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At least 19 recordsLinked to original sources

PubMed2006

A retrospective study of aplastic pancytopenia in the dog: 9 cases (1996-2003).

BACKGROUND: Aplastic pancytopenia is defined by the presence of pancytopenia in blood and a hypocellular bone marrow with the hematopoietic space replaced by adipose tissue. Several causes of acquired aplastic pancytopenia are known; however, in some cases, an underlying cause is never determined. OBJECTIVE: The objective of this retrospective study was to identify the incidence, potential causes, and outcome of aplastic pancytopenia in dogs. METHODS: Bone marrow cytologic and core biopsy reports were reviewed to identify dogs diagnosed with aplastic pancytopenia between July 1, 1996 and June 30, 2003. Four-hundred eighty-six bone marrow reports that included aspirate and core biopsy evaluations were reviewed. Signalment, treatment given, previous and current disease conditions, clinical signs of disease, clinical laboratory data, therapy, response to therapy, and survival time were recorded. RESULTS: Nine dogs (1.85% of bone marrow samples reviewed) met the criteria for inclusion. Two dogs (22%) had associated diseases that included monocytic ehrlichiosis and Sertoli cell tumor. In 7 dogs (78%), the cause of aplastic pancytopenia could not be definitively determined, although an idiosyncratic drug reaction to griseofulvin was suspected in 1 of the dogs. The median age of dogs diagnosed with aplastic pancytopenia was 3.2 years, and apparent breed or sex predilection was not identified. Median HCT, total WBC count, and platelet count on the day of presentation were 21.8%, 1.0 x 10(3)/microL, and 2.0 x 10(3)/microL, respectively. Six of 9 dogs diagnosed with aplastic pancytopenia died or were euthanized within 21 days. Two dogs had complete hematologic recovery. One dog was living 3 years after diagnosis, but hematologic recovery was never documented. CONCLUSIONS: Aplastic pancytopenia is diagnosed infrequently and idiopathic aplastic pancytopenia may account for up to 67% or more of canine cases. Although the prognosis is guarded, some dogs with aplastic pancytopenia recover.

Animals↗

PubMed1996

Pancytopenia secondary to methotrexate therapy in rheumatoid arthritis.

OBJECTIVE: To assess the frequency of methotrexate (MTX)-induced pancytopenia in rheumatoid arthritis (RA). METHODS: A MEDLINE literature search was conducted to identify articles published during the last 15 years (1980-1995) that presented data on MTX-associated pancytopenia. Two case reports of our own experience are also presented. In addition, articles that examined risk factors associated with MTX-related pancytopenia were identified. RESULTS: A total of 70 patients with pancytopenia related to MTX therapy were identified (68 reported in the literature, 2 from our own experience). Sixty-one of the patients were described in published case reports, 7 patients were from 5 long-term prospective studies. In many of these cases, predisposing factors for the development of pancytopenia were described. The 5 long-term prospective studies reported toxicity data on patients who had been treated with MTX for at least 13 weeks. A total of 511 patients were included in the prospective trials, yielding an overall incidence of pancytopenia of 1.4% (7 of 511). Of the 70 cases reported, 12 patients died (17%). Most of them had impaired renal function, hypoalbuminemia, concurrent infection, and/or concomitant medication with more than 5 drugs. The minimal cumulative MTX dose leading to fatal pancytopenia was 10 mg, observed in one of our patients. CONCLUSION: Pancytopenia is not an uncommon side effect of low-dose pulse MTX therapy in RA. It can lead to serious complications, including death.

Administration, Oral↗

PubMed2005

Methotrexate-induced pancytopenia: serious and under-reported? Our experience of 25 cases in 5 years.

