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Biomedical subjects

R P Warrier

Publications and source records attributed to R P Warrier.

At least 19 recordsLinked to original sources
PubMed2003

Effects of iron deficiency on the secretion of interleukin-10 by mitogen-activated and non-activated murine spleen cells.

Interleukin (IL)-10 plays crucial regulatory roles in immune responses by inhibiting the secretion of several cytokines (IL-2, IL-12, interferon-gamma (IFN-gamma)) and lymphocyte proliferation. Iron deficiency, a public health problem for children, alters these immune responses. To determine whether these changes are related to altered IL-10 secretion, we measured IL-10 in 24 and 48 h supernatant of spleen cell cultures from iron deficient (ID), control (C), pairfed (PF), and ID mice fed the control diet (iron repletion) for 3 (R3) and 14 (R14) days (d, n = 12/group). Mean levels of hemoglobin, hematocrit, and liver iron stores varied as follows: C approximately equal PF approximately equal R14 > R3 > ID (P < 0.01). Mean baseline IL-10 levels of ID mice tended to be higher than those of other groups (P > 0.05, ANOVA). Mean IL-10 levels secreted by concanavalin A (Con A) and antibody raised against cluster of differentiation molecule 3 (anti-CD3)-treated cells (+/-background) were lower in ID than in C (48 h) and iron replete mice (P < 0.05). Underfeeding also reduced IL-10 secretion by anti-CD3-treated cells (48 h, P < 0.05). Lymphocyte proliferative responses to anti-CD3 +/- anti-CD28 antibodies were lower in ID than in C and PF mice, and they were corrected by iron repletion (P < 0.05). IL-10 levels negatively correlated with indicators of iron status (r <or= -0.285) and lymphocyte proliferation (r <or= -0.379 [r <or= -0.743 for ID mice]), but positively correlated with IFN-gamma levels (r <or= 0.47; P < 0.05). Data suggest that iron deficiency has a generalized deleterious effect on cells that secrete both cytokines. Reduced IL-10 secretion by activated cells does not overcome the inhibition of lymphocyte proliferation due to other factors of T cell activation that are regulated by iron.

Animals↗
PubMed2003

Acute perforative appendicitis during preoperative chemotherapy for Wilms tumor.

Infectious complications are not uncommon in children undergoing treatment for cancer. Abdominal pain, especially right lower quadrant pain secondary to appendiceal and cecal inflammation, is a major concern in immunocompromised hosts and a potential source of sepsis. The authors report the case of a child who developed acute perforative appendicitis requiring appendectomy while on preoperative chemotherapy for Wilms tumor, stage IV, favorable histology. Problems related to diagnosis and management of acute abdominal pain and infection in an immunocompromised child with an abdominal mass are discussed along with a review of the literature.

Abdominal Pain↗
PubMed2001

Immunotactoid glomerulopathy in sickle cell anemia.

A 12-year-old African American male with homozygous sickle cell disease (SCD) was admitted with insidious onset of periorbital and scrotal edema. The initial evaluation failed to reveal any underlying monoclonal gammopathy, or cryoglobulinemia, or other systemic causes for the renal disease. A percutaneous renal biopsy was consistent with immunotactoid glomerulopathy (ITG), which is rare in children and is characterized histologically by fibrillar deposits in the glomeruli. Children can present with symptoms of nephrotic syndrome and progress to end stage renal disease. Our patient was treated with an ACE inhibitor and is currently free of edema and with normal renal function on follow-up at 1 year. Immunotactoid glomerulopathy should be considered in the differential diagnosis of nephrotic syndrome in children with sickle cell disease. Renal biopsy is indicated in children with sickle cell disease and nephrotic syndrome and ITG should be considered as potential cause. Although there is no effective treatment for this condition, ACE inhibitors can decrease the protein-uria and possibly delay the progression to end stage renal disease. The side effects related to the use of ACE inhibitors should be monitored. These include renal impairment, hyperkalemia, anemia, neutropenia, and angioedema. Since we have a short follow-up in our patient, the role and safety of ACE inhibitors in the management of ITG need further evaluation.

Anemia, Sickle Cell↗
PubMed2000

Association between increased levels of TNF-alpha, decreased levels of prealbumin and retinol-binding protein, and disease outcome.

We determined whether there is an association between tumor necrosis factor-alpha (TNF-alpha), undernutrition [prealbumin (PA) <160 mg/L, retinol binding protein (RBP) <30 mg/L], disease stage, outcome (death or survival), and race in children with leukemia. TNF-alpha, PA, and RBP were measured in 52 patients (0.8 to 17 years old): 18 African Americans, 34 whites; 27 newly diagnosed (ND), and 25 in clinical remission (CR). Mean levels of TNF-alpha were higher in patients than in 46 healthy children (p < 0.05), but were not different between ND and CR groups. Mean acute phase proteins (APP) were different among groups: ND > CR > controls (p < 0.05). Mean levels of PA and RBP were lower in patients than in controls (p < 0.051, and tended to be higher in CR than in ND patients. African-American patients had lower concentrations of TNF-alpha, PA, and RBP but higher APP than white patients (p < 0.05). CR patients and African-American patients who died tended to have higher levels of TNF-alpha and APP, but lower PA and RBP than those who survived. A higher percentage of ND African Americans (45%) than of ND whites (13%) died. Results suggest that undernutrition and inflammation in CR patients and African Americans were associated with poor survival, and that ND African Americans have a poorer outcome than whites independently of TNF-alpha levels.

