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Biomedical subjects

H D Alexander

Publications and source records attributed to H D Alexander.

At least 55 records · Page 3Linked to original sources
PubMed1993

Monocyte esterase deficiency in gastrointestinal cancer.

AIM: To substantiate the high incidence of monocyte esterase deficiency (MED) in gastrointestinal carcinoma already reported in a small group of patients; to compare the clinical findings in esterase deficient and esterase positive patients. METHODS: Peripheral blood smears (n = 22) or cytocentrifuge preparations (n = 52) of mononuclear cells from the peripheral blood of patients with gastrointestinal carcinoma were stained by the non-specific esterase stain (pH 5.8) using a batch technique. Samples containing > or = 85% esterase negative monocytes were identified at light microscopic examination. RESULTS: Seven of 74 patients were identified as having MED. This correlated exactly with the proportion (five of 46) found before, using an automated method, and was significantly higher than the 0.8% incidence in normal blood donors shown in that study. Comparison of the clinical details of the 12 MED patients with those of 105 esterase positive patients showed a significantly longer disease free survival in the MED cohort and increased occurrence of benign neoplasms--largely colorectal polyps--in this group also. Three patients had a borderline degree of deficiency and were excluded from comparisons, although they showed the same clinical tendencies as the MED group. CONCLUSIONS: There is a strong degree of association between monocyte esterase deficiency and gastrointestinal carcinoma. Further evidence must be sought to prove that the deficiency precedes the disease and therefore may predispose to it, or at least may identify subjects with such a predisposition. This could lead to early diagnosis and effective treatment of gastrointestinal carcinoma in a sizeable proportion of patients.

Aged↗
PubMed1992

Cell sizing in chronic lymphoproliferative disorders: an aid to differential diagnosis.

AIMS: To determine if leucocyte volume distribution analysis (