruloplasmin deficiency with hemosiderosis.

Hereditary ceruloplasmin deficiency with hemosiderosis (aceruloplasminemia) is a new disease characterized by systemic hemosiderosis, diabetes mellitus, neurological abnormalities and pigment degeneration of the retina. Loss of the ferroxidase activity of ceruloplasmin results in systemic iron deposition and tissue damage. Neuroimaging studies reveal iron deposition in basal ganglia and in the red and dentate nuclei. Cerebellar ataxia, extrapyramidal signs and dementia develop after middle age. We report a patient with undetectable serum ceruloplasmin levels and the above clinical manifestations. Sequence analysis of the cDNA of ceruloplasmin from this patient revealed an insertion of adenine in exon 3; this produced a premature stop codon.

Amino Acid Sequence↗
PubMed2000

Idiopathic pulmonary hemosiderosis.

Two cases of idiopathic pulmonary hemosiderosis in children are reported. Both cases presented with a combination of acute/recurrent respiratory symptoms along with iron deficiency anemia. In one case diagnosis was delayed for 18 months after onset of symptoms. After initial stabilisation with corticosteroid therapy, both cases were put on chloroquine therapy and showed improvement. Various other forms of therapy and outcome are discussed. It is suggested that in cases with recurrent respiratory symptoms, idiopathic pulmonary hemosiderosis should also be considered after excluding infectious etiology.

Adrenal Cortex Hormones↗
PubMed1975

Alveolar capillary basement membrane lesions in Goodpasture's syndrome and idiopathic pulmonary hemosiderosis.

An ultrastructural study of lung distinguised between lesions of the alveolar capillary basement membrane in a case of Good pasture's syndrome and in three cases of idiopathic pulmonary hemosiderosis. In Goodpasture's syndrome, diffuse vascular injury with wide endothelial gaps, diffusely fragmented basement membranes and an electron dense layer on the basement membrane was found. In idiopathic pulmonary hemosiderosis, focal ruptures of the basement membrane were associated with hydropic changes in pneumocytes and, although fibroblasts were not seen, collagen deposition occurred within the basement membrane. immunofluorescent studies failed to show deposition of immunoglobulins G (IgG), A (IgA), M (IgM) or C3 in the lung in either disease. The ultrastructural lesions appear to separate these clinically similar entities.

Adolescent↗
PubMed1978

Asymptomatic IgA nephropathy associated with pulmonary hemosiderosis.

A glomerular lesion identical to that of IgA nephropathy was demonstrated unexpectedly in a 17 year old boy who presented with clinical manifestations of pulmonary hemosiderosis and with no evidence of renal disease. This subclinical glomerular lesion would have remained undetected in this patient unless kidney tissue was obtained and examined by immunofluorescence or electron microscopy. It is unknown if the glomerular lesion in this case is causally related to pulmonary hemosiderosis.

Adolescent↗
PubMed1995

Hemosiderin deposition in portal endothelial cells: a novel hepatic hemosiderosis frequent in chronic viral hepatitis B and C.

We have recently noted a hitherto undescribed hepatic hemosiderosis confined to endothelial cells of the portal tract in chronic viral hepatitis. In this study, this lesion was surveyed in 156 liver biopsy specimens from patients with chronic hepatitis C and in 21 liver biopsy specimens from patients with chronic hepatitis B. As controls, we examined 110 liver biopsy specimens from patients with primary biliary cirrhosis (PBC), 36 from patients with alcoholic liver injury, nine from patients with autoimmune hepatitis (AIH), and five from patients with primary hemochromatosis. Hemosiderin deposition was found in the endothelial cells of venous vessels in portal tracts regardless of the presence or degree of hemosiderin deposition in hepatic parenchyma. This phenomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C and in eight of 21 (38%) cases of chronic hepatitis B. In controls, this lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and alcoholic liver injury (11%). The incidence of this lesion showed significant differences between chronic hepatitis C, B, and AIH, and between PBC and alcoholic liver injury. There was a positive correlation between the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder chronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectively, in more severe cases. However, this correlation was not evident in either PBC or alcoholic liver injury. This hemosiderin deposition was positively correlated with the degree of piecemeal necrosis in chronic hepatitis C, and to a lesser degree, the positive correlation was shown in chronic hepatitis B. These findings suggest that the progression of chronic hepatitis and the piecemeal necrosis in chronic hepatitis C and B, followed by the release of hepatocellular iron to portal and periportal areas, are directly or indirectly responsible for endothelial hemosiderosis. Further studies focusing on this peculiar phenomenon in relation to choice of therapy and evaluation of chronicity of viral hepatitis are encouraged.