OBJECTIVE: To ascertain the extent of methotrexate (MTX)-related pancytopenia at the Norfolk and Norwich University Hospital (NNUH) between 1999 and 2004. METHODS: Patients were identified by a department database search, review of pharmacy records and personal communication. Pancytopenia was defined as white blood cell count (WBC) <3.5 x 10(9)/l, haemoglobin (Hb) <11 g/dl and platelet count <130 x 10(9)/l. Severe pancytopenia was defined as WBC <2.0 x 10(9)/l, Hb <10 g/dl and platelet count <50 x 10(9)/l. RESULTS: Twenty-five patients had MTX-induced pancytopenia. Eleven patients were taking folic acid and one folinic acid. The median dose of MTX was 12.5 mg weekly (interquartile range 5.625 mg) and median duration of treatment 36 months (interquartile range 40.5 months). The severity of pancytopenia correlated with the dose (P = 0.04). The numbers of patients with potential risk factors were: renal insufficiency, 8; pre-existing folate deficiency, 7; age >75 yr, 15; hypoalbuminaemia, 18; pre-existing infection with hip prosthesis, 1; possible drug interactions, 18; dosing errors, 1; and polypharmacy, 15. Pancytopenia was detected by routine blood monitoring in nine patients. There were seven deaths (28% mortality), five from sepsis and two from acute myeloid leukaemia. CONCLUSION: This is the largest reported individual case series of MTX-induced pancytopenia. With the increasing long-term use of MTX, it is important that patients be monitored for haematological side-effects as pancytopenia can be a late manifestation. Pharmacogenetics may hold the answer to predicting who is at risk of this potentially fatal complication of MTX.

Aged↗

PubMed1996

Pancytopenia with chromosomal fragility: vitamin B12 deficiency.

PURPOSE: Pancytopenia in children may have many etiologies. Chromosomal abnormalities with pancytopenia is of particular concern because clonal abnormalities indicate a neoplastic process. We describe three children who had vitamin B12 deficiency and who displayed pancytopenia with multiple chromosomal breaks, rearrangements, and deletions consistent with chromosomal fragility. Severe vitamin B12 deficiency is rare in children and should be considered in the differential diagnosis of a child with pancytopenia, dyserythropoiesis, and multiple chromosomal abnormalities. PATIENTS AND METHODS: Three children displayed pancytopenia with dyserythropoiesis in the bone marrow. Routine cytogenetic analyses in all three patients were performed and chromosome breakage study was performed on the peripheral blood of one patient after vitamin B12 supplementation. RESULTS: All three patients had severe vitamin B12 deficiency. Spontaneous chromosomal fragility was seen in routine cytogenetic analyses in all three patients. Vitamin B12 supplementation resolved the pancytopenia in all three patients and spontaneous and diepoxybutane-induced breakage rates in chromosomes were well within normal rates after therapy in one patient. CONCLUSION: The presence of pancytopenia with cytogenetic abnormalities in a child is worrisome. However, careful interpretation of dyserythropoiesis and megaloblastic changes in bone marrow in the aforementioned clinical situation would result in the correct diagnosis of a disorder that is easily cured.

Bone Marrow↗

PubMed1997

[Allopurinol induced pancytopenia in a patient with myeloproliferative disorder].

We reported a rare case of pancytopenia caused by allopurinol. A 61-year-old man was first admitted in May 1993, because of thrombocytosis. He had suffered from chronic glomerulonephritis. He was administered allopurinol for hyperuricemia from March 1993. On first admission the laboratory findings revealed leukocytosis (10,100/microliter) and thrombocytosis (971 x 10(3)/microliter) in the peripheral blood. Myelofibrosis was strongly suspected due to increased number of MgK and reticular fiber in the bone marrow. Two months later, he readmitted due to pancytopenia (WBC 1,300/microliter, Hb 6.2g/dl, Plt 10 x 10(3)/microliter). His bone marrow showed markedly hypocellular. Because we suspected that pancytopenia was induced by allopurinol, we discontinued allopurinol and administered oxymetholone, G-CSF, and EPO, WBC, RBC, and platelet count had been recovered about one and half months later. In vitro co-culture indicated that CFU-G, E, and Meg in the bone marrow cells after recovery from pancytopenia were markedly suppressed in the presence of patient's serum and oxipurinol. Pancytopenia due to allopurinol was reported to be rare, and some authors showed that it will sometimes be fatal. Because pancytopenia of this case had been recovered in a relatively short time with cytokine therapy, it was thought to be effective for pancytopenia due to drug like this case.

Allopurinol↗

PubMed1999

A retrospective study of canine pancytopenia.

