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A leukemoid reaction is a complex and poorly understood response by the bone marrow to a variety of stresses; although any peripheral blood cell line may be involved, it is rarely a purely monocytic event. A case is reported of a true monocytic leukemoid reaction in a patient with myelodysplastic syndrome related to the effect of corticosteroids on the underlying marrow disorder.
A transplantable murine breast carcinoma in mice was associated with marked leukemoid reaction. Within 1 week of subcutaneous implantation of tumor the leukocyte count began to increase and reached average levels of 165,000 leukocytes per cubic millimeter within 18 days. This represented an increase in mature neutrophils primarily, although other blood leukocytes were modestly increased as well. The total number of neutrophils per humerus was increased but no increase was detected in the number of myloblasts, promyelocytes, or myelocytes. The tritiated thymidine-labeling index of the latter three cells was not significantly changed during tumor growth. The number of progenitor cells forming granulocytic and mononuclear cells in vitro was decreased in the marrow during tumor growth. Colony-stimulating activity in plasma was slightly increased during the early phase of tumor growth and decreased during later phases. Emergence time of blood neutrophils was normal, as measured by labeling with tritiated thymidine, but decline in labeled cells was abnormally slow in tumor-bearing mice. There was a shift of erythropoiesis to the spleen, but total erythropoiesis appeared to be normal in most mice. Surgical excision of the tumor resulted in prompt reversal of the leukemoid reaction. In the aggregate these results are consistent with a hypothesis that the leukemoid reaction was the result of increased blood transit time of neutrophils primarily, rather than increased neutrophil production.
A case of leukemoid reaction associated with renal carcinoma is presented. On account of the high leukocyte count and a palpable abdominal mass in the upper left quadrant, interpreted as an enlarged spleen, the primary tentative diagnosis was chronic granulocytic leukemia. Abdominal ultrasonographic scan revealed an enlarged left kidney and subsequent nephrectomy revealed a large hypernephroma. Leukemoid reactions associated with malignant disease are described in general with emphasis on the differential diagnosis.
A 57-year-old female with a large retroperitoneal tumor was atutopsied. She showed through the entire course of illness marked leukocytosis with the appearance of immature marrow cells, and this finding was hematologically interpreted as granulocytic leukemoid reaction. An intermittent pyrexia was also seen without infective etiology. The histologic diagnosis of the tumor was liposarcoma of the pleomorphic type. The tumor showed extensive necrosis, but no metastatic invasion was found. So-called leukemoid reaction appears sometimes together with malignant neoplasms. The majority of these tumors show widespread bone marrow metastases, and without bone marrow invasion they only rarely induce this reaction. Besides it is not common for leukemoid reaction to be evoked by the development of malignant mesenchymal tumors except for malignant lymphomas. The pathophysiologic process of the present of the present case is thought to be a rare occurrence.
Host genetic factors influencing the occurrence of leukemoid reaction in BALB/cMk strain mice bearing transplanted tumors were studied. A Mendelian hybridization experiment was performed with BALB/cMk and C57BL/6 strains, and their strain hybrids; the first filial (F1) generation hybrids; the second filial (F2) generation hybrids; and the backcrosses to the two parental strains. The results of these studies suggested a genetic regulation of leukemoid reaction occurrence in BALB/cMk mice bearing transplanted tumors. Genes permissive to the occurrence of the reaction seemed to be dominant to their nonpermissive alleles.
A transient leukemoid reaction in a neonate with Down syndrome is reported. The blastic proliferation was identified as T lymphoblastic in an early stage of maturation (prethymocytes) using morphological, cytochemical, and immunological methods. A spontaneous complete remission occurred in 8 weeks. No additional cytogenetic alterations were found, except for those concerning chromosome 21. Other cases reported in the literature reveal that cytogenetic studies may be useful to distinguish these transient leukemic reactions from true leukemias in newborns with Down syndrome. The in vitro growth pattern of peripheral blood and bone marrow may also be useful for this purpose.
Paroxysmal nocturnal hemoglobinuria (PNH) has been observed to evolve into myelofibrosis and acute myeloid leukemia. Myeloblastic leukemoid reaction has not been described in PNH. We described a patient with PNH with myelodysplasia and septicemia. The marrow aspirates showed a picture of myeloblastosis which subsided when sepsis was controlled. The myeloblastic leukemoid reaction in our patient related to overwhelming sepsis, splenectomy and overt hemolysis.
