Patients are progressively at greater risk of serious infections with worsening neutropenia, with patients whose ANC is 100.4☏ should be admitted immediately to the hospital. There are virtually no data concerning these patients in the literature and, as noted, the pathogenesis of their neutropenia remains a mystery.īefore initiating an evaluation of newly discovered neutropenia in an adult patient, clinicians should consider a fundamental question: Is the patient acutely ill? Evaluation and treatment of an acutely ill patient not previously known to be neutropenic is a medical emergency ( Figure 1). Despite their very low neutrophil counts, these patients usually follow a benign clinical course, although some may require G-CSF for recurrent infections. This mild phenotype is distinct from another subset of patients with CIN who have profound neutropenia (ANC <200). 55, 56 However, the neutropenia in that population is quite mild, with ANCs usually no lower than 800, and may reflect at least a component of constitutional neutropenia. Studies from the island of Crete, where neutropenia is quite common, have shown an association between neutropenia and myeloid hypoplasia, with a selective decrease in CD34 +/CD33 – progenitors or with increased production of TNF-α. It is a diagnosis of exclusion that can only be made after a thorough and unrevealing search for other causes, including negative testing for autoimmune disease and nutritional deficiency and a normal bone marrow examination with normal cytogenetics. Neutropenia that is acquired in adulthood but eludes a specific diagnosis is termed chronic idiopathic neutropenia (CIN). Semisynthetic penicillins (amoxicillin, ampicillin *)Īntiarrhythmic agents (procainamide, * flecainide *)
In the few studies that have corrected for the rate of prescription, a handful of drugs (clozapine, methimazole, sulfasalazine, trimethoprim-sulfamethoxazole, and β-lactam antibiotics as a class) have shown the highest odds ratios for causing serious neutropenia. 41 It is important to note that the true potential of each drug to cause neutropenia may not be accurately reflected by the incidence calculated from case reports, because these are not usually normalized to the prescription rate of the drugs. 38 Other drugs commonly implicated in neutropenia include phenothiazines (eg, chlorpromazine), 39 semisynthetic penicillins (eg, ampicillin) and cephalosporins, 40 thionamides (methimazole, propylthiouracil), and nonsteroidal antiinflammatory drugs. 37 In the case of clozapine, agranulocytosis appears to result from the toxic effect of a drug metabolite that may also have an impact on the marrow stroma this may cause a somewhat more prolonged neutropenia than is usually seen in drug-induced agranulocytosis. The antipsychotic agent clozapine, the antiplatelet drug ticlopidine, and the antiinflammatory drug sulfasalazine all have well-known associations with idiosyncratic agranulocytosis. The most obvious are chemotherapeutic drugs, many of which cause bone marrow suppression as an expected consequence of their mechanisms of action. However, certain common offenders bear specific recognition. 36 Neutropenia has been reported in association with an extensive array of medications ( Table 2). For CME questions, see page 1378.ĭrugs and toxins are among the most common causes of acquired neutropenia. To participate in this journal CME activity: (1) review the learning objectives and author disclosures (2) study the education content (3) take the post-test with a 75% minimum passing score and complete the evaluation at and (4) view/print certificate. Physicians should claim only the credit commensurate with the extent of their participation in the activity.Īll other clinicians completing this activity will be issued a certificate of participation. Medscape, LLC designates this Journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™.
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