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We retrospectively evaluated (18)fluoro-2-deoxyglucose positron emission tomography (FDG-PET) scans in 172 patients with lymphoma and correlated results with pathologic diagnosis using the World Health Organization (WHO) classification system. In total, FDG-PET detected disease in at least one site in 161 patients (94%) and failed to detect disease in 11 patients (6%). The most frequent lymphoma diagnoses were diffuse large B-cell lymphoma (LBCL; n = 51), Hodgkin lymphoma (HL; n = 47), follicular lymphoma (FL; n = 42), marginal zone lymphoma (MZL; n = 12), mantle cell lymphoma (MCL; n = 7), and peripheral T-cell lymphoma (PTCL; n = 5). FDG-PET detected disease in 100% of patients with LBCL and MCL and in 98% of patients with HL and FL. In contrast, FDG-PET detected disease in only 67% of MZL and 40% of PTCL. Comparison with bone marrow biopsies showed that FDG-PET was not reliable for detection of bone marrow involvement in any lymphoma subtype.

Veno-occlusive disease (VOD) of the liver remains a major complication after hematopoietic stem cell transplantation (SCT). VOD is thought to develop after hepatic endothelial cells are damaged by high-dose chemotherapy or radiation, causing microthrombosis in hepatic venules. However, the precise mechanisms leading to VOD are not well defined, and a diagnosis is often difficult to establish. It is also difficult to predict which patients are most likely to develop VOD. Elevated levels of homocysteine (HC) have been associated with thrombosis, and prothrombin fragment 1 + 2 (F1 + 2) is a measurable marker for coagulation. Therefore, we performed a prospective cohort study to determine if HC or F1 + 2 levels could be used to predict the development of VOD prior to SCT, or to help establish a diagnosis of VOD in association with other clinical parameters. Plasma levels of these factors were measured before conditioning and serially for 21 days after SCT in 42 consecutive patients undergoing SCT. Eleven of 26 allogeneic SCT recipients developed VOD, whereas no autologous SCT recipient (n = 16) developed VOD (p = 0.008). In patients who developed VOD, HC levels were consistently higher than those seen in non-VOD patients after day 7 of SCT. Patients with VOD also had higher levels of F1 + 2 after SCT, although this marker was less consistently elevated over time. A logistic regression model that evaluated all serial measures of HC and F1 + 2 showed a moderate sensitivity and specificity in diagnosing VOD in allogeneic SCT patients, but neither marker was useful to predict development of VOD when tested prior to SCT.

Nonmyeloablative allogeneic transplantation is an emerging therapy for hematologic and solid malignancies and potentially offers patients reduced transplant-related toxicity. Data regarding infectious complications of these protocols are limited, but early studies have demonstrated little infectious morbidity, particularly low rates of invasive fungal infections (IFIs). In the present study, 31 consecutive cases of nonmyeloablative transplantation were reviewed over a 2.5-year period, with a specific focus on infectious complications. Twenty-six patients (84%) had at least 1 significant infection during the year after transplantation, and infection-related mortality was 37%. Cytomegalovirus end-organ disease was diagnosed in 3 patients (10%). Ten patients (32%) were given the diagnosis of IFI; 7 (23%) met criteria for proven IFI. Fungal-related mortality was 80% within the group of patients with IFI and accounted for a significant portion of the overall mortality in the study. Severe graft-versus-host disease, high-dose corticosteroid use, recurrent neutropenia, and relapsed or refractory disease were factors associated with development of IFI.

Treatment options are limited for patients with relapsed acute myelogenous leukemia (AML), particularly when the disease is refractory to standard cytotoxic chemotherapy. Targeted drug therapy offers the advantage of delivering higher doses of non-cross resistant chemotherapy with potentially less systemic toxicity. Gemtuzumab ozogamicin (Mylotarg, Wyeth-Ayerst Laboratories) is an immunoconjugate that consists of humanized anti-CD 33 antibody linked to the potent anti-tumor antibiotic calicheamicin and has been an effective therapy for some patients with relapsed AML. However, the overall utility of gemtuzumab ozogamicin is not well defined. For instance, it is not known how well this antibody will target extramedullary disease. This article reports gemtuzumab treatment of refractory AML in a 32-year-old man. At the time of recurrence, his bone marrow was hypoplastic and without leukemia, but the condition progressed resulting in marked leukemic infiltration of the oral mucosa. This case history raises the possibility that leukemic sanctuary sites may exist, and that monoclonal antibody therapy may have sub-optimal activity in non-medullary sites of disease.

