Background: Increased incidence of cardiac involvement and pulmonary hypertension (PH) has been reported in patients with chronic myeloproliferative disorders (CMPD). Most studies are small and retrospective except one where majority of the patient had essential thrombocytosis (ET). Method: We conducted a study to assess the incidence of PH in patients with CMPD. Patients were excluded if they had secondary cause of PH. Diagnosis of PH was established if right ventricular systolic pressure (RVSP) by transthoracic echocardiography (TTE) and Doppler study was ≥ 35 mmHg. 27 patients with diagnosis of CMPD established by standard criterion were included in the study. 9 patients had ET, 14 had polycythemia vera (PV) and 3 had chronic myeloid leukemia (CML). Results: Diagnosis of PH was established in 14/27 patients. 2 patients were excluded form analysis because of poor ejection fraction on TTE, 1 with PV and 1 with CML, giving final diagnosis of PH in 12/25 (48%) patients. 9 patients were males and 16 were females. Mean age at diagnosis in the entire cohort was 56.2 years and that with and without PH was 54.5 vs. 57.7 years respectively. Mean duration of follow up was 8.7 years and that with and without PH was 7.8 vs. 9.9 years respectively. 7/9 ET, 5/14 PV AND 0/2 CML patients had PH, mostly of mild to moderate severity. All patients were asymptomatic at the time of their last visit within last 2 months. The results are depicted in the table 1. There was no relation of PH to duration of disease, platelet count and hematocrit at diagnosis or during follow up period for the entire group or specific diagnosis of ET or PV. Because of erratic and variable duration of aspirin use by individual patients, we could not determine its significance. Discussion: The results of our study are similar to the study reported by Garypidou et al with regard to ET. However they had only 2 patients with PV and both of them had no evidence of PH. In our study 5/14 PV (36%) patients had PH, indicating PV patients also have significant risk of having PH. Pathogenesis of PH can be reliably related to CMPD because: Cases of secondary PH were excluded TTE excluded cardiac causes of PH Incidence of primary PH is very low (0.2cases/100,000) and usually occurs in 3rd or 4th decade. Moreover autopsy studies have demonstrated the presence of atypical megakaryocytes and thrombotic material in the lung capillaries of pulmonary hypertension patients and CMPD. Increased level of thrombopoietin also has been demonstrated in pulmonary artery of patients with PH. Thus platelets are implicated in pathogenesis of PH in patients with CMPD. Since PH seems to be common in patients with CMPD, more studies are needed to study the long-term impact of PH on survival in these patients. Impact of therapy including platelet lowering agents and ASA on development and progression of PH also needs to be studied. Table 1 CMPD Total No (%) MeanAge at Dx(yrs) Duration of Ds(yrs) Mean Plt at Dx(k/muL) Mean Plt at fu(k/muL) Mean Hct at Dx(%) Mean Hct at fu(%) Dx-diagnosis, Ds-disease, yrs-years, Plt-platelet, fu-follow up, Hct-hematocrit, PH-pulmonary hypertension, +-present, − absent ET PH + 7/9(77.8) 56.3 7.2 877.7 488.6 41.1 36.7 ET PH − 2/9(22.2) 65.0 8.0 698.0 492.0 45.3 40.0 PV PH + 5/14(35.7) 52.0 10 528.8 320.4 53.9 43.2 PV PH − 9/14(64.3) 58.7 10.6 511.9 316.8 58.9 41.9 CML PH − 2/2 46.5 4.0 620.5 387.5 36.9 36.2

Prostate cancer is the most common malignancy and the second most common cause of cancer-associated mortality in males. Bone metastasis is frequent and generally multiple and osteoblastic. Presentation of a pure osteolytic and solitary metastasis from a prostate carcinoma is extremely rare. We report a case of prostate cancer in a 70-year-old man who presented with progressive severe right hip pain and stiffness with no urinary symptom. A whole-body bone scan revealed a solitary metastasis to the right hip. A prostate biopsy revealed prostate adenocarcinoma. We believe this is the first reported case of presentation of a solitary osteolytic bone metastasis in the pelvis from carcinoma of the prostate.