To better define the incidence and causes of canine pancytopenia, we retrospectively evaluated the results of complete blood counts submitted to the University of Minnesota Veterinary Teaching Hospital during a 1-year period. Pancytopenia was defined as packed cell volume < 36%, total leukocyte count < 6,000/microliter or total segmented neutrophil count < 3,000/microliter, and platelet count < 200,000/microliter. Of 4,560 complete blood counts, 110 (2.4%) samples from 51 dogs met the criteria for pancytopenia. Eleven different disease processes were identified. These included chemotherapy-associated pancytopenia (n=22), parvovirus infection (n=5), malignant histiocytosis (n=5), idiopathic aplastic anemia (n=3), sepsis (n=3), myelodysplastic syndrome (n=3), immune-mediated hematologic disease (n=3), lymphoblastic leukemia (n=2), ehrlichiosis (n=2), estrogen toxicity (n=2), and multiple myeloma (n=1). Malignant histiocytosis and idiopathic aplastic anemia occurred more frequently than was expected. Doxoruicin was the chemotherapeutic agent associated with pancytopenia. Hematologic recovery and patient survival time varied with the cause of pancytopenia; therefore, a specific diagnosis was essential for establishing prognosis. Differentiation among causes of pancytopenia requires a systemic approach that includes elimination of infectious and drug-induced causes, and examination of bone marrow aspiration and core biopsy specimens.

Journal Article↗

PubMed2002

Auto-immune pancytopenia in a child with DiGeorge syndrome.

UNLABELLED: We report on the development of auto-immune pancytopenia in a child with DiGeorge syndrome carrying the 22q11 microdeletion. She had congenital heart disease, dysmorphic facies, thymic hypoplasia, immunodeficiency, velopharyngeal insufficiency, scoliosis, and a hearing deficit. She had a low T-cell count with a normal CD4/CD8 ratio, IgA deficiency and a normal lymphoblastic response to mitogens. She has presented with pancytopenia since 10 years of age (leucocytes 3,300/mm(3), haemoglobin 107 g/l, platelets 80,000/mm(3)). Platelet-associated antibodies, anti-neutrophil antibodies and Coombs' positive red cells were present. At 14 years of age, she presented with a severe episode of haemolysis with pancytopenia. Steroids were effective in treating the pancytopenia at a dose of 2 mg/kg per day for 6 weeks. Since 15 years of age, she has had episodes of acrocyanosis. At 16 years of age, she still had mild pancytopenia without any treatment. CONCLUSION: the clinical spectrum of the 22q11 microdeletion syndrome is very broad. This case suggests that auto-immune disease such as pancytopenia is part of the 22q11 microdeletion syndrome.

Adolescent↗

PubMed2005

Pancytopenia in children: etiological profile.

Pancytopenia is a common occurrence in pediatric patients. Though acute leukemias and bone marrow failure syndromes are usual causes of pancytopenia, etiologies such as infections and megaloblastic anemia also contribute. The aim of this study was to evaluate the clinico-hematological profile of varying degrees of childhood cytopenias with special reference to the non-malignant presentations. This is a retrospective study carried out in a tertiary care children's hospital. We retrospectively analyzed 109 pediatric patients who presented with pancytopenia for different etiologies. Acute leukemia (including ALL, AML and myelodysplastic syndrome) and aplastic anemia accounted for 21 per cent and 20 per cent cases respectively. Megaloblastic anemia was found in 31 (28.4 per cent) patients and was single most common etiological factor. Severe thrombocytopenia (platelet < or = 20 x 10(9)/l) occurred in 25.2 per cent of these patients. Various skin and mucosal bleeding occurred in 45.1 per cent of patients with megaloblastic anemia. Infections accounted for 23 (21 per cent) patients who presented with pancytopenia. Amongst infections, enteric fever occurred in 30 per cent patients. Malaria, kala-azar and bacterial infections were other causes of pancytopenia at presentation. The study focuses on identifying easily treatable causes such as megaloblastic anemia and infections presenting with pancytopenia. These conditions though look ominous but respond rapidly to effective therapy.

Acute Disease↗

PubMed1999

Pancytopenia in Zimbabwe.

