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Results for “HEMOSIDEROSIS”

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At least 595 records · Page 33Linked to original sources
PubMed1978

Localized hemosiderosis as a sequela of acne.

Dark blue-black pigmentation has persisted in areas of previous acne scarring in a young woman. By histologic and electron microscopic examination, the pigment is demonstrated to represent hemosiderin. Much of the hemosiderin is lying free within macrophages, not bound by lysosomal membranes that normally would protect the cell from this toxic material.

Acne Vulgaris↗
PubMedDate not supplied

Methods for evaluating iron stores and efficacy of chelation in transfusional hemosiderosis.

An accurate determination of the total amount and distribution of body iron stores is essential for prognostic purposes and to evaluate the efficacy of chelation therapy. In the clinical setting, a rough estimate of the total body iron burden may be obtained in patients with transfusion-dependent anemias by calculating the amount of blood administered plus the amount absorbed by the gastrointestinal route, which is influenced by the level of Hb and by bone marrow activity. An increase in serum iron and a decrease in total iron binding capacity are early indicators of iron overload, but their sensitivity and specificity are not very high. In normal individuals, serum ferritin correlates well with iron stores, as measured by phlebotomy, and with directly measured liver iron. However, plasma ferritin, being an acute phase reactant, is increased in cases of chronic disease, disseminated malignancy, or inflammatory disorders. Non-transferrin bound iron, i.e. iron that circulates in plasma unbound to transferrin, is potentially toxic since it is capable of taking part in free radical-mediated reactions that result in irreversible tissue damage. This iron can be measured with a HPLC based assay. At present the most accurate way of estimating the iron burden is by direct measurement of iron concentration in tissues. The liver is the most accessible. The measurement is done by atomic absorption spectrometry on ashed or lyophilized samples obtained by needle biopsy, and correlates well with the total amount of blood transfused and with the extent of hepatic fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Chelation Therapy↗
PubMed1991

[Relation between circulating immune complexes and serum ferritin in hemosiderosis of different etiologies].

Parameters of iron metabolism and humoral immunity were studied in patients with chronic diffuse diseases of the liver (cirrhosis, chronic hepatitis), beta-thalassemia major, dyserythropoiesis, hereditary hemochromatosis. High ferritin content has been recorded in the plasma of these patients, that leads to the formation of antibodies to this protein followed by the production of circulating immune complexes inducing metabolic disorders that aggravate the pathologic process. Plasmapheresis and deferoxamine therapy result in a decrease of ferritin and circulating immune complex content in the plasma, that produces a favourable effect on the patients' condition.

Adult↗
PubMed1991

[Calcipenic osteopathy in transfusion hemosiderosis and idiopathic hemochromatosis].

Bone metabolism studies were performed on 5 patients with transfusion haemosiderosis (2 male, 3 female; mean age: 30.8 years) and 5 patients with idiopathic haemochromatosis (2 male, 3 female; mean age: 48.8 years). In the majority of the patients, the modern osteodensitometric method showed a significant decrease of the mineral content of the trabecular and cortical bones. Low calcitonin and dehydroepiandrosterone-sulphate concentrations were measured in the majority of the patients with calcipenic osteopathy. Besides marked bone loss, hypogonadotropic hypogonadism was found in 3 male patients, while normal LH, FSH concentration values were measured in 3 female patients. The prolactin concentration was normal in all 6 patients. The authors suppose that besides the already known pathogenetic factors, insufficient calcitonin effect and especially the partial lack of dehydroepiandrosterone-sulphate can play a role in the development of bone loss connected with iron overload. Further study with a greater number of patients in required to support the above findings.

Adult↗
PubMed1991

Siderophilic bodies associated with hemosiderosis and atypical mycobacterial infection in an island siamang (Hylobates syndactylus).

Laminated iron concretions were noted in the liver of an aged siamang (Hylobates syndactylus) that had granulomatous enteritis and hepatitis due to Mycobacterium avium intracellulare infection. Preexisting hepatic siderosis, iron sequestration in macrophages, and compromised macrophage function due to mycobacterial infection are proposed as the basis for the abundance and size of the concretions. Similar siderophilic bodies and concomitant siderosis occurred in other siamangs. The concretions are similar to Schumann bodies and Michaelis-Gutmann bodies associated with granulomatous disease in other species.

Animals↗
PubMed1991

[Long-term treatment of patients with transfusion hemosiderosis using oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1)].

A new oral iron chelator, L1, was given for 14 to 16 months to four patients with transfusion haemosiderosis. These patients could no longer be treated with deferoxamine because of allergic reactions or psychological problems. Serum ferritin values at the start of the treatment ranged from 2220 to 4530 microgram/l. L1 was given in a total daily dose of 3 g, at first in a single dose, later 3 times 1 g daily. The 24-hour urinary excretion of iron varied greatly from day to day. The mean urinary iron excretion of the four patients ranged from 19.3 to 45.7 mg/day. In two patients an important decrease of ferritin was found. These patients had been given no more or only sporadic transfusions. In one patient transient agranulocytosis was seen which was probably not caused by L1.

Adolescent↗
PubMed1991

[Changes in the pleura and review of idiopathic pulmonary hemosiderosis Ceelen-Gellerstedt disease].

Ceelen's disease has been considered after the first description as a rather well defined nosological entity with severe pathological findings in the kind of a "brownish induration of the lung without a detectable extrapulmonary circulation". Nowadays this disease enter into the general discussion of uncertain pulmonary bleeding mechanism. So far not further characterized structural changes in the pleura in an open lung biopsy of a 28-year-old woman with Ceelen's disease are reported. Basically the alterations consists of disruption of the elastic laminae associated with a giant cell reaction with incorporation of elastica fragments. In a survey of mainly pathological anatomical reports on Ceelen's disease the hypothesis of a primary alteration of the elastic tissue is confronted with the hypothesis of a primary not yet in detail characterised defect of the alveolar-capillary entity and brought in relation to the particular findings in the pleura.

Adult↗