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PubMed1995

Resistance to erythropoietin in iron-overloaded haemodialysis patients can be overcome by ascorbic acid administration.

Haemodialysis patients with iron overload sometimes develop resistance to erythropoietin therapy due to 'functional iron deficiency'. It is known that this resistance may be overcome by iron supplementation; however, the latter could worsen haemosiderosis. Therefore, we treated four iron-overloaded haemodialysis patients who had developed relative resistance to erythropoietin (among whom three had features of 'functional iron deficiency') with ascorbic acid (500 mg intravenously after haemodialysis, 1-3 times a week). The erythropoietin doses were voluntarily kept unchanged during the study. After a latency of 2-4 weeks, haematocrit and haemoglobin had increased respectively from 26.5 +/- 0.7 to 32.7 +/- 0.4 vol% and from 8.8 +/- 0.3 to 10.8 +/- 0.2 g/dl (means +/- SEM, P < 0.001). While serum ferritin remained unchanged, transferrin saturation increased from 27 +/- 7 to 54 +/- 12% (P < 0.05), suggesting that ascorbic acid supplementation had allowed mobilization of iron from tissue burdens. In one patient, haematocrit declined after withdrawal of vitamin C and increased again after rechallenge. Also, ascorbate supplementation was continued after the study in two patients and allowed the erythropoietin doses to be decreased, 8 and 11 weeks, respectively, after the start of the trial. When a control group of seven patients with normal iron status and without resistance to erythropoietin were challenged in the same manner with ascorbate, no elevation of haematocrit or transferrin saturation was noted. We conclude that ascorbate supplementation may circumvent resistance to erythropoietin that sometimes occurs in iron-overloaded patients, in particular, in the setting of 'functional iron deficiency'.

Adult↗
PubMed1990

Recombinant erythropoietin reverses polymorphonuclear granulocyte dysfunction in iron-overloaded dialysis patients.

Iron overload increases the risk of bacterial infection in dialysis patients, partly by impairing functions of the polymorphonuclear granulocytes (PMNs). PMN defence was studied sequentially in haemodialysis patients with transfusional haemosiderosis, treated for 6 +/- 1.5 months (n = 8) to 13 +/- 1.7 months (n = 4) with recombinant human erythropoietin (rHuEpo). Over this period, signs of iron overload (increased serum ferritin and serum iron) improved, and stainable iron disappeared in PMNs. Simultaneously, phagocytosis of Yersinia enterocolitica by PMNs improved. The decrease in serum ferritin was significantly related to the improved phagocytosis. Killing of Y. enterocolitica by PMNs also improved. It is anticipated that rHuEpo therapy in iron-overloaded dialysis patients could decrease the incidence of bacterial infection by improving PMN functions in these patients.

Adult↗
PubMed1992

Pharmacokinetics of aluminoxamine and ferrioxamine and dose finding of desferrioxamine in haemodialysis patients.

We investigated the pharmacokinetics of desferrioxamine and its chelated compounds aluminoxamine and ferrioxamine in normal volunteers and haemodialysis patients with and without iron overload. Desferrioxamine was administered in a single dose of 30 mg per kg body-weight was a 30-min infusion to five healthy volunteers and to 20 haemodialysis patients (five patients without haemosiderosis and 15 patients with haemosiderosis). The interdialytic half-life of ferrioxamine was 2.2 h in normal volunteers, 13.3 h in dialysis patients without haemosiderosis, and 24.6 h in patients with haemosiderosis. There was no interdialytic elimination of aluminoxamine. In a second study, seven dialysis patients received 5, 10, and 20 mg per kg body-weight desferrioxamine in a random order with a time interval of 2 weeks. The peak serum concentrations after these doses were 4.1 +/- 2.9, 6.4 +/- 2.9, and 10.7 +/- 7.1 mumol/l for ferrioxamine and 2.8 +/- 1.5, 3.1 +/- 1.5, and 4.2 +/- 1.7 mumol/l for aluminoxamine. Thus, a 4-fold increase in desferrioxamine dosage resulted in a 2.7-fold increase in peak ferrioxamine levels and in only a 1.5-fold increase in peak aluminoxamine levels. We conclude that dialysis patients, especially those with haemosiderosis, are exposed to persistently elevated ferrioxamine levels. Weekly doses of 5-10 mg/kg of desferrioxamine would be sufficient for aluminium chelation therapy.