Acute-Phase Proteins↗
PubMed1999

Lack of difference in iron status assessed by soluble transferrin receptor between children with cerebral malaria and those with non-cerebral malaria.

We conducted this study to determine whether children with cerebral malaria are less likely to have tissue iron deficiency than those with non-cerebral malaria. Iron status was assessed by soluble transferrin receptor (sTfR), serum ferritin, and haemoglobin in 44 Zaïrian children: 15 with cerebral malaria, 14 with non-cerebral malaria, and 15 without malaria (age range 0.5-16 years). Although there was no significant difference in the mean concentrations of sTfR, serum ferritin, or haemoglobin between either group of patients, a higher percentage of children with cerebral malaria (27 per cent) than those with non-cerebral malaria (14 per cent) or controls (7%) had sTfR levels above 7.3 mg/l (suggestive of tissue iron deficiency). A higher percentage of children with cerebral malaria (40 per cent) than with non-cerebral malaria (29 per cent) or controls (20 per cent) also had either serum ferritin < 100 micrograms/l and inflammation or sTfR > 7.3 mg/l or both. The data suggest that children with cerebral malaria are as likely to have tissue iron deficiency as those with non-cerebral malaria.

Adolescent↗
PubMed1998

Iron deficiency reduces the hydrolysis of cell membrane phosphatidyl inositol-4,5-bisphosphate during splenic lymphocyte activation in C57BL/6 mice.

Iron deficiency impairs lymphocyte proliferation in humans and laboratory animals by unknown mechanisms. In this study, we investigated whether this alteration can be attributed in part to impaired hydrolysis of cell membrane phosphatidyl inositol-4, 5-bisphosphate (PIP2), a required early event of T-lymphocyte activation. The study involved 46 iron-deficient (ID), 26 control (C) and 23 pair-fed (PF) mice, and ID mice that were repleted for 3 (n = 16), 7 (n = 17) or 14 d (n = 18). Mice were killed after 40-63 d (mean, 48 d) of consuming the test diet (0.09 mmol/kg iron) or the control diet (0.9 mmol/kg). The mean (+/-SEM) hemoglobin concentrations were 57 +/- 16.7, 176 +/- 2.6 and 181 +/- 9.7 g/L for ID, C and PF groups, respectively. After splenic lymphocytes were labeled in vitro with 3H-myoinositol for 3 h, PIP2 hydrolysis was estimated by measuring the radioactivity recovered as a mixture of inositol mono-, di- and triphosphate (IP) from concanavalin A (0, 1, 2.5, 5 and 10 mg/L) activated cells. Although cells from ID mice and those from mice repleted for 3 d incorporated slightly more radioactivity in cellular phospholipids than did cells from C or PF mice, less (P < 0.005) was recovered as IP than in controls, suggesting impaired conversion of the precursor to PIP2. At almost all incubation periods (10-120 min) and mitogen concentrations, the rate of PIP2 hydrolysis expressed as the ratio of radioactivity obtained in Con A-treated to untreated cells was significantly (P < 0.05) reduced in cells from ID mice compared with those obtained from C and PF mice. For cells that were activated for 60 min or less, iron repletion for 14 d significantly (P < 0.05) improved the rate of PIP2 hydrolysis. PIP2 hydrolysis positively and significantly (P < 0.05) correlated (r = 0.27-0.56) with indicators of iron status. Mitogenic response was also significantly (P < 0.05) reduced in ID but not PF mice, and it was corrected by iron repletion for 3, 7 or 14 d. Lymphocyte proliferation positively (r = 0.27-0.37, P < 0.01) correlated with indices of iron status and IP ratios. The data suggest that reduced PIP2 hydrolysis contributes to impaired blastogenesis in iron deficiency.

Animals↗
PubMed1997

Hemoglobin A2 levels in healthy persons, sickle cell disease, sickle cell trait, and beta-thalassemia by capillary isoelectric focusing.

Simultaneously measuring major and minor hemoglobin (Hb) variants by capillary isoelective focusing, we obtained HbA2 intervals in healthy volunteers (n = 412) (reference value) and patients with HbS or beta-thalassemia. We classified normal HbA2 reference intervals into three age groups: 5 months or younger (1.2% +/- 1.5%), 6 months to 1 year (2.2% +/- 0.9%), and 1 year or older (2.4% +/- 0.9%). These intervals were comparable to those used with other methods. Patients 1 year of age or older with HbS had significantly higher HbA2 levels (sickle cell trait, 2.9% +/- 0.9%; sickle cell anemia, 2.8% +/- 1.0%; P < .05). Although reference HbA2 intervals overlapped those in patients with HbS, no overlap in HbA2 levels was noted between these groups and patients with beta-thalassemia (observed range, 4.3% to 7.5%). The higher than normal HbA2 interval in patients with HbS must be considered before a diagnosis of sickle cell trait or sickle cell disease with beta-thalassemia is made.

