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Pernicious anemia (PA) is the most common cause of vitamin B12 (cobalamin) deficiency anemia in the world. It is an autoimmune disease, comprising of salient features of autoimmune chronic atrophic gastritis (CAG) and cobalamin deficiency (CD). Although the anemia was first described as pernicious, it may well be controlled with vitamin B12 replacement. The onset and progression of PA is often insidious. Alternatively, patients may have no anemic symptoms since they become acclimatized to the subtle nature of the disease. Oftentimes, there is a possibility that the underlying disease may be missed unless a full blood count (FBC) is investigated, leading to hindrance in the treatment journey. Diagnostic challenges remain tangible for many practicing clinicians, since there is lack of reliable cobalamin assays to diagnose CD as well as clinical mimics, which simulate many other hematological conditions, such as myelodysplastic syndrome, acute leukemia, sideroblastic anemias, bone marrow failure states, thrombotic microangiopathy, and thromboembolism. Moreover, prompt recognition of the symptoms of CD is also vital, because some neurologic sequalae may become irreversible despite replenishing cobalamin. Herein, we discuss a literature review on the pathophysiology, challenging clinical presentations and diagnostic difficulties of PA. Since the cobalamin replacement therapy for PA is straightforward, it will not be discussed in this review. [ABSTRACT FROM AUTHOR]

Background: Thromboembolism (TE) is a leading cause of death in cancer patients. Primary thromboprophylaxis (PTP) in ambulatory cancer patients receiving chemotherapy has been debated and considered to potentially improve survival by reducing TE occurrence. Objective: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) in ambulatory lung cancer (LC) patients on chemotherapy to determine the benefit and risk of PTP with low-molecular-weight heparins (LMWHs). Method: A literature search using MEDLINE and EMBASE databases was performed through June 2016. RCTs with venous thromboembolism (VTE) reduction as primary or secondary endpoints were included. Mantel-Haenszel method was used to estimate the pooled event risk ratio as well as pooled absolute risk difference with 95% confidence interval (CI). Result: A total of 4315 LC patients from six studies were available for analysis. PTP lasted for 4 to 6 months. The venous thromboembolism (VTE) incidence was 4.0% and 7.9% in LMWH and control groups, respectively (risk ratio, 0.510 (95% CI, 0.397-0.654, P < 0.001). The absolute risk difference in VTE was -0.039 (95% CI, -0.053 to -0.025, P < 0.001), with an estimated number needed to treat (NNT) of 25 to prevent one VT Eevent. The pooled risk ratio for major bleeding was 1.468 (95% CI, 0.785-2.746, P = 0.229). The pooled risk ratio for overall survival was statistically nonsignificant at 1.020 (95% CI, 0.938-1.109, P = 0.648). Conclusion: Routine PTP for ambulatory LC patients receiving chemotherapy is not recommended and further studies are necessary to define a subset of ambulatory LC patients receiving chemotherapy who may benefit from PTP. [ABSTRACT FROM AUTHOR]

Recognizing Gaucher disease in elderly patients can be challenging. We present a Gaucher disease type 1 case diagnosed in an elderly patient with thrombocytopenia and lung adenocarcinoma. The diagnosis of Gaucher disease was delayed due to lack of familiarity about Gaucher Disease type 1 which can manifest in adulthood. [ABSTRACT FROM AUTHOR]

Key Clinical Message Total parenteral nutrition can be complicated by the marrow sea-blue histiocytes as well as copper deficiency-related bone marrow changes. Cytoplasmic vacuoles in the erythroid and myeloid precursors raise the possibility of copper deficiency anemia. If the diagnosis is delayed, the clinical course can be complicated by neurologic deficits. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Detection of paroxysmal nocturnal hemoglobinuria clones to exclude inherited bone marrow failure syndromes" by A. E. Dezern, H. J. Symons, and colleagues in the 2014 issue.