Myeloid leukemoid reaction after initial azacitidine therapy for chronic myelomonocytic leukemia.

The development of myeloid leukocytosis in leukemia patients during antileukemic treatment requires a differential diagnosis between myeloid leukemoid reaction and leukemia progression. We herein report the case of an 80-year-old Japanese man with chronic myelomonocytic leukemia (CMML) who developed marked myeloid leukocytosis (36.3 × 109/L) with 32.5% monocytes and 48% neutrophils about 4 weeks after the initial 5-azacitidine (AZA) treatment. The leukocytosis was unlikely to be attributed to infection and adverse drug reaction. As it resolved in a few days without any interventions, the transient myeloid leukocytosis was confirmed to be a myeloid leukemoid reaction. After four cycles of AZA treatment, leukemic blasts in the bone marrow decreased and the patient became transfusion-independent. Interestingly, levels of serum G-CSF showed a similar trend to the myeloid leukocytosis, while those of serum GM-CSF and IL-17 were undetectable throughout the clinical course, suggesting that a differentiation response to AZA treatment might lead to the myeloid leukemoid reaction. Our case implies that a marked but transient myeloid leukemoid reaction mimicking CMML progression can develop during AZA treatment, which requires careful clinical monitoring and differential diagnosis.

Leukemoid reaction: a rare paraneoplastic event in a case of advanced penile cancer and its management.

Leukemoid reaction is a paraneoplastic phenomenon associated predominantly with solid tumours. Malignancies presenting with leukemoid reaction have a grave prognosis. It is defined as persistent neutrophil count greater than 50×103 cells/µL. We report a case of leukemoid reaction in a patient with metastatic penile cancer. A 60-year-old man with partial penectomy status for squamous cell carcinoma of penis on neoadjuvant chemotherapy, presented with left fungating inguinal lymphadenopathy and total leucocyte count 96×103 cells/µL and hypercalcaemia. Leucocytealkaline phosphatase (LAP) score was excessively elevated. The patient underwent left ilioinguinal block dissection along with vastus lateralis flap for defect reconstruction. Postoperatively, the neutrophil counts and serum calcium level normalised. The patient improved clinically and was discharged.

Tigecycline-induced Drug Fever and Leukemoid Reaction: A Case Report.

In this study, we describe a patient in whom tigecycline-induced drug fever and leukemoid reaction (LR) after 3 weeks of therapy for pneumonia.A 62-year-old man developed aspiration pneumonia on February 1, 2015. He had received multiple antibiotics at another hospital, but did not respond well. Disease rapidly progressed, and he was referred to our department on February 14. We adjusted the antibiotic therapy to tigecycline + vancomycin, and added voriconazole to empiric antifungal therapy. Pneumonia largely improved, and we discontinued vancomycin and voriconazole on February 28. With tigecycline monotherapy, his clinical status remained stable.On March 7, he developed high fever and LR (white blood cell count: 38.25 × 10(9)/L). Erythrocyte sedimentation rate and C-reactive protein were elevated, and CD8+ T cells had been abnormally activated. After a careful physical examination and laboratory investigation, we confirmed that primary infection did not progress and no other cause was evident. So we figured fever and LR might be induced by tigecycline. After discontinuing tigecycline and adding low-dose steroid, fever and LR totally resolved in 3 days, which further confirmed our diagnosis.According to this case and literature review, drug-induced hypersensitivity should be considered in the differential diagnosis of fever and LR when the therapeutic duration of tetracycline approximates 3 weeks. Monitoring T-cell subsets may facilitate early diagnosis. When necessary, we should discontinue the suspected drug to confirm diagnosis.

Leukemoid reaction secondary to hypersensitivity syndrome to phenobarbital: a case report.

The most important adverse effects of phenobarbital, an anticonvulsant drug, are behavior and cognitive alterations. Hypersensitivity syndrome caused by phenobarbital presenting with a leukemoid reaction is a rare side effect, which is rarely ever reported and needs to be known. We report on a 27-year-old Chinese woman who experienced hypersensitivity syndrome three weeks after the initiation of phenobarbital. The patient developed fever, skin rash, face swelling, lymphadenopathy, myalgia, hepatitis, eosinophilia, atypical lymphocytes and leukocytosis. Along with the pathological progress of the disease, the patient noticed a gradual exacerbation of her symptoms. And the highest leukocyte count was up to 127.2 x 10(9)/L. After discontinuing of phenobarbital and administration of methylprednisolone combined with the intravenous immunoglobulin shock therapy, all initial symptoms improved and the leukocyte count normalized. This case is reported because of its rarity of the leukemoid reaction secondary to hypersensitivity syndrome to phenobarbital.

Leukemoid reaction after methotrexate-induced pancytopenia in a patient undergoing continuous ambulatory peritoneal dialysis.

Methotrexate has been used as an important alternative therapy in the treatment of various rheumatic diseases. Life threatening marrow suppression in end-stage renal disease patients undergoing hemodialysis or continuous ambulatory peritoneal dialysis has been reported. A 33-year-old woman with systemic lupus erythematosus undergoing chronic peritoneal dialysis developed severe mucositis and pancytopenia after low-dose methotrexate treatment for arthritis. The leukocyte count recovered after methotrexate was withdrawn but a leukemoid blood picture developed during her recovery. No evidence of leukemia was found on bone marrow biopsy. The leukocyte count gradually returned to normal with conservative therapy.