Adult↗
PubMed1996

Dark ring sign: finding in patients with fungal liver lesions and transfusional hemosiderosis undergoing treatment with antifungal antibiotics.

OBJECTIVE: To describe the MR appearance of necrotizing fungal granulomas occurring in the liver of leukemic patients with hepatosplenic fungal disease and transfusional hemosiderosis on antifungal antibiotics. SUBJECTS AND METHODS: Four patients with acute myelogenous leukemia (n = 2) or acute lymphocytic leukemia (n = 2) who developed hepatosplenic fungal disease, and were treated with antifungal medication, underwent MRI examination on a 1.5 T MR imager. MR images were prospectively evaluated and correlated with liver biopsy (three patients), and clinical picture (one patient). RESULTS: Multiple liver lesions measuring approximately 1 cm in diameter were identified in all patients. Lesions possessed a distinctive MR appearance: central mild hyperintensity with a peripheral ring of very low signal intensity on precontrast T1- and T2-weighted images. The central region of the lesions enhanced following gadolinium administration with the peripheral ring remaining low in signal intensity. CONCLUSION: Necrotizing fungal granulomas in the liver of patients with transfusional hemosiderosis on treatment with antifungal antibiotics have a distinctive appearance of moderate high signal intensity center on T1- and T2-weighted and postgadolinium MR images with a peripheral rim of low signal intensity. This appearance reflects the presence of iron-laden macrophages in the periphery of granulomas and may be expected in processes that initiate an immune response involving aggregation of macrophages in the liver of patients with transfusional iron overload.

Acute Disease↗
PubMed2005

Idiopathic pulmonary hemosiderosis in pregnancy: anesthetic implications.

Idiopathic pulmonary hemosiderosis is a rare disorder that results in significant anemia and pulmonary compromise. The case of a patient with new onset of disease diagnosed during labor is presented, and after urgent cesarean delivery, both the neonate and the mother survived. The anesthetic implications of a parturient with idiopathic pulmonary hemosiderosis, including monitoring, preoperative evaluation, and perioperative care, are discussed.

Adult↗
PubMed1975

Hyperreactivity to cow milk in young children with pulmonary hemosiderosis and cor pulmonale secondary to nasopharyngeal obstruction.

Six black infants and young children with high titers of milk precipitins were identified by screening the sera of 160 children with idiopathic chronic lung disease. None of the six had immunoglobulin deficiency, elevation of sweat chlorides, SS hemoglobin, or recurrent aspiration. All six children had typical manifestations of milk-induced pulmonary hemosiderosis: recurrent pulmonary infiltrates (6/6), hemosiderin-laden pulmonary macrophages (5/6), intermittent wheezing (5/6), eosinophilia (4/6), anemia (4/6), iron deficiency (4/4), failure to thrive (4/6), and elevated levels of serum IgE (4/4). Three children also had chronic rhinitis and eventually developed large adenoids, hypercapnia and acidosis during sleep, and right heart failure. Elimination of cow milk from the diet, symptomatic therapy, and adenoidectomy when indicated resulted in improvement of all six patients. Pulmonary hemosiderosis and some cases of upper airway obstruction with pulmonary hypertension appear to be two stages, early and delayed, of the same immunophysiologic process. Early dietary intervention may prevent the cardiovascular complications of this process.

Black or African American↗
PubMed1983

Epidemiologic observations in idiopathic pulmonary hemosiderosis.

We did an epidemiologic survey of 30 children in whom idiopathic pulmonary hemosiderosis was diagnosed. Eighteen patients had died; 12 patients were still living. The majority of the cases were diagnosed in between 1962 and 1971, mainly in the spring and fall. Eighty percent of the patient lived in villages, whereas only 30% of the total population resided in the same type of rural area. Only one (5%) of the deceased children lived in the city, whereas four (33%) of the living children were city dwellers. The socioeconomic conditions were poor, and in 50% of the cases continuous exposure to highly toxic insecticides was elicited by history and investigation of housing conditions. The incidence of newly diagnosed cases decreased with the improvement of living conditions and the prohibition of the use of certain insecticides. We believe that environmental factors, perhaps insecticides, may cause idiopathic pulmonary hemosiderosis in genetically predisposed persons. An epidemiologic history and genetic investigation should be included in the evaluation of patients with any disease when the cause is obscure.

Child↗