Successful treatment of prolonged agranulocytosis caused by acute parvovirus B19 infection with intravenous immunoglobulins

Herzog-Tzarfati, Katrin; Shiloah, Eli; Koren‐Michowitz, Maya; Minha, Sa’ar; Rapoport, Micha J.

doi:10.1016/j.ejim.2006.02.014

Cited by 13 publications

(13 citation statements)

References 6 publications

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“…When severe agranulocytosis persists beyond this period, unusual circumstances have been reported. For example, some patients with persisting agranulocytosis unresponsive to G‐CSF have parvovirus B19 infection, and recover after administration of IVIgG (implicating removal of circulating virus by IgG anti‐parvovirus antibody, reversing virus‐induced inhibition of granulopoiesis) …”

Section: Discussionmentioning

confidence: 99%

Sepsis and persisting neutropenia in a drug addict

2017

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A 38-year-old woman was brought in to the emergency room (ER) because of altered level of consciousness. She had a known history of seizure disorder but was not on any prescription medications. She also had a history of intravenous (IV) drug abuse, including cocaine, methamphetamine, and heroin. She recently described herself as being "pill-sick" which according to her partner meant that she felt unwell after a recent administration of an illicit drug.In the ER, she was hypoxemic and was intubated. She was febrile, her blood pressure was 90 systolic, heart rate 120/min, and oxygen saturation undetectable by the digital probe. Admission hemoglobin was 11.6 g/dL (mean corpuscular volume [MCV] 86), white blood count 0.8 3 10 9 /L (absolute neutrophil count [ANC], 0.2), and platelet count 97 3 10 9 /L. Rare nucleated red blood cells were seen, but no myeloblasts or other primitive cells. Coagulation studies showed INR 3.1, activated partial thromboplastin time (aPTT) 81 s, and fibrinogen 1.9 g/L. The serum creatinine was 320 mmol/L (reference range, 50-98); serum lactate measured 13.0 mmol/L (reference range, 0.5-2.2). A chest X-ray showed multiple pulmonary infiltrates and right-sided pleural effusion. A CT head scan was negative for any acute abnormality. CT chest was suspicious for a right-sided empyema, but no vegetations were seen on the heart valves. The most striking finding on her admission blood work was leukopenia with near-absence of neutrophils in the peripheral blood. The clinical picture of hypotension, tachycardia, lactic acidosis, renal failure, pulmonary infiltrates, and pleural effusion in the setting of IV drug abuse, together with thrombocytopenia, coagulopathy, and normoblastemia, suggests septicemia in the setting of pneumonia or right-sided infective endocarditis, most likely complicated by disseminated intravascular coagulation (DIC)-although fibrin D-dimer levels would be helpful in supporting the last diagnosis. Severe sepsis can result in a transient leukopenia/neutropenia, 1 although complete absence of circulating neutrophils is unusual and points to a possible de novo neutropenic disorder such as drug-induced agranulocytosis 2,3 (although the patient was not receiving any prescription medications). Current guidelines do not recommend starting this patient on G-CSF on admission due to lack of proven mortality benefit. 4,5 Circulating nucleated red blood cells (normoblastemia) portend a poor prognosis in a critically ill patient. 6 She had a central venous catheter inserted into her right internal jugular vein and was transferred to the intensive care unit (ICU) on vasopressin and norepinephrine. Blood and urine cultures were sent and the patient was started on piperacillin-tazobactam and vancomycin. Repeat blood work showed progressive thrombocytopenia, with the platelet count measuring 9 3 10 9 /L 20 h later, and with the leukocytes and ANC remaining profoundly reduced at 0.1 and 0, respectively. Repeat coagulation studies showed INR 3.9, aPTT >150, fibrinogen 2.0, and D-dimer > 20,00...

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Section: Discussionmentioning

confidence: 99%

Sepsis and persisting neutropenia in a drug addict

2017

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“…As the parvovirus B19 was originally thought to only affect erythroid progenitor cells, this finding was unexpected. However, few case reports have been published describing the occurrence of neutropenia in previously healthy subjects with a parvovirus B19 infection, suggesting that inhibition of the myeloid progenitor cells can occur [19, 20]. In fact, this is not so surprising as the globoside receptors to which parvovirus B19 binds are also present on cardiac myocytes, white blood cells, platelets and trophoblasts [14].…”

Section: Discussionmentioning

confidence: 99%

Leukopenia due to <i>Parvovirus B19</i> in a Crohn's Disease Patient Using Azathioprine

Asseldonk

Kanis²,

Boer³

et al. 2009

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Thiopurines such as azathioprine (AZA) and 6-mercaptopurine are frequently used for the treatment of inflammatory bowel diseases. Patients with low or absent thiopurine S-methyltransferase (TPMT) activity, resulting in high 6-thioguanine nucleotide levels, have an increased risk of developing leukopenia. Alternatively, certain viral infections could induce leukopenia. We present the case of an adult Crohn’s disease patient with a parvovirusB19 infection and leukopenia during long-term AZA therapy. The uncomplicated long-term use of adequately-dosed AZA and stable non-toxic metabolite levels could not acknowledge TPMT deficiency as a primary cause of the leukopenia. ParvovirusB19 was assumed to induce the leukopenia by restraining myeloid proliferation. In addition, AZA probably potentiated susceptibility to this viral infection and may have inhibited adequate immunological defense. Leukopenia during thiopurine therapy not explained by TPMT deficiency could be induced by parvovirusB19 infection and compels temporal but not permanent cessation of thiopurine therapy.

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“…8 Parvovirus B19 infects mainly erythroblasts and is responsible for a transient aplastic crisis with reticulocytopenia, although other hematologic abnormalities, neutropenia and agranulocytosis, appear to be much more frequently associated with parvovirus B19 infection than previously reported, probably immunological-mediated. 9 In this case, it would be of particular interest to discuss whether the severe pancytopenia was mainly a side effect from azathioprine, or if it was mainly caused by the dual viral infection. Most probably the patient's immunosuppression state, conditioned by both the disease and the drug, predisposed to both infections, which by immunological-mediated pathways led to the severe pancytopenia.…”

Section: To the Editormentioning

confidence: 97%