Epstein-Barr virus (EBV) is known to be involved in the majority of patients who develop post-transplant lymphoproliferative disorder after solid organ transplant. We conducted a retrospective study to determine the utility of qualitative and quantitative Epstein-Barr virus polymerase chain reaction (PCR) for the diagnosis and monitoring of post-transplant lymphoproliferative disorder in adult solid organ transplant patients. Peripheral blood leukocytes obtained from 35 adult solid organ transplant patients consecutively referred for evaluation of possible post-transplant lymphoproliferative disorder, were tested by EBV PCR at the time of initial evaluation and at time points thereafter. Eighteen of 35 (51%) patients were ultimately diagnosed with post-transplant lymphoproliferative disorder by tissue biopsy. Fifteen of 18 (83%) patients were found to have EBER-1 positive tumors by in situ hybridization. EBV PCR was positive in 7 of 15 patients, suggesting a sensitivity of 39%. Seventeen patients without post-transplant lymphoproliferative disorder and three with EBER-1 negative post-transplant lymphoproliferative disorder all had negative EBV PCR tests, suggesting a specificity of 100%. We observed that declines in EBV DNA load were associated with response to therapeutic interventions, such as reduction in immunosuppression, rituximab therapy and chemotherapy. We conclude that peripheral blood EBV PCR may have a role in the diagnosis and monitoring of post-transplant lymphoproliferative disorder in adult solid organ transplant patients.

Nonmyeloablative allogeneic stem cell transplantation (NMASCT) can be used to exploit the graft-versus-tumor (GVT) potential of allogeneic donor cells in the setting of reduced conditioning regimen toxicity. This approach is particularly attractive for patients who have received extensive prior therapy and are poor candidates for traditional allogeneic stem cell transplantation. However, toxicity in heavily pretreated patients remains uncertain. Additional immunosuppression in already immunocompromised patients may result in unexpected toxicity. We report a case of probable progressive multifocal leukoencephalopathy (PML) responsive to interleukin-2 (IL-2) following a NMASCT in a 29-year-old woman with relapsed Hodgkin's lymphoma. The patient developed severe neurological symptoms approximately 6 weeks following NMASCT associated with low CD4+ cell counts and magnetic resonance imaging (MRI) was consistent with PML. IL-2 therapy resulted in increasing CD4+ counts and progressive resolution of neurological symptoms. Disruption of IL-2 therapy led to neurological deterioration, which responded to reinstitution of IL-2 therapy. The patient's lymphoma initially progressed following NMASCT, but has responded to donor leukocyte infusions (DLI). This case reiterates the potent GVT potential of NMASCT in patients with Hodgkin's disease. However, it demonstrates the potential for severe complications related to immunosuppression, especially in heavily pretreated patients. The toxicity after NMASCT should not be understated and will need to be explored further.

F-18 fluorodeoxyglucose positron emission tomography (FDG PET) is highly sensitive and specific for the detection of nodal and extranodal disease in patients with malignant lymphoma. However, no previous reports have shown lymphomatous involvement of the small bowel that was recognized on the basis of FDG-PET imaging findings. The authors present two cases of clinically unsuspected small bowel involvement by mantle cell lymphoma that were initially detected on FDG PET.

Acute myelogenous leukemia (AML) describes a group of related hematologic malignancies that are being approached therapeutically from several perspectives. Conventional chemotherapeutic agents, such as anthracyclines and cytosine arabinoside (Ara-C), are useful in treating AML but now appear to have reached their maximum potential. Newer therapeutic approaches to AML have recently focused on immune-based therapy through monoclonal antibodies that target and destroy malignant cells via specific cell receptors. One such agent is gemtuzumab (CMA-676), an agent that targets the CD33 antigen on malignant myeloid cells. Initial studies have shown significant anticancer activity. We will discuss traditional and newer therapeutic approaches to AML and review the role of monoclonal antibody based therapies for patients with AML. A case of a 30-year-old man with refractory AML who was treated with gemtuzumab will be mentioned, highlighting potential applications and possible limitations to this novel therapy. Despite the effective reduction in the number of malignant cells in bone marrow, gemtuzumab ineffectively treated extramedullary leukemic gingival infiltrate. Regardless of limitations, monoclonal-based therapy offers an exciting and potentially safer adjunctive therapy for patients with AML.