Anemia, Sickle Cell↗
PubMed1997

Tumor necrosis factor alpha in children with sickle cell disease in stable condition.

Tumor necrosis factor alpha (TNF-alpha) is known to induce wasting in humans and animals. This study was undertaken to determine TNF-alpha concentrations in children with sickle cell disease (SCD) and whether high TNF-alpha levels are more likely to be present in children with growth deficits, infection, or pain crisis. Tumor necrosis factor alpha was measured using enzyme immunoassay in 143 blood samples obtained from 101 children. Mean TNF-alpha levels were higher in patients (50 pg/mL) than in 21 control children (19 pg/mL) and in 26 laboratory employees (20 pg/mL). During the follow-up period, 35%, 38%, and 28% of children with SCD had infection, pain crisis, or a blood transfusion, respectively. Mean TNF-alpha concentrations were higher in children who had an infection than in those who did not. No significant effect of pain crisis or blood transfusion was observed. Tumor necrosis factor alpha concentrations were above normal (> 40 pg/mL) in 15% of controls, 34% of children with SCD, and 52% of children with SCD who had an infection and 33% of those who did not. A higher percentage of children who had elevated TNF-alpha levels had weight (46% versus 31%) or height (50% versus 28.6%) deficits than children who had normal TNF-alpha levels. These results indicate that most children with SCD in stable condition have normal TNF-alpha concentrations and that those with high TNF-alpha levels are more likely to have growth deficits.

Adolescent↗
PubMed1996

Serum transferrin receptor concentrations in women with mild malnutrition.

We determined the influence of undernutrition on blood soluble transferrin receptor (sTfR) concentrations, an indicator of iron deficiency, in 99 Zairean women (aged 16-45 y) without inflammation. They were recruited during a survey on iron deficiency in rural Bas-Zaire. sTfR was measured by enzyme immunoassay, and indicators of nutritional status [albumin, transthyretin (or prealbumin), and retinol binding protein] were measured by radial immunodiffusion. Undernutrition was diagnosed if the concentration of any one of the indicators was below normal: albumin < 35 g/L, transthyretin < 160 mg/L, and retinol binding protein < 30 mg/L. The sTfR concentration ranged from 1.89 to 19.1 mg/L (mean: 8.7 mg/L). Mean values for indicators of nutritional status, serum ferritin, and transferrin saturation were within the normal range for health subjects. Regardless of the iron status (iron sufficiency, anemia, or iron deficiency with or without anemia) and whether women were pregnant or nonpregnant, undernutrition did not significantly reduce sTfR concentrations. A higher percentage (80%) of iron-deficient women with two or three protein values below normal had sTfR concentrations > 8 mg/L (which are suggestive of iron-deficiency erythropoiesis) compared with iron-deficient women with no (72.7%) or one (66.7%) protein value below normal, anemic women (46-60%) and iron-sufficient women (18.2-36.8%). Results suggest that sTfR can be used as an indicator of iron deficiency in field studies without in-depth assessment of nutritional status. However, the effect of severe malnutrition on this index requires further investigation.

Adolescent↗
PubMed1996

Immune thrombocytopenia and hemolytic anemia associated with Hodgkin disease.

PURPOSE: We discuss an unusual clinical presentation of Hodgkin disease with immune thrombocytopenia and autoimmune hemolytic anemia. PATIENTS AND METHODS: A 4-year-old boy presented to us with a large anterior mediastinal mass, thrombocytopenia, and Coombs' positive hemolytic anemia refractory to transfusion therapy. Biopsy of the anterior mediastinal mass was possible only after administration of intravenous immunoglobulin to raise the platelet count. The immune manifestations decreased with initiation of appropriate chemotherapy. RESULT: The child was able to successfully complete chemotherapy and radiation therapy and has no clinical or laboratory evidence of persistent autoimmune phenomena. CONCLUSION: Immune thrombocytopenia with autoimmune hemolytic anaemia is a rare presenting manifestation of Hodgkin disease and can present difficulty in diagnosis and management.

Anemia, Hemolytic, Autoimmune↗
PubMed1996

The evolution of chemotherapeutic agents for the treatment of pediatric musculoskeletal malignancies.

The incorporation of antineoplastic agents in the treatment of pediatric musculoskeletal malignancies and their impact in the management and outcome of patients with these types of malignancies are briefly reviewed. The role of chemotherapy in the management of these tumors with special emphasis on osteosarcoma, Ewing's sarcoma family of tumors, and rhabdomyosarcoma and undifferentiated sarcomas is discussed. Also included are complications and side effects of the antineoplastic agents.

Antineoplastic Agents↗
PubMed1996

Langerhans' cell histiocytosis.

Langerhans' Cell Histiocytosis, formerly known as Histiocytosis X, and its related syndromes (i.e., eosinophilic granuloma, Hand-Schuller-Christian disease, and Letterer-Siwe disease) are briefly reviewed. The biology, clinical manifestations, and treatment options of the localized, single form and the disseminated, multisystem form are also discussed.

Histiocytosis, Langerhans-Cell↗