4224 Low-dose of methotrexate (MTX), less than 20 mg per week, is a regimen, widely used for rheumatoid arthritis (RA) treatment. Whereas the hepatotoxicity of MTX is well recognized, the bone marrow toxicity is still a concern, with pancytopenia being a rare, but potentially fatal complication. Risk factors for pancytopenia include advanced age, renal impairment, infection and hypoalbuminemia. Myelosupression is more likely if MTX is taken daily. However, RA by itself can cause hematologic abnormalities, such as Felty's and large granulocyte lymphocytes syndromes. Because the management of pancytopenia secondary to MTX toxicity is completely different from the treatment of hematologic complications, bone marrow examination is important. We reported a case of pancytopenia in a patient receiving low-dose of MTX for disabling RA. A 82-year-old woman with coronary artery disease, renal insufficiency and mild dementia was admitted with 1 months history of weakness, oral ulcers and bruising. Patient's medications list included totally 15 drugs, with aspirin, tylenol, ibuprophen and low-dose of methotrexate for rheumatoid arthritis. The patient had normal CBC 4 weeks prior to admission. Upon examination, she had bruises, petechia and multiple arthritic deformities, especially of small joints. She had severe mucositis and mild pretibial edema. Laboratory investigations revealed: hemoglobin: 9.3 g/dL; MCV: 110 fl; total leukocyte count: 2.300/mm3 with neutrophil count of 800/mm3; platelets count: 6 K/uL; BUN: 17 mg/dL; creatinin: 1.4 mg/dL; folic acid level: 2.53 ng/ml; vit-B12 level, thyroid function and liver function tests were normal, except of mild hypoalbuminema. Peripheral smear showed rare megaloblasts, leucopenia, and thrombocytopenia; no blasts or large granular lymphocyte were found. Biopsy revealed markedly hypocellular bone marrow; immunophenotyping failed to show lympho- or myeloprolipherative disorders or leukemia. A diagnosis of pancytopenia secondary to MTX toxicity was made. MTX was discontinued, the patient was placed on neutropenic precautions and was treated with blood and platelets transfusions, folic acid and G-CSF. She was discharged on day 14 with normal hematologic parameters. Although infrequent, pancytopenia is a severe complication of low-dose MTX therapy. Because the main route of MTX elimination is via renal excretion, which can be inhibited by many medications (aspirin, NSAID's, probenecid, antibiotics), throughout the therapy a number of precautions are important: periodic creatinine clearance and serum albumin determination, especially in elderly patients. Dosing schedule should be clearly printed on MTX boxes. In severe cases of pancytopenia bone marrow biopsy is warranted. Consensus does not exist, but folate supplementation may reduce MTX toxicity and does prevent discontinuation of therapy. Because folate may have a benefit of cardioprotection due to its ability to prevent MTX-induced hyperhomocysteinemia, it is especially important in the treatment of elderly patients with cardiac problems. Disclosures: No relevant conflicts of interest to declare.

BackgroundHuman immunodeficiency virus (HIV) is associated with numerous hematological disorders—anemia, pancytopenia, and hemostatic abnormalities being the most common ones. Direct antiglobulin test has frequently been observed in the clinical syndrome of HIV, but autoimmune hemolytic syndrome (AIHA) is rare. Review of other reports of DAT and AIHA in patients with HIV infections suggests that these autoantibodies may be associated with anemia in this population. Many of these patients are also concurrently infected with hepatitis C virus (HCV). We recently reported a significantly higher incidence of autoantibodies to red blood cells in patients with HCV infection as compared to healthy blood donors. We also noted an even higher incidence of autoantibodies to red blood cells in patients concurrently positive for both HCV and HIV. We hypothesized that HCV infection in patients with HIV confers a much higher risk of developing autoantibodies against red blood cells.MethodSixty-eight patients with HCV and HIV were randomly screened for DAT and AIHA in our hospital from June 2001 to June 2004.ResultsThirty-four patients were positive for HIV. Among them 16 were positive for HCV and 18 were negative. Thirty-four patients were positive for HCV only.We noted an incidence of 18.8% of DAT positivity in patients with concurrent HIV and HCV infection. One of these three patients had clinical AIHA, with high LDH, indirect bilirubinemia, and low haptoglobin. Five percent of the patients with HIV in the absence of HCV had positive DAT. There was no clinical AIHA in this group, and 14.7% of patients with HCV infection alone had positive DAT. One of these five patients had clinical AIHA.ConclusionOur study indicates that HIV-positive patients who are concurrently infected with HCV have a higher incidence of autoantibodies against erythrocytes.