During the growth of five of ten primary tumors that were induced by 3-methylcholanthrene in BALB/cMk and BALB/cMk X C57BL/6F1 mice, leukemoid reactions, characterized by increase in number of granulocytes in peripheral blood, and splenomegaly were observed. However, no such reactions occurred in five C57BL/6 mice bearing primary tumors induced by 3-methylcholanthrene. The results of leukemoid reactions in mice bearing 3-methylcholanthrene-induced primary tumors are compared with the reactions found in mice bearing transplanted tumors.
A retrospective study was performed on bone marrow biopsies of 50 untreated patients with leukemoid reactions (LR) and 50 untreated patients with early chronic granulocytic leukemia (CGL). A comparison was made between hematopoietic and adipose tissues, bone and its cells, as well as other stromal components in these two disorders. Histologic and histomorphometric analyses revealed significant differences in trabecular structure, in localization of fat cells, in numbers of sinusoids, capillaries and various stromal elements. No significant differences between LR and CGL were detected in the quantity of erythro- and granulocytopoiesis and of megakaryocytes, but these were smaller in CGL than in LR. This histologic and histomorphometric evaluation demonstrates that certain histologic features may serve as valuable aids in distinguishing LR from CGL.
The authors present a unique case of bladder cancer that presented as paraneoplastic syndrome of fever and leukemoid reaction. Furthermore, the patient had a left renal tumor histologically similar to the bladder tumor. We discuss whether the foregoing was a metastatic or a primary tumor coexisting with a bladder tumor. The neoplastic syndromes affecting patients with bladder neoplasms are briefly discussed.
Two infants with Down syndrome, one 4 weeks old and the other stillborn, at necropsy showed hepatic and pancreatic fibrosis, which was very severe in the liver of the liveborn infant and in the pancreas of the stillbirth. The liveborn infant had typical hematological features of the transient congenital leukemoid reaction of Down syndrome, and the identification of a megakaryoblastic component was consistent with recent opinion that this is a spontaneously-remitting congenital megakaryoblastic leukemia. The hydropic stillborn infant had intense extramedullary megakaryocytosis. The visceral fibrosis may have had a pathogenesis similar to that postulated for the myelofibrosis of megakaryoblastic leukemia in older children.
We describe a patient with severe alcoholic hepatitis, markedly elevated white blood cell count, and high fever. After review of the English literature, we discovered reports of other cases similar to our case. The striking feature in all of these cases was a high short-term mortality rate, despite predictions of a favorable outcome. We therefore believe these patients represent a subgroup of patients with alcoholic hepatitis and that the leukemoid reaction is a poor prognostic sign in this disease.
A 55-year-old woman had progressive weakness, weight loss, night sweats, fever, right-sided facial weakness, and hepatomegaly. Reticulonodular infiltrates were seen on chest x-ray film and a central filling defect was noted on liver scan. Study of the peripheral blood was noted on liver scan. Study of the peripheral blood revealed pancytopenia and myeloblasts. The bone marrow was not markedly hypercellular but contained noncaseating granulomas and myeloblasts. The patient's condition deteriorated and she died on the 22nd hospital day. Autopsy disclosed disseminated sarcoidosis but no evidence of leukemic infiltrates. Although concomitant "smoldering" acute leukemia cannot be ruled out, the findings in this patient can be best explained on the basis of a myeloblastic leukemoid reaction accompanying sarcoidosis.
Reactive leukocytosis has been reported in patients with non-Hodgkin's lymphoma of different histologic types. On the other hand, the blastic crisis of chronic myelocytic leukemia (CML) can sometimes be localized outside the bone marrow and simulate lymphoma, particularly when the blasts are of lymphoid lineage and the blastic crisis is the presenting feature of the disease. We report two patients in whom the differential diagnosis between lymphoblastic lymphoma with reactive leukocytosis and blastic crisis of CML outside the bone marrow was raised. They were two males aged 32 and 22 years, respectively, with lymphadenopathy (and one with splenomegaly), who were initially diagnosed of T lymphoblastic lymphoma. In both cases, leukocytosis was detected with myelemia and dysgranulopoiesis in the onset in one of them and when lymphadenopathy reappeared after remission in the other one. In addition, one patient had marked eosinophilia. In the bone marrow there was marked granulopoietic hyperplasia, with a reduction of fatty cells, and the granulocyte alkaline phosphatase index was reduced. However, the cytogenetic study did not disclose the existence of Philadelphia (Ph) chromosome, and bcr/abl molecular rearrangement was also not observed in the molecular study of both cases. We discuss the basic aspects of differential diagnosis between T lymphoblastic lymphoma with leukemoid reaction and T lymphoid lymphadenopathic blastic crisis of Ph-negative, bcr/abl-negative CML.
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