BACKGROUND: There has been little systematic study of the clinical spectrum of pancytopenia, and the optimal diagnostic approach to pancytopenia remains undefined. METHODS: The authors studied 134 hospitalized pancytopenic patients in Zimbabwe in both consecutive and nonconsecutive fashion. RESULTS: The most common cause of pancytopenia was megaloblastic anemia, followed by aplastic anemia, acute leukemia, acquired immunodeficiency syndrome (AIDS), and hypersplenism. Severe pancytopenia was usually due to aplastic anemia. Patients with aplastic anemia and acute leukemia were usually children, whereas those with megaloblastic anemia were adults. Moderate to severe anemia was noted throughout the series, but was most striking in patients with megaloblastic anemia, aplastic anemia, and acute leukemia. The mean corpuscular volume (MCV) was elevated in most patients with megaloblastic hematopoiesis, aplastic anemia, and acute nonlymphocytic leukemia. Normal or low MCV values were noted in almost one third of patients with megaloblastic anemia. Anisocytosis, poikilocytosis, macroovalocytosis, microcytosis, fragmentation, and teardrop erythrocytes were more prominent on the blood films of patients with megaloblastic anemia. CONCLUSIONS: Megaloblastic anemia, aplastic anemia, and AIDS are the most common causes of pancytopenia in Zimbabwe. Aplasia is the most frequent cause of severe pancytopenia. The authors have formulated tentative guidelines for the evaluation of pancytopenic patients in this setting.

Acquired Immunodeficiency Syndrome↗

PubMed1990

Diagnoses in patients with severe pancytopenia suspected of having aplastic anemia.

There were 100 patients with pancytopenia notified to the Swedish part of an international study of aplastic anemia (Aa) (1983-1986). Aa was the cause in 16 patients and 50 patients had different conditions explaining their pancytopenia, whereas in 34 patients no obvious explanation was found at the time of discovery of their pancytopenia. A follow-up study in 1987 comprised the patients with Aa (n = 16) and the patients with uncharacterized pancytopenia (n = 34.3 additional patients had then been diagnosed as having Aa whereas 3 patients had a diagnosis of a low-grade NHL and 8 patients a diagnosis of MDS. No (or an inadequate) bone marrow sample had been taken in 9 of the 34 patients. This study shows that pancytopenia may be found in many serious conditions. Patients with pancytopenia should be carefully followed as Aa can develop slowly and as the MDS diagnosis can be difficult to establish at an early stage.

Anemia, Aplastic↗

PubMed2004

Leflunomide-associated pancytopenia with or without methotrexate.

OBJECTIVE: To report 18 cases of pancytopenia associated with leflunomide use in Australia, 5 of which were treated at Princess Alexandra Hospital, Brisbane. case summaries: Leflunomide was used in the treatment of rheumatoid arthritis in 17 of 18 patients; the other patient was diagnosed with systemic lupus erythematosus. Median age was 65.5 years (range 18-79), and 15 of the patients were female. Fourteen patients were on combined treatment with methotrexate. Pancytopenia was typically severe, requiring hospital admission, withdrawal of the immunosuppressant(s), intensive supportive therapy, and treatment of neutropenic sepsis. Five patients died, 4 of whom were receiving concomitant methotrexate. Time to onset of pancytopenia ranged from 11 days to 4 years (median 4 mo). In one case in which the patient had been stable while receiving leflunomide, methotrexate, and hydroxychloroquine for 4 years, fatal pancytopenia was triggered by acute renal failure secondary to dehydration and use of nonsteroidal antiinflammatory drugs. The Naranjo probability scale suggested a probable causal association in 5 cases and possible association in the remainder. DISCUSSION: Leflunomide, indicated for treatment of active rheumatoid arthritis, inhibits pyrimidine synthesis in lymphocytes and other rapidly dividing cells and may rarely be associated with life-threatening pancytopenia. Combination therapy with methotrexate may increase the risk. Time to onset is variable, and clinicians should remain vigilant, particularly when there is a change in the patient's baseline health status. CONCLUSIONS: The risk of pancytopenia during leflunomide therapy appears to be increased when the drug is combined with methotrexate and in older patients. Onset may be delayed, and ongoing monitoring of blood counts is essential.

Aged↗

PubMed2005

Death related to albendazole-induced pancytopenia: case report and review.