Background: Posttransplant lymphoproliferative disorder (PTLD) is an Epstein-Barr virus-associated malignancy that occurs in the setting of pharmacologic immunosuppression after organ transplantation. With the increased use of organ transplantation and intensive immunosuppression, this disease is becoming more common. We explore reduction in immunosuppression as an initial therapy for PTLD., Methods: We analyzed our organ transplant patient database to identify patients with biopsy-proven PTLD who were initially treated with reduction of their immunosuppressive medications with or without surgical resection of all known disease., Results: Forty-two adult patients were included in this study. Thirty patients were treated with reduction in immunosuppression alone. Twelve patients were treated with both reduction in immunosuppression and surgical resection of all known disease. Thirty-one of 42 patients (73.8%) achieved a complete remission. Of those patients who were treated with reduction in immunosuppression alone, 19 of 30 (63%) responded with a median time to documentation of response of 3.6 weeks. Multivariable analysis showed that elevated lactate dehydrogenase (LDH) ratio, organ dysfunction, and multi-organ involvement by PTLD were independent prognostic factors for lack of response to reduction in immunosuppression. In patients with none of these poor prognostic factors, 16 of 18 (89%) responded to reduction in immunosuppression in contrast to three of five (60%) with one risk factor and zero of seven (0%) with two to three factors present. The analysis also showed that increased age, elevated LDH ratio, severe organ dysfunction, presence of B symptoms (fever, night sweats, and weight loss), and multi-organ involvement by PTLD at the time of diagnosis are independent prognostic indicators for poor survival. With median follow-up of 147 weeks, 55% of patients are alive with 50% in complete remission., Conclusions: Reduction in immunosuppression is an effective initial therapy for PTLD. Clinical prognostic factors may allow clinicians to identify which patients are likely to respond to reduction in immunosuppression.

Bone marrow involvement can be found in patients with low-, intermediate-, or high-grade non-Hodgkin's lymphoma. A 40-year-old woman experienced onset of low back pain radiating into her entire right lower extremity. Plain x-rays of her right leg and computed tomography of chest, abdomen, and pelvis were unremarkable. Magnetic resonance imaging of pelvis and thighs revealed diffusely abnormal marrow signal (low T1 and high T2 weighted) in the pelvis and femora. The patient underwent (18)F-fluorodeoxyglucose positron emission tomography (FDG-PET) scan to evaluate the extent of her disease. The scan revealed diffuse scattered foci of abnormal FDG uptake in the bone/bone marrow, which was particularly intense in the axial bones. Bone marrow biopsy confirmed extensive involvement of the bone marrow with diffuse large B-cell lymphoma. This case report highlights the utility of FDG-PET in the detection of bone marrow involvement by aggressive lymphoma.

Allogeneic donor leukocytes can be used after nonmyeloablative conditioning to exploit their graft-versus-tumor (GVT) activity in the setting of reduced conditioning-regimen toxicity. This approach may be particularly useful for patients who relapse after autologous stem cell transplantation (SCT). However, GVT activity, toxicity, and ability to establish mixed chimerism may differ in patients who were heavily pretreated prior to SCT compared with patients treated earlier in the course of their disease. We have performed a series of studies of nonmyeloablative allogeneic transplantation and present data on the subset of 14 patients treated for relapse after autologous SCT: 4 patients received no conditioning and unstimulated donor leukocyte infusions (DLI), 10 patients received conditioning with fludarabine and cyclophosphamide followed by unstimulated or granulocyte-colony-stimulating factor (G-CSF)-stimulated allogeneic peripheral blood stem cells (PBSCs), 4 patients received no graft-versus-host disease (GVHD) prophylaxis, and 10 patients received cyclosporine GVHD prophylaxis. All but 1 patient had sustained donor chimerism at least 30 days after allogeneic cell therapy (ACT), and 8 patients had more than 80% donor chimerism after ACT. Acute GVHD developed in 11 patients (grade III-IV, n = 6). Aplasia was more frequent in the patients receiving unstimulated PBSCs, despite the development of mixed chimerism. There were 6 complete responses and 4 partial responses; response was independent of conditioning and growth-factor stimulation of the donor graft. Five patients died of treatment-related causes and 4 patients died from progressive disease. Four patients remained alive 27 to 194 weeks (median, 66 weeks) after ACT. Prior autologous SCT may define a subset of patients at particularly high risk for GVHD and other toxicity after ACT. However, these data show that ACT with either DLI or G-CSF-stimulated blood cells results in direct GVT activity in some patients with Hodgkin's disease, myeloma, and non-Hodgkin's lymphoma, even after relapse from autologous SCT. Most patients developed donor chimerism with minimal conditioning. Alternative prophylactic regimens that control GVHD while maintaining GVT are needed to improve outcomes in these heavily pretreated patients.