Adult↗
PubMed2000

Idiopathic pulmonary haemosiderosis.

Idiopathic pulmonary haemosiderosis (IPH) is a rare disorder characterized by recurrent bouts of haemoptysis, iron deficiency anaemia, and pulmonary infiltrates on chest radiograph. We present such a case and believe that it is the first report from the Middle East.

Child, Preschool↗
PubMed1980

Ferrugination caused by Monsel's solution. Clinical observations and experimentations.

Ferrugination of fibrin, dermal collagen, and striated muscle fibers may result from the application of Monsel's solution (20% ferric subsulfate) for hemostasis to wounds caused by excisions of skin. The collagen fibers in the dermis are coated with a slightly refractile, gray-brown substance which is strongly positive with Perl's reaction for iron. Ferruginated collagen fibers are eliminated through the epidermis as the epidermis regenerates. Some of the ferruginated fibers become calcified. Siderophages are present in these and adjacent areas. Seepage of Monsel's solution into deeper tissues at the site of biopsy may result in ferrugination of skeletal muscle, perichondrium, and even cartilage. We applied Monsel's solution to biopsy sites caused experimentally in a rabbit and confirmed the capacity of the solution to produce ferrugination of collagen fibers and skeletal muscle. Ferrugination of collagen fibers becomes less pronounced as the wounds heal and as iron pigment is taken up by macrophages. Ferruginated fibers of skeletal muscle act as foreign bodies to elicit a granulomatous reaction. Comparison of biopsy sites to which Monsel's solution had been applied with biopsy sites to which the solution had not been applied indicates that the substance does not seem to interfere with the rate of epidermal regeneration. However, when there is injury to skeletal muscle and other deep tissues by Monsel's solution, an inflammatory reaction persists at these sites for weeks.

Administration, Topical↗
PubMed1980

Unusual histiocytic reaction to Monsel's solution.

Monsel's solution for hemostasis was applied to a wound produced at the site of a punch excision biopsy from the wrist of a 51-year-old white man. The biopsy specimen showed an incompletely excised basal cell carcinoma. Thirty days later, the residual carcinoma was excised. Adjacent to a basal cell carcinoma in the second biopsy specimen was an intradermal nodule composed of large polygonal cells and multinucleated histiocytic giant cells containing granules and clumps of dark brown and black pigment. This pigment was strongly positive for iron when stained by Perl's method. This unusual histiocytic reaction to topically applied ferric subsulfate must be differentiated from malignant melanomas and from histiocytic neoplasms with siderosis.

Biopsy↗
PubMed2000

Pulmonary hemosiderin in deceased infants: baseline data for further study of infant mortality.

Infant lung samples were obtained prospectively at autopsy by medical examiner pathologists in five areas of the United States. Tissues were submitted regardless of the cause of death. Lung sections were stained with Prussian blue to detect deposits of hemosiderin. Fifty-nine cases were evaluated for the study. The four sections examined for each case were taken from the anterior and posterior aspects of the right and left upper lung. Three pathologists independently scanned the lung sections microscopically using a 10x objective lens (with 10x ocular lens) and indicated an "iron score" by indicating for each section if it showed no staining for iron-hemosiderin (Score 0), occasional staining with most fields negative (Score 1), focally abundant staining with most fields having no staining (Score 2), focally abundant staining with most fields showing positive staining (Score 3), or prominent staining throughout the section (Score 4). There was good agreement between pathologists on the iron score for each case. A total iron score was calculated by adding the scores based on each pathologist's observations. The mean total iron score was 6 (range, 1-44), with the range of possible total iron scores being 0 to 48. There was no significant difference between the four lung sections in a given case. Six cases had total iron scores that were at least twice the mean (i.e., total iron score > 12); in five of these cases death was caused by conditions other than sudden infant death syndrome, including one case in which asphyxia was the cause of death. These data are consistent with other reports that pulmonary hemosiderin in deceased infants is suggestive of a cause of death other than sudden infant death syndrome. The data may be useful as baseline data for further studies of infant mortality involving possible pathologic changes in the lungs.

