Heredofamilial deficiency of monocyte esterase in patients with rheumatoid arthritis.

Bell, A. L.; Markey, G. M.; McCaigue, M. D.; Middleton, D.; Mccormick, J. A.; Wilson, Anthony G.; Morris, T. C. M.

doi:10.1136/ard.51.5.668

Cited by 6 publications

(3 citation statements)

References 11 publications

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“…A 41% familial incidence of MED has been previously demonstrated by study of 14 families who had a member with MED and either autoimmune disease ( N = 5 ; including 1 renal unit patient) or lymphoproliferative disease (N = 8) and a renal unit patient with familial nephritis (1)(2)(3). The 2 sibs of the latter patient were not esterase deficient but all 5 clinically normal sibs of the patient with an autoimmune basis for renal failure (microscopic vasculitis) had MED.…”

Section: Discussionmentioning

confidence: 93%

“…Lactofemn stimulated the cytotoxicity of esterase positive monocytes for Tr-labeled K562 cells but not that of constitutionally esterase negative monocytes (6). Epidemiological studies have shown a significantly increased incidence of monocyte esterase deficiency (MED) in autoimmune and lymphoproliferative disease, and family studies in subjects with these diseases have shown a 41% familial incidence of the trait, demonstrating that the trait was not caused by the disease (1,2,3). The latter evidence suggested that a possible reason for the increased incidence of the anomaly in these cohorts was that the esterase negativity predisposed to or was linked to a predisposition for these diseases.…”

Section: Introductionmentioning

confidence: 99%

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Renal Failure and Esterase-Negative Monocytes

Hull¹,

Markey²,

Morris³

1997

Renal Failure

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Monocyte esterase deficiency (MED) has been found to be linked with autoimmune (1,2) and lymphoproliferative (2,3) disease. The incidence of MED where > 85% of peripheral blood monocytes are consistently negative in the cytochemical stain for monocyte esterase activity, was shown to be significantly raised in patients with renal failure (3.8%) as compared to the incidence in normal blood donors (0.8%) in a survey performed at the Belfast City Hospital in 1987 (2). The overall occurrence of any proportion of esterase-negative monocytes (ENMs) in patients with renal disease has not been previously studied. The aims of this study were to document this occurrence, and by examining the clinical and biochemical parameters associated with ENMs to identify possible reasons for their occurrence. The original survey data were reexamined and further information previously unreported regarding the occurrence of ENMs was extracted from the renal patient cohort data. Clinical and biochemical data were obtained from the hospital notes of the renal patients and associations sought between these parameters and the occurrence of ENMs. ENMs occurred in a significantly higher proportion (31%) of the renal patients than in the normal population (8%; p < 0.001 chi-sq.) or any other hospital population. A highly significant association between rising serum phosphate levels and increasing proportions of ENMs was identified (p < .001) and this association proved to be independent of serum creatinine levels and renal dialysis status. There is a marked increase in occurrence of esterase-negative monocytes in patients with renal failure. This increase was not caused by the degree of renal failure as reflected by serum creatinine levels, nor by renal transplantation or immunosuppressive therapy. A significant association between rising serum phosphate and increasing proportion of esterase-negative monocytes was identified. This new information, when considered with the previously described experimental and epidemiology evidence for malfunction of esterase negative monocytes, identifies a phenomenon which may contribute to the immunological difficulties of patients with chronic renal failure.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Renal Failure and Esterase-Negative Monocytes

Hull¹,

Markey²,

Morris³

1997

Renal Failure

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“…An increased prevalence of MED (up to 10 times greater than that found in blood donors) has been reported in lymphoproliferative and gastrointestinal malignant neoplastic diseases, as well as in patients with autoimmune disease ( Markey et al , 1990,1993 ). MED is a familial trait and has been demonstrated in 46% of members in affected families ( Markey et al , 1986,1987,1990 ; Bell et al , 1992 ; Hull et al , 1998 ). The patterns of inheritance suggest that the trait is predominantly an autosomal dominant characteristic ( Fig 2).…”

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confidence: 99%

Quantitative deficiency of monocyte‐specific esterase (MSE) mRNA in monocyte esterase deficiency (MED)

et al. 2000

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Summary. Cytochemical staining of monocyte-specific esterase (MSE) is widely used for identification of the monocytic lineage in leukaemias. Deficiency of this enzymatic activity occurs as a familial trait and the deficiency has been shown to occur with greater frequency in patients with lymphoproliferative or gastrointestinal malignant neoplastic diseases than in normal blood donors. Reverse transcriptase polymerase chain reaction (RT-PCR), sequencing and quantification by Northern blot analysis was conducted on the MSE mRNA of 12 subjects with monocyte esterase deficiency (MED) and seven MSE-positive subjects to examine whether mutations were present or whether the defect was quantitative. Mutations were not found in the mRNA sequences. However, MED subjects had significantly less MSE mRNA than MSE-positive subjects (P 0´001). These findings show that deficiency of monocyte esterase activity in MED is not as a result of the presence of inactive isoenzymes and may be owing to an abnormality in the regulation of mRNA production.

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