The prognosis of patients with progressive intermediate-grade non-Hodgkin's lymphoma (NHL) after high-dose chemotherapy and autologous peripheral stem-cell transplantation (PSCT) is poor, with survival measured in months. The advent of monoclonal antibody therapy for NHL has created new options for effective therapy with relatively mild side effects. We report on two patients with progressive intermediate-grade NHL after PSCT who were treated with monoclonal antibody therapy. Both patients initially received rituximab (unlabeled anti-CD20 monoclonal antibody) and were subsequently treated with (90)Y-epratuzumab (yttrium-90-labeled humanized anti-CD22 monoclonal antibody) at relapse. One patient received (90)Y-epratuzumab alone while the other was treated with higher doses in combination with autologous peripheral stem-cell infusion. Both patients achieved a rapid response to the radiolabeled antibody with minimal toxicity. Monoclonal antibody therapy may be an effective and tolerable treatment for progressive NHL after PSCT.

The purpose of this study was to determine the efficacy, engraftment kinetics, effect of bone marrow tumor contamination, and safety of high-dose therapy and granulocyte-colony stimulating factor (G-CSF) mobilized peripheral blood progenitor cell (PBPC) support for patients with responding metastatic breast cancer. Forty two patients underwent G-CSF (10 microg/kg) stimulated PBPC harvest. PBPC and bone marrow aspirates were analyzed by histologic and immunocytochemical methods for tumor contamination. Thirty-seven patients received high-dose therapy consisting of cyclophosphamide 6 g/m2, thiotepa 500 mg/m2, and carboplatin 800 mg/m2 (CTCb) given as an infusion over 4 d followed by PBPC reinfusion and G-CSF (5 microg/kg) support. No transplant related deaths or grade 4 toxicity was recorded. CD34+ cells/kg infused was predictive of neutrophil and platelet recovery. With a median follow-up of 38 months, three year survival was 44% with relapse-free survival of 19%. Histological bone marrow involvement, found in 10 patients, was a negative prognostic factor and was associated with a median relapse-free survival of 3.5 months. Tumor contamination of PBPC by immunohistochemical staining was present in 22.5% of patients and found not to be correlated with decreased survival. G-CSF stimulated PBPC collection followed by a single course of high dose chemotherapy and stem cell infusion with G-CSF stimulated marrow recovery leads to rapid, reliable engraftment with low toxicity and promising outcome in women with responding metastatic breast cancer.

Serum soluble transferrin receptor (sTfR) concentration has been evaluated in the diagnosis of iron deficiency in otherwise healthy individuals and in patients with rheumatoid arthritis, but has not been studied in a general population of patients with complicated clinical presentations. In this study, 145 anaemic patients with a variety of medical conditions undergoing diagnostic bone marrow aspiration for any reason were tested by a complete blood count, a panel of biochemical tests to evaluate iron status, bone-marrow aspirate iron stain, and serum sTfR concentration. Sixteen per cent lacked stainable iron in the marrow aspirate. All biochemical parameters differed significantly between patients with or without stainable marrow iron. The sTfR assay was significantly more sensitive but less specific than other iron status assays in identifying the absence of stainable iron. Logistic regression analysis demonstrated that only sTfR and ferritin contributed independently to the prediction of marrow iron status. Serum ferritin alone was highly specific but insensitive. A decision algorithm combining serum ferritin and sTfR was as sensitive as TfR and as specific as serum ferritin. The measurement of serum sTfR, especially in conjunction with serum ferritin, is a valuable addition to the existing methods for predicting the results of marrow aspirate iron stains.