Albendazole is a benzimidazole with wide spectrum coverage as an antiparasitic drug. Reported side effects have been minimal. We report the case of a patient who died with severe prolonged pancytopenia beginning during the third week of therapy for a pulmonary echinococcal cyst. This case was a 68-year-old man who presented with a large cystic lung mass. His medical history was significant for Child-Pugh class B cirrhosis. A prolonged course of albendazole was initiated. Two weeks later, the patient presented in septic shock with severe pancytopenia. The patient was initially resuscitated, but died after 10 days with no marrow recovery. Autopsy was consistent with albendazole-induced pancytopenia. This is the third human case of pancytopenia and the first death reported in relation to albendazole-induced pancytopenia. Neutropenia seems to be related more to higher dosage and longer duration of use. Albendazole sulfoxide peak dose and half life are significantly prolonged by liver disease and concomitant administration of certain drugs. The severity and duration of albendazole-induced pancytopenia in this case was likely related to the underlying liver disease. Frequent serial monitoring of blood counts and cessation of medication with any evidence of marrow toxicity in such patients is warranted.

Aged↗

PubMed2005

[Role of vitamin deficiency in pancytopenia in Djibouti. Findings in a series of 81 consectutive patients].

The purpose of this study of patients with pancytopenia in Republic of Djibouti was to identify etiologic factors and attempt to define diagnostic and therapeutic strategies adapted to local conditions. Clinical, biological and radiological assessment was performed in 81 patients hospitalized for pancytopenia. There were 56 men and 25 women. Mean hemoglobin, leukocyte and platelet rates were 56,5 +/- 22,7 g/l, 2,1 +/- 0,7.g/l and 56,2 +/- 24,7 g/l respectively. Vitamin deficiency was the most common cause of pancytopenia (49%), followed by hypersplenism (9%), HIV infection (6%) and leishmaniasis (6%). Vitamin-deficient patients had significantly more severe anemia and thrombopenia and significantly higher mean corpuscular volume than patients with pancytopenia related to other causes. Hemoglobin rate lower than 40 g/L and platelet rate lower than 35 G/L showed a positive predictive values of 90% and 100% respectively for a vitamin deficient pancytopenia. Vitamin deficiency is the most frequent etiology of pancytopenia and causes the most severe cytopenia in Djibouti. Rapid vitamin supplementation after minimal etiologic assessment including a myelogram is an effective treatment strategy for this public health problem.

Adult↗

PubMed1997

[Toxicity of low-dose methotrexate in rheumatoid arthritis--clinical characteristics in patients with MTX-induced pancytopenia and interstitial pneumonitis].

Pancytopenia and interstitial pneumonitis are one of the most serious and unpredictable adverse effects of low dose, pulse methotrexate (MTX) in treating rheumatoid arthritis (RA). It is important to investigate the historical, clinical or immunologic features associated with the development of such toxicity, in order to use MTX more appropriately. Two hundred eighty four patients (female 230 male 54) with rheumatoid arthritis had been treated with pulse weekly oral MTX with a mean follow-up of 33.2 months. Adverse effects which required the discontinuation of MTX occurred in 47 patients (16.5%). Gastrointestinal toxicity occurred most frequently (14 patients) and liver dysfunction occurred in 9 patients. Four patients (1.4%) developed pancytopenia, and six patients (2.1%) developed interstitial pneumonitis. All patients who developed pancytopenia were old female with long history of active, deforming rheumatoid arthritis, The cumulative dose of MTX ranged from 15 mg to 760 mg at the time pancytopenia developed. Impaired renal function, hypoalbuminemia, and multiple medication were observed, and antinuclear antibodies were positive in most patients. It should be noted that severe stomatitis preceded or accompanied with pancytopenia in all patients. Blood counts returned to the normal level in 7 to 14 days. All patients who developed interstitial pneumonitis were old female. The cumulative dose ranged from 65 mg to 580 mg. Pre-existance of lung diseases, history of adverse effects of other DMARDs, the presence of Raynaud's phenomenon, and antinuclear antibodies appeared to be risk factors for interstitial pneumonitis. All patients recovered with high dose of corticosteroid and mechanical ventilation. Such clinical characteristics that are associated with MTX-induced pancytopenia or interstitial pneumonitis should be reminded in the treatment of rheumatoid arthritis with MTX.