Autopsy↗
PubMed1999

Hobnail hemangioma: a pseudomalignant vascular lesion with a reappraisal of targetoid hemosiderotic hemangioma.

The clinicopathologic features of 15 cutanous hemangiomas having a distinctive and frequently pseudomalignant morphologic appearance are presented. There were 5 male and 9 female patients, whose ages at diagnosis ranged from 11 to 58 years (median 30.5). An angiomatous/pigmented, nontargetoid, flat, or exophytic lesion of variable duration was the main presenting sign. The tumor sizes ranged from 0.4 cm to 2 cm (median 1 cm). The locations included the lower limb, particularly the thigh (8); the trunk, including the shoulder area (4); the head (1); the gingiva (1); and the tongue (1). One patient had two lesions; none had a concomitant vascular anomaly or was suspected to have HIV infection. Treatment consisted of excisional biopsy in all cases. Follow-up information on 10 patients (range 4-66 months; median 13 months) showed no recurrence. On microscopic examination, the lesion showed a biphasic pattern characterized by the presence of well-formed, dilated, vascular channels in superficial dermis and a collagen-dissecting, pseudoangiosarcomatous pattern as the lesion infiltrated deeper into the dermis. The lining endothelium consistently showed distinctive hobnail cytomorphology; although there were endoluminal stromal papillae, there was no endothelial multilayering or tufting. Cytologic atypia was minimal or absent, and there were no mitoses. In 3 cases, the morphologic features were reminiscent of retiform hemangioendothelioma. Immunohistochemistry performed in 8 cases showed variable reactivity of endothelial cells with CD31, CD34, Factor VIII-related antigen, and Ulex europaeus agglutinin-1 in all cases; smooth muscle actin-positive pericytes were observed focally around some of the abnormal vascular spaces. The above-described hemangiomatous lesions share many features with so-called targetoid hemosiderotic hemangioma (a clinically descriptive term), but show a variable, often minimal, amount of hemosiderin deposition. The histologically descriptive term hobnail hemangioma is proposed to designate these lesions. Hobnail hemangioma should be distinguished from well-differentiated angiosarcoma, patch-stage Kaposi's sarcoma, and retiform hemangioendothelioma, with which it may be confused.

Adolescent↗
PubMed2001

Prognostic significance of pulmonary lymphangioleiomyomatosis histologic score.

Correlations were made between clinical and follow-up data and histopathologic findings in 105 women (mean age +/- standard deviation, 38.3 +/- 9.0 years) with pulmonary lymphangioleiomyomatosis (LAM). The actuarial survival (to pulmonary transplantation or death) of the patients from the time of lung biopsy was 85.1% and 71.0% after 5 and 10 years respectively. The histologic severity of LAM, graded as a LAM histologic score (LHS), was determined on the basis of semiquantitative estimation of the percentage of tissue involvement by the two major features of LAM: the cystic lesions and the infiltration by abnormal smooth muscle cells (LAM cells) in each case: LHS-1, <25%; LHS-2, 25% to 50%; and LHS-3, >50%. Analysis using the Kaplan-Meier method revealed significant differences in survival for patients with LHS-1, -2, and -3 (p = 0.01). The 5-and 10-year survivals were 100% and 100% for LHS-1, 81.2% and 74.4% for LHS-2, and 62.8% and 52.4% for LHS-3. Increased degrees of accumulation of hemosiderin in macrophages also were associated with higher LHS scores (p = 0.029) and a worse prognosis (p = 0.0012). Thus, the current study suggests that the LHS may provide a basis for determining the prognosis of LAM.

Adolescent↗
PubMed2001

Diffuse alveolar hemorrhage syndromes.

Diffuse alveolar hemorrhage (DAH) is a rare yet serious and frequently life-threatening complication of a variety of conditions. DAH may result from coagulation disorders, inhaled toxins, or infections. Most cases of DAH are caused by capillaritis associated with systemic autoimmune diseases such as antineutrophil cytoplasmic antibodies-associated vasculitis, anti-glomerular basement membrane disease, and systemic lupus erythematosus. Early recognition is crucial, because the prompt institution of supportive measures and immunosuppressive therapy is required for survival. Our understanding of DAH and its management is largely empiric and based on small case series and individual reports, many dating back more than one decade. To provide the practicing specialist with a rational diagnostic and management approach to the patient with DAH, this review summarizes the most recent publications and salient information derived from older publications.