We examined the clinical characteristics of six patients with myelofibrosis secondary to myeloproliferative diseases whose clinical courses were complicated by pulmonary hypertension to determine possible causal links between the two disorders. Six patients (four male, two female), with diagnoses of myeloproliferative disease, myelofibrosis (one with polycythemia vera, three with agnogenic myeloid metaplasia, one with unclassified myeloproliferative syndrome, one with essential thrombocytosis), and pulmonary hypertension are presented. Measurement of the pulmonary artery pressure was performed by Doppler echocardiography in all patients and by right sided heart catheterization in four patients. The range of resting pulmonary artery systolic pressure was 35 to 47 mmHg above the mean right atrium by echocardiography. One patient had autopsy evidence of pulmonary myeloid metaplasia and interstitial fibrosis; another had acute leukemic infiltration of the lung parenchyma. All patients had thrombocytosis; symptomatology in one patient with marked thrombocytosis improved with plateletpheresis. Two patients suffered systemic thrombosis. All patients had severe hepatomegaly. Two patients had evidence of left ventricular dysfunction. The interval between the development of dyspnea and death was less than seven months in five of the patients. A causal link between pulmonary hypertension and myelofibrosis secondary to myeloproliferative diseases is suggested for each patient. Hematopoietic infiltration of the pulmonary parenchyma, portal hypertension, thrombocytosis, hypercoagulability, and left ventricular failure may account in part for the development of pulmonary hypertension in these patients. Patients with myelofibrosis and dyspnea should have Doppler echocardiography to evaluate pulmonary artery pressures.

We report a case of extramedullary myeloid cell tumor of the urinary bladder in an elderly male with a three year history of myelodysplastic syndrome (refractory anemia with excess blasts), noninvasive papillary transitional cell carcinoma of the urinary bladder, and in situ transitional cell carcinoma of the left ureter. Light microscopy demonstrated a poorly differentiated neoplasm composed of medium to large cells with eosinophilic cytoplasm. The tumor cells showed immunohistochemical expression of myeloperoxidase, lysozyme, CD15, CD68 and CD43. Bone marrow examination following cystectomy demonstrated refractory anemia with excess blasts (6-10%) and a normal karyotype. Cytogenetics, approximately 1 year after cystectomy, demonstrated a deletion of the short arm of chromosome number 12. Four years after presentation, the patient succumbed to pulmonary aspergillosis.

We describe a patient who presented with a neutrophilic leukocytosis, normal karyotype, and IgA lambda multiple myeloma. One year after diagnosis she developed diffuse myelofibrosis as well as multiple lytic lesions of bone. Given the myeloproliferative features of her case, the clonality of her peripheral leukocytes was determined prior to treatment. Analysis of X-chromosome inactivation at the X-linked human androgen-receptor gene locus (HUMARA) proved that granulopoiesis was polyclonal. Subsequent treatment of the myeloma reversed with myelofibrosis and normalized her WBC count. This is the first case of multiple myeloma with myelofibrosis in which a concomitant clonal myeloproliferative disease was ruled out at a genetic level. The myeloproliferative features in this case are presumed to be induced by cytokines produced by the plasma cell clone.

A patient with a high level serum monoclonal IgM lambda paraprotein (3,850 mg/dL) was found to have a mass infiltrating the gastric mucosa. Gastric biopsy with immunohistochemical stains showed a B-cell lymphoplasmacytoid infiltrate expressing IgM lambda, consistent with Waldenström's macroglobulinemia. The patient's response to gastric radiation indicated that the primary source of the macroglobulinemia was the stomach. This is an extremely rare presentation, with only six other reported cases of this entity with gastric involvement.

We examined erythropoietin (EPO) gene expression and EPO production during hypoxia in two Sprague-Dawley rat strains with divergent polycythemic responses to hypoxia. Hilltop (H) rats develop severe polycythemia, severe hypoxemia, and pulmonary artery hypertension. The H rats often die from a syndrome indistinguishable from chronic mountain sickness (CMS) in humans. Madison (M) rats develop polycythemia and pulmonary artery hypertension that is modest and suffer no excess mortality. We tested the hypothesis that these rat strains have different stimulus-response characteristics governing EPO production. Rats of each strain were exposed to hypoxia (0.5 atm, 73 Torr inspired PO2), and renal tissue EPO mRNA and EPO levels, plasma EPO, ventilation, arterial and renal venous blood gases, and indexes of renal function were measured at fixed times during a 30-day hypoxic exposure. During extended hypoxic exposure, H rats had significantly elevated renal EPO mRNA, renal EPO, and plasma EPO levels compared with M rats. Ventilatory responses and indexes of renal function were similar in the strains during the hypoxic exposure. H rats had greater arterial hypoxemia from the onset of hypoxia and more severe renal tissue hypoxemia and greater polycythemia after 14 days of hypoxic exposure. When EPO responses were expressed as functions of renal venous PO2, the two strains appeared to lie on the same dose-response curves, but the responses of H rats were shifted along the curve toward more hypoxic values. We conclude that H rats have significantly greater polycythemia secondary to poorer renal tissue oxygenation, but the stimulus-response characteristics governing EPO gene expression and EPO production do not seem to differ between M and H rats. Finally, the regulation of EPO levels during hypoxia occurs primarily at the transcriptional level.