Eosinophilic leukemoid reaction associated with carbamazepine hypersensitivity.

Carbamazepine is widely used in the treatment of epilepsy, neuralgic pain, and bipolar affective disorders. Several adverse drug reactions have been described during the course of carbamazepine administration, including exanthemata and hematological reactions. Carbamazepine is one of the common drugs that have been implicated in the etiology of drug hypersensitivity syndrome. A 50-year-old male presented with generalized erythroderma following 10 weeks of ingestion of carbamazepine 200 mg daily for idiopathic epilepsy. His systemic examination was within normal limits. Blood counts revealed marked eosinophilia of 52% (absolute eosinophil count of 10,400 per mm3). Bone marrow aspiration revealed a moderate increase in the eosinophilic series with cells showing normal morphology. The eosinophil counts returned to normal after 2 weeks of oral prednisolone therapy. This case is reported because of its rarity in the Indian medical literature.

Leukemoid response in ethylene glycol intoxication.

A 33-y-old male developed severe acidosis, renal failure, and profound neutrophilia after ingesting ethylene glycol. Workup for his neutrophilia excluded infectious and malignant causes. An elevated leukocyte alkaline phosphatase (LAP) level confirmed a leukemoid response, and the neutrophila resolved. Although several leukemoid reactions have been published due to therapeutic agents these reports are often incomplete or inaccurate; this is the first case of leukemoid response to a toxin. Leukemoid response is distinguishable from leukemia by the absence of clonally derived cells, although this is not easily apparent in extreme neutrophilia. Elevated LAP is useful in identifying leukemoid reaction from leukemia in cases of extreme neutrophila. If a patient develops extreme neutrophila in association with drug or toxin exposure, a leukemoid reaction should be considered and an LAP obtained.

[Severe side effects of the treatment of acute promyelocytic leukemia with all-trans retinoic acid].

Sixty-three cases with acute promyelocytic leukemia (APL) were treated with all-trans retinoic acid (ATRA). The rates of hyperleukocytosis, intracranial hypertension, retinoic acid syndrome were 57.1%, 9.5%, and 3.2% respectively. Mortality of the treatment was 11.1%. Under ATRA treatment, hyperleukocytosis leading to leukostasis was the cause of death in patients with APL. We therefore suggest that the patients with such leukocyte levels (that is, 5.0 x 10(9).L-1 on the 6th day, 10.0 x 10(9).L-1 on the 10th day, 15.0 x 10(9).L-1 on the 15th day) can be used as guidelines for starting chemotherapy(homoharringtonine); before ATRA treatment, while leukocyte counts are > 10 x 10(9).L-1, the patients only receive homoharringtonine; when leukocyte counts are < or = 5.0 x 10(9).L-1, the patients receive a combination of homoharringtonine and ATRA. Retinoic acid syndrome is a distinctive complication of ATRA therapy in the patients with APL. While the syndrome occurs, the treatment of ATRA must be stopped and corticosteroids must be used.

Suspected betamethasone-induced leukemoid reaction in a premature infant.

The use of antenatal corticosteroids in threatened pregnancies of less than 34 weeks' duration is a valuable tool for assisting fetal lung maturation. Although this practice has existed for over 20 years, little is known about a rare extreme elevation of the newborn's white blood cell count, called a leukemoid reaction. A case of leukemoid reaction is discussed to assist the clinician with the current thought processes and diagnostic differential behind this benign condition.

Agranulocytosis, plasmacytosis, and thrombocytosis followed by a leukemoid reaction due to acute acetaminophen toxicity.

OBJECTIVE: To describe a patient who developed hepatotoxicity, reactive plasmacytosis with thrombocytosis and life-threatening agranulocytosis, followed by a leukemoid reaction, apparently caused by acute acetaminophen toxicity. SETTING: University-affiliated hospital. CASE SUMMARY: A 19-year old white women who took an overdose of acetaminophen developed hepatotoxicity and reactive plasmacytosis with thrombocytosis and life-threatening agranulocytosis, followed by a leukemoid reaction. Symptoms, signs, and laboratory findings regressed with symptomatic therapy during the follow-up period. CONCLUSIONS: We believe that acute acetaminophen toxicity was responsible for these hematologic abnormalities. This profile of hematologic adverse effects associated with acetaminophen toxicity has not been reported previously.

Leukemoid reaction induced by prenatal administration of betamethasone.

A case of leukemoid reaction in a premature baby whose mother was antenatally treated by betamethasone is reported. The neonatal and maternal factors which might lead to leukocytosis or leukemoid reaction were excluded. The presented case is the last in a series of eight previously reported cases of leukemoid reaction, in which the common denominator was the antenatal administration of betamethasone.

Monocytic leukemoid reaction, glucocorticoid therapy, and myelodysplastic syndrome.

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.

Hypersensitivity to carbamazepine presenting with a leukemoid reaction, eosinophilia, erythroderma, and renal failure.

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.

Maternal ritodrine hydrochloride therapy associated with transient leukemoid reaction in the infant.

We have described a preterm infant who had a transient self-limited leukemoid reaction apparently due to maternal ritodrine therapy.