A 26-year old woman with diagnosis Anorexia Nervosa, restricting type presented to the ED with refusal to eat, weakness and amenorrhea. She weighted 29.2 kg, which at a height of 5 ft made her BMI 12.6 kg/m2. Laboratory data showed a hemoglobin of 9.3/dl, hematocrit of 28.4%, leukocyte count of 8.9 K/ul, platelets count 131 K/ul. Ferritin was 168.4 ng/ml, serum iron 80 mcg/dL, transferin saturation 35.7%. Initial chemistries revealed albumin of 3.5 g/dl, prealbumin 12.4 mg/dl. Following hydration, the hemoglobin level fell to 6.9 g/dl, hematocrit to 22.0%. Remarkably, patient also experienced transient leukopenia (3.0 K/ul) and thrombocytopenia (92 K/ul). Peripheral blood smear revealed anisocytosis, polychromasia, hypochromia and RBC fragments. The histological examination of bone marrow biopsy and aspirate showed almost complete depletion of hematopoietic tissue with rare erythroid, myeloid cells and occasional megakaryocyte. Fat tissue was completely melted presenting Gelatinous Degeneration, no stainable iron was seen. The flow cytomery did not show abnormal myeloid maturation, increased blast population or lymphoproliferative disorder. Smear prepared from the flow sample contained maturing myeloid and erythroid cells. Reticulocytes were preserved and accounted for 0.7%. The patient was treated with blood transfusions and nutritional support. After 2 months, all biochemical imbalances and hematological parameters normalized. This is reflected in a hemoglobin level of 10.5g/dL, hematocrit of 31.3%, leukocyte count of 5.7 K/ul and platelet count of 371 K/ul. On the day of discharge to Anorexia Nervosa Clinic patient weighted 32.0 kg. Although abnormalities in the peripheral blood are common in anorexia nervosa, in the rare cases anorexia may be associated with hypo- and aplasia, variable hypocellularity and complete Gelatinous Degeneration Bone Marrow. GDBM is an extreme condition significantly related to bone marrow necrosis and characterized by reduction of fat spaces and accumulation of material rich in acid mucopolysacharides, what we observed in our patient. The bone marrow fat depletion could adversely affect the local environment and interfere with normal hematopoiesis by way of an alteration in the release cytokines or growth factors. We have hypothesized that Gelatinous Degeneration Bone Marrow related only to the amount of weight loss; not to other factors such as duration of caloric deprivation, age or clinical type of anorexia. In most anorexia cases in the literature, alterations of bone marrow were reflected in the peripheral blood as mild or no cytopenia. However, we found that peripheral blood findings do not correlate with bone marrow changes, and are not good predictors of bone marrow involvement in anorexia nervosa. As a result, bone marrow morphology should be reviewed to assess severity of hematologic abnormalities in this instance. Our findings confirmed that even severe aplastic bone marrow alterations as gelatinous degeneration, as well as abnormalities in the peripheral blood is a reversible process conditioned to weight recovery after establishment of adequate nutrition. Importantly, clinical significance of the laboratory abnormalities and medical findings in anorexia nervosa patients has not been firmly established. We do not have risk-stratification for treatment, what is crucial for reversing a common, but seems under recognized problem in our ‘obsessed with weight loss’ culture.