A contemporary health system seeks to overcome the excesses and shortcomings of the medical model by integrating wholistic concepts and practices into the medical care it provides. Established on the grounds of an acute care hospital as one of its departments, the Franciscan Wholistic Health Center's (FWHC) goal-explicit spirituality and the involvement of FWHC staff in their own as well as their client's spiritual development-distinguishes it from other efforts.

Acquired inhibitors of factor VIII have rarely been reported in the presence of systemic lupus erythematosus (SLE). Treatment is usually corticosteroids, with or without immunosuppressive agents such as cyclophosphamide or azathioprine. We report here case histories of 2 patients, one with documented SLE, the other with a forme fruste of SLE. Both patients had inadequate responses to corticosteroids and immunosuppressive agents. Both responded to intravenous immunoglobulin, with a decrease in their titers of factor VIII inhibitor and significantly decreased frequency of bleeding episodes despite persistent low-level inhibitor titers. Better control of their SLE symptoms and findings was also observed. Previously reported treatments of acquired factor VIII inhibitors in SLE are discussed.

We have used in situ hybridization to determine the localization and distribution of cells expressing the erythropoietin (EPO) gene in kidneys of rats exposed to reduced oxygen tensions to characterize the control of renal EPO formation during hypoxic hypoxia. Animals were subjected to severe hypoxia (7.5% O2) for 4, 8 and 32 hours to assess changes related to the duration of hypoxic exposure, and additionally to 9% and 11.5% O2 for eight hours to define changes related to the degree of hypoxia. The number of cells containing EPO mRNA were counted on tissue sections and compared to tissue concentrations of EPO mRNA and to the serum hormone concentrations. In situ hybridization revealed expression of the EPO gene exclusively in peritubular cells that were predominantly located in the cortical labyrinth under all conditions tested. After four hours of severe hypoxia (7.5% O2) approximately 170-fold more cells were found to contain EPO mRNA than under normoxic conditions. The number of EPO producing cells did not change significantly between four and eight hours exposure to 7.5% O2, but the amount of EPO mRNA per kidney increased approximately threefold. Further continuation of hypoxia resulted in down-regulation of renal EPO mRNA levels, which was mainly due to a reduction in the number of cells containing EPO mRNA. Comparison of graded degrees of hypoxia applied for eight hours showed an inverse exponential relationship between oxygen tension and the number of EPO producing cells. This recruitment of cells expressing the EPO gene occurred along a gradient extending from the corticomedullary border to the subcapsular tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

The cellular origins of erythropoietin were investigated in the rat using a probe derived from a cloned rat erythropoietin cDNA. In anaemic-hypoxic rat liver, in situ hybridization detected erythropoietin mRNA primarily in hepatocytes and less frequently in nonparenchymal sinusoidal or perisinusoidal liver cells. An RNase protection assay was used to compare the erythropoietin mRNA contents of separated rat liver cell fractions and also suggested that hepatocytes are the major source of extrarenal erythropoietin with nonparenchymal liver cells contributing less than 1% to total hepatic erythropoietin production. In kidney, in situ hybridization localized erythropoietin mRNA in nonepithelial cells, as yet of undefined lineage, in the cortical and outer medullary interstitium. These results indicate that, in the rat, the primary sources of erythropoietin in liver and kidney are different types of cells.

Parenchymal iron deposition occurs in hemochromatosis, while iron is deposited in reticuloendothelial (RE) cells after blood transfusions or rhabdomyolysis. Magnetic resonance images of patients with decreased liver signal intensity on T2-weighted images at 1.5 T were blindly compared in an effort to distinguish these conditions. In each of five patients with hemochromatosis, the pancreas had low signal intensity, but splenic signal intensity was decreased in only one. In contrast, only three of the 16 patients with RE iron overload had low pancreatic signal intensity, while all of these patients either had low splenic signal intensity (n = 14) or previously underwent splenectomy (n = 2). Distinction among these causes of iron deposition is clinically important because parenchymal iron overload from hemochromatosis may produce significant tissue damage, while the RE iron of transfusions and rhabdomyolysis is of little clinical consequence.