Anti-Glomerular Basement Membrane Disease↗
PubMed1986

Changes in proton relaxation times of the rat spleen during adjuvant-induced immunologic reaction.

Possible changes in magnetic resonance (MR) relaxation times resulting from an immune reaction were evaluated in the rat spleen by means of in vitro proton spectroscopy and an established model of immune disease. Heat-killed Mycobacterium butyricum in Freund's adjuvant was injected intradermally into the tail of 28 rats. Ten normal rats served as controls. At different times following the injection of adjuvant (day 7, day 10, day 12, day 14, or day 22), the spleens were removed and weighed, and proton T1 and T2 relaxation times were measured with a 0.25-T spectrometer (10.7 MHz). Water content was also determined. Specimens of each spleen were histologically examined; this included Prussian-blue staining for detection of hemosiderin. In 22 of the 28 adjuvant-injected rats, spleen T1 values increased significantly, from a mean value of 451 msec +/- 23 S.D. (control rats) to a maximum mean value of 571 +/- 15 S.D., which occurred on day 12; this T1 increase paralleled an increase in weight and water content and a histologic appearance of granulomatous inflammation. In these rats, T2 changes were not significant. In the other six adjuvant-injected rats, spleen T2 relaxation time significantly decreased from a mean value of 42 msec +/- 5 S.D. to a mean value of 32 msec +/- 1 S.D. Histologic evaluation indicated that the origin of this T2 decrease was probably the presence of hemosiderin in the spleens of only these six rats. Mean T1 of these spleens decreased slightly, but not significantly.

Adjuvants, Immunologic↗
PubMedDate not supplied

MR evaluation of liver iron overload.

Children and young adults with hemolytic anemias requiring frequent transfusions develop increased liver iron content. We evaluated 15 chronically transfused children with sickle cell disease to determine whether spin-echo magnetic resonance (MR) imaging was useful in assessing the degree of iron overload. Quantitative MR parameters were correlated with liver biopsy iron determinations and serum ferritin levels. The best predictor of liver iron was the ratio of the intensities between the liver and paraspinal musculature on somewhat T1 weighted sequence (repetition time 0.5 s, echo time 28 ms), R2 = 0.58. Magnetic resonance was able to separate those patients with liver iron levels greater than 100 micrograms/mg (intensity ratios approximately 0.4), from those with levels less than 100 micrograms/mg (intensity ratios near 1). However, MR was unable to quantitate liver iron in patients with values ranging from 100 to 400 micrograms/mg since similar intensity ratios were present in this range. Thus, MR provides a qualitative rather than quantitative assessment of liver iron overload.

Anemia, Sickle Cell↗
PubMedDate not supplied

Pilot study of the relationship between histologic progression and hepatic iron concentration in chronic hepatitis C.

Hepatic iron deposition is common in patients with chronic hepatitis C (HCV) and may play a role in progression of liver disease. This pilot study examines the relationship between hepatic iron concentration (HIC) and histologic progression over time in patients with HCV. HIC was retrospectively measured in 14 patients with HCV who had 2 serial liver biopsies prior to the era of interferon therapy. The mean interval between biopsies was 56 +/- 46 months. Mean Knodell score worsened between first and second biopsies (10.0 +/- 2.8 versus 12.4 +/- 3.3; P = 0.007). There was increased portal inflammation (3.2 +/- 0.4 versus 3.6 +/- 0.5; P = 0.028) and fibrosis (1.8 +/- 1.3 versus 2.7 +/- 1.2; P = 0.002), but no significant change in piecemeal necrosis or lobular degeneration. There was no significant change in HIC between first and second biopsy (P = 0.66). However, HIC was noted to increase significantly among patients with cirrhosis on initial biopsy or those who progressed to cirrhosis (P = 0.009). In this pilot study, histologic progression in patients with precirrhotic HCV was not associated with an increase in HIC, whereas hepatic iron accumulation was observed in 3 patients once cirrhosis was present. The interaction between progression of hepatitis C and iron deposition warrants further study.

Adult↗