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A case of amoebic liver abscess with leukemoid reaction is described. This patient also had jaundice as the presenting feature. Therapy with metronidazole resulted in improved general condition and both blood picture and liver function tests also became normal.
The most common etiologies of hypercalcemia are hyperparathyroidism or malignancy, most often of the lung, breast or hematological system, but rarely occur in transitional cell carcinoma. The appearance of this metabolic disorder and other paraneoplastic signs like leukemoid reaction or thrombocytosis is a potential marker for malignant behaviour and poor prognosis in advanced tumours. Simultaneous presentation of that three paraneoplastic signs have only been described in two patients with wellknown bladder carcinoma. Most paraneoplastic syndromes appear only during the late stages of malignancy when the diagnosis has long been established, but sometimes may be an early sign of the malignancy. We describe a case of a previously unknown infiltrating transitional cell carcinoma of the kidney without bony metastasis, that presented itself with hypercalcemia, hyperleukocytosis resembling a leukemoid reaction and thrombocytosis. We think recognizing the paraneoplastic syndrome is very important because it is an alarm sign of malignancy.
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 female newborn was delivered prematurely at gestational age of 26 weeks with birth weight of 1,000 grams. Her initial white blood cell count was 68,900/mm3, which increased to 207,000/mm3 on the fifth day of life with a remarkable shift-to-left pattern. The most immature myeloid series in the peripheral blood smear was promyelocyte; and the promyelocyte, myelocyte and meta-myelocyte accounted for 38% of the peripheral white blood cells. Neither hepatosplenomegaly nor skin rash was noted, but the platelet count dropped to 86,000/mm3 transiently on Day 8. Cytogenetic study for the bone marrow aspiration revealed normal results. The leukemoid reaction recovered within three weeks without specific treatment. Antenatal usage of steroid to promote lung maturation was considered to be one possible cause of the transient leukemoid reaction.
Bladder carcinoma associated with leukemoid reaction, though it rarely occurs, is considered highly malignant and has proved to produce granulocyte colony-stimulating factor (G-CSF). Interest exists in whether G-CSF itself or G-CSF producing ability reflects the malignant potential of such a tumor, possibly through an autocrine mechanism. In a patient with invasive bladder carcinoma, we found that the tumor cells produced G-CSF responsible for a remarkable leucocytosis. However, we could not detect the rearrangement and amplification of the G-CSF gene nor the expression of G-CSF receptor in the tumor cells. Our immunohistological and molecular biological study failed to demonstrate a crucial role for G-CSF in mediating a growth advantage for the tumor.
The responsiveness of marrow granulocyte progenitors (CFU-D) to macrophage-derived stimulatory and inhibitory factors has been studied using diffusion chamber technique in 12 patients with neutrophilic leukemoid reaction (with granulocyte count in the range between 10-40 G/l) and ten healthy subjects. CFU-D from patients with neutrophilic leukemoid reaction (NLR) revealed a normal reactivity to colony-stimulating activity, whereas they were hyporesponsive to macrophage-derived indomethacin-sensitive inhibition. This altered response was correlated both with the concentration of granulocyte progenitors in the S phase and with blood neutrophilic leukocytosis. In patients with higher granulocyte count and increased concentration of CFU-D during active DNA synthesis a more pronounced hyporesponsiveness of granulocyte progenitors to macrophage-induced inhibition has been found.
This paper details the simultaneous occurrence of a severe leukemoid reaction, non-bacterial thrombotic endocarditis (NBTE) (marantic endocarditis), and a consumptive thrombocytopathy without signs of micro-angiopathic hemolysis on peripheral blood smear in a patient with terminal metastatic, undifferentiated, large cell bronchogenic carcinoma. The case is presented and the condition is discussed in detail.
Authors present three cases of leukemoid reaction in very low birth weight preterm infants. Hematologic evolution is detailed and was characterized by the presence of intense leukocytosis with marked shift to the left abundant immature forms. Leukocyte counts reached values of 70,000 and 106,000/mm3 between the second and third day of life, becoming normal around the eight day. No pathology known to cause such intense leukocytosis was observed in any case. Bibliography is reviewed and possible etiology is discussed, as until now this entity has been attributed to prenatal administration of glucocorticoids.