Aged↗

PubMed2001

Severe pancytopenia associated with low-dose methotrexate therapy for rheumatoid arthritis.

OBJECTIVE: To report the occurrence of severe pancytopenia associated with low-dose methotrexate (MTX) therapy for rheumatoid arthritis. CASE SUMMARY: Two patients developed severe pancytopenia after 10 days (cumulative dose 15 mg) and 23 months (cumulative dose 1030 mg), respectively, of low-dose MTX therapy for rheumatoid arthritis. Both patients had renal impairment. One died and the other recovered completely. DISCUSSION: Pancytopenia is a rare adverse effect of low-dose oral MTX therapy. The exact mechanism for development of pancytopenia is unknown, although it is likely that several factors play a role. The most important risk factor for MTX toxicity is impaired renal function. This adverse effect may occur at any time during MTX therapy. CONCLUSIONS: Severe pancytopenia associated with low-dose MTX therapy for rheumatoid arthritis is a potentially serious complication that may occur at any time during therapy. This adverse effect is more likely to occur in patients with renal impairment.

Administration, Oral↗

PubMed2001

A case of thyrotoxicosis with pancytopenia.

We report a 49-year-old man with primary hyperthyroidism who presented with pancytopenia. The patient presented with leg edema, sinus tachycardia, cardiomegaly, and pleural effusions, all from congestive heart failure. Laboratory data showed pancytopenia and primary hyperthyroidism; echocardiogram showed diffuse hyperkinesis of the left ventricular wall and right ventricular overloading. The bone marrow was moderately hypercellular and compatible with arrested hematopoiesis. Pancytopenia and heart failure improved after administration of methimazole and diuretics. However, high levels of thyroid hormone recurred with pancytopenia 4 months after admission. Therefore, subtotal thyroidectomy was performed, and the levels of thyroid hormones and peripheral blood cell counts have remained normal. Pancytopenia may be caused by hyperthyroidism.

Antithyroid Agents↗

PubMed2004

Pancytopenia, a rare hematologic manifestation of brucellosis in children.

The records of 54 children with brucellosis were evaluated retrospectively. Among them, eight patients (14.8%) with pancytopenia were identified in a 7-year period between 1996 and 2003. Six of the eight patients with pancytopenia had Brucella melitensis isolated from blood cultures, and all eight patients had Brucella agglutination titers of at least 1:320. Agglutination test titers did not correlate with the degree of pancytopenia. Fever was the most common manifestation, followed by malaise, anorexia, sweating, weight loss, and gastrointestinal symptoms. Most patients had hepatosplenomegaly, and bone marrow aspiration specimens showed hyper-cellularity or normocellularity. Hemophagocytosis (3 patients) and histiocytic hyperplasia (4 patients) were observed in bone marrow examinations of eight patients, but bone marrow aplasia and granulomas were not detected. All children recovered completely; the pancytopenia was transient and resolved after the antibiotic treatment of Brucella infection. Brucellosis should be considered as a possible diagnosis among patients with pancytopenia.

Adolescent↗

PubMed1995

Pancytopenia related eosinophilia in rheumatoid arthritis: a specific methotrexate phenomenon?

Methotrexate (MTX) induced pancytopenia has been reported in about 3% of patients with rheumatoid arthritis (RA) receiving low dose MTX. We describe 4 additional patients with RA (2M, 2F; mean age 65 yrs; mean duration of RA 9 yrs) who developed pancytopenia while receiving low dose MTX. Risk factors identified for the development of pancytopenia in our patients included impaired renal function, hypoalbuminemia, advanced age, low folate level, concurrent use of multiple comedication, nonsteroidal antiinflammatory drugs, and cotrimoxazole). Remarkably, pancytopenia related eosinophilia was observed in blood and bone marrow after restoring the intracellular folate level by folinic acid. The range of eosinophils was 22-56% of the number of peripheral white blood cells (mean nadir 33%). The peak level of eosinophilic granulocytes was reached after a mean of 6 days in hospital (range 4-8), whereas the peak of neutrophils was reached after a mean of 11 days (range 9-13 days). The duration of the eosinophilic response was 11 days. As eosinophilia has not been observed in other drug induced pancytopenias in patients with RA this could be a specific MTX induced phenomenon.

Aged↗