Glutathionyl hemoglobin is elevated in iron deficiency anemia.

There are few good biomarkers of iron deficiency anemia (IDA). Since IDA patients have evidence for increased oxidative stress, we used mass spectrometry (MS) [i.e. matrix-assisted laser desorption/ionization (MALDI) and electrospray ionization] to identify novel biomarkers. Using MALDI-MS, the following oxidative modifications of hemoglobin with the following mass-to-charge ratios were identified: 1,087.5 (α32-40), 1,545.7 (α17-31), 1,290.0 (ß31-40) and 2,076.1 (ß41-59). On electrospray ionization MS, the IDA patients had significantly elevated glutathionyl hemoglobin (GSHb) compared with the controls (16.9 ± 9.6 vs. 7.7 ± 3.7%; p = 0.002). GSHb levels correlated inversely with serum ferritin (Spearman rho -0.485; p = 0.003) and positively with serum transferrin receptor (0.460; p = 0.002). GSHb also demonstrated inverse correlations with hemoglobin (-0.512; p = 0.001), mean cell volume (-0.419; p = 0.026), serum iron (-0.446; p = 0.008) and transferrin saturation (-0.460; p = 0.008). For the first time, we show that GSHb is elevated in patients with IDA and has potential as a biomarker of this form of anemia.

Risks of routine iron and folic acid supplementation for young children.

CONTEXT: Almost 70% of young children in India are anemic. Current policy recommends routine iron-folic acid (IFA) supplementation to all under 5 children. A potential risk of this approach is an increase in infectious diseases in general, and malaria in particular. EVIDENCE ACQUISITION: An extensive literature search including PubMed, the World Health Organization (WHO) document library, and the Indian Government database, for documents regarding IFA supplementation in under-5 children. RESULTS: Previously, systematic reviews had suggested adverse effects of IFA supplementation in malaria endemic settings. However, a recent large trial in Tanzania has found clear evidence of increased mortality, chiefly due to malaria, among children receiving routine IFA, whilst a simultaneous study in Nepal (a non-malarious region) found no adverse effects on morbidity or mortality from infectious disease attributable to IFA. These findings have prompted the World Health Organization to revise recommendations regarding IFA supplementation in malaria endemic areas. CONCLUSIONS: India has a non-homogenous distribution of malaria endemicity. We propose that although no change to IFA supplementation be made in non-malarious regions, routine IFA should be provided in malarious regions once malaria control and primary health care infrastructure are functioning well.

Melioidosis.

Melioidosis is an emerging infectious disease in India acquired through percutaneous inoculation or contaminated water. Known risk factors include diabetes mellitus, renal failure, cirrhosis, and malignancy. Melioidosis presents with a febrile illness, with protean manifestations ranging from septicemia to localized abscess formation. We present the case of a 42-year-old male from a non-endemic region who presented with fever of 2 months duration, sepsis, persistent pneumonia, right hip joint pain and hepatic and splenic abscesses. Aspiration of the joint and soft tissue fluid collection and subsequent culture yielded gram negative bacilli identified as Burkholderia pseudomallei. The epidemiology, clinical features, and laboratory diagnosis of this rare infection and its treatment is reviewed.

A guide to murine platelet structure, function, assays, and genetic alterations.

Platelets play an important role in hemostasis, thrombosis and several other biological processes. The adaptability of mice to genetic manipulation and their genetic similarity to humans has resulted in a plethora of murine models to study platelet function. Although murine platelets differ from human platelets with regard to size, number and structure, functionally they are very similar. Thus, studies which employed these model systems have greatly improved our current understanding of the contribution of platelets to hemostasis and thrombosis. This review presents general recommendations with respect to collection, isolation and processing of murine platelets. It also describes the assays currently available to study platelet function and critically assesses their utility. The extensive literature on the effects of genetic alterations on murine platelet function is considered in detail. This review is intended to provide a convenient source of reference for platelet investigators.

A guide to murine coagulation factor structure, function, assays, and genetic alterations.

Murine blood coagulation factors and function are quite similar to those of humans. Because of this similarity and the adaptability of mice to genetic manipulation, murine coagulation factors and inhibitors have been extensively studied. These studies have provided significant insights into human hemostasis. They have also provided useful experimental models for evaluation of the pathophysiology and treatment of thrombosis. This review contains recommendations for obtaining, processing and assaying mouse blood hemostatic components, and it summarizes the extensive literature on murine coagulation factor structure and function, assays and genetic alteration. It is intended to be a convenient reference source for investigators of hemostasis and thrombosis.

Chronic myelogenous leukemia: mechanisms underlying disease progression.

Chronic myelogenous leukemia (CML), characterized by the BCR-ABL gene rearrangement, has been extensively studied. Significant progress has been made in the area of BCR-ABL-mediated intracellular signaling, which has led to a better understanding of BCR-ABL-mediated clinical features in chronic phase CML. Disease progression and blast crisis CML is associated with characteristic non-random cytogenetic and molecular events. These can be viewed as increased oncogenic activity or loss of tumor suppressor activity. However, what causes transformation and disease progression to blast crisis is only poorly understood. This is in part due to the lack of a good in vivo model of chronic phase CML even though animal models developed over the last few years have started to provide insights into blast crisis development. Thus, additional in vitro and in vivo studies will be needed to provide a complete understanding of the contribution of BCR-ABL and other genes to disease progression and to improve therapeutic approaches for blast crisis CML.