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.
We have described a preterm infant who had a transient self-limited leukemoid reaction apparently due to maternal ritodrine therapy.
Alcoholic hepatitis (AH) is a clinicopathologic syndrome resulting from an excessive intake of alcohol. Leukemoid reactions (LRs) are characterized by a strikingly elevated granulocyte count over 40,000-50,000 cells/mm(3). Although a leukocytosis of 15,000-18,000 cells/mm(3) is frequently seen in AH, LRs are rare in this context. AH-associated LRs are a sign of poor prognosis and have a high mortality. A 64-year-old male with a history of heavy alcohol intake underwent a right hemicolectomy for cecal carcinoma. Preoperative laboratory data were normal with the exception of an albumin of 2.1 g/dL. Liver biopsies that were taken because of a nodular appearance revealed micronodular cirrhosis, steatohepatitis, and Mallory bodies. Postoperatively, the patient developed a leukocytosis that progressively increased to 72.6 cells/mm(3). He also developed signs of impaired hepatic and renal function. Extensive workup failed to reveal a source of infection. A trial of intravenous antibiotics had no impact on the leukocytosis. Methylprednisolone at a dose of 40 mg IV daily was started on postoperative day 9. The patient experienced a progressive decline in white blood count (WBC), which reached 25.2/mm(3) on postoperative day 14. However, he died on postoperative day 16. We conclude that the patient had AH-associated LR in the postoperative period, but died despite successful treatment of the LR with steroids.
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We investigated whether histological chorioamnionitis (HCA) is a risk factor predisposing to leukemoid reaction (LR) and whether LR is associated with the preterm parturition syndrome and the systemic fetal inflammation response syndrome. A prospective histological study on placentas was performed in preterm infants (<or=32(+6) weeks' gestation) admitted to level III neonatal intensive care unit of Padua University from January 1998 to December 2003. Development of LR was related to evidence of HCA. Among the placentas of the 223 preterm examined infants, 61 (27%) were diagnosed with HCA. Overall incidence of LR was 5.3%. Of 61 preterm neonates with HCA, 8 (13%) developed LR; moreover, 4 (2%) of 162 preterm infants without HCA developed LR (odds ratio = 7.4). Neonates with both LR and HCA differ from neonates with LR and without HCA in occurrence of prolonged rupture of membranes (62.5% versus 0%, P < .01), mode of delivery (37.5% versus 100% cesarean delivery, P < .01), gestational age (26 +/- 1.6 versus 29.7 +/- 1.7 gestational weeks, P < .01), and bronchopulmonary dysplasia incidence (63% versus 25%, P < .01). Histological chorioamnionitis placental findings increase the risk for neonatal LR. The LR in low-birth-weight neonates with HCA is significantly associated with earlier delivery and bronchopulmonary dysplasia. Pathogenetic mechanisms of neonatal LR in low-birth-weight infants without HCA remain undefined.
We report a patient in whom hypersensitivity to carbamazepine presented with generalized erythroderma, a severe leukemoid reaction, eosinophilia, hyponatremia, and renal failure. This is the first report of such an unusual reaction to carbamazepine.
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This is a description of a case in a man who developed non-Hodgkin lymphoma of small cleaved cells preceded by erythroderma with leukemoid reaction. Non- caseous granulomas with Langhans' cells were found in the skin biopsy. The etiologic agent was not identified until the neoplasia that killed him was demonstrated. Autopsy study showed lymphomatous infiltration in all ganglionaries groups, the skin, lungs, kidney, liver, spleen, adrenal glands and bone marrow. One of the interesting aspects of the case in the tissue reaction to the neoplastic process, a fact already described but rarely observed.
We reviewed 4 patients with urothelial bladder cancer and hypercalcemia but without evidence of bony metastasis. Of the patients 2 presented with a leukemoid reaction (1 also had thrombocytosis). None of the patients had evidence of bone metastases or other causes of hypercalcemia, such as hyperparathyroidism, sarcoidosis or vitamin D intoxication. All 4 patients received aggressive therapy for the tumors. In each instance the serum calcium returned to normal following radiation therapy or tumor removal, lending support to the theory of humoral hypercalcemia of cancer. A diagnostic and therapeutic approach to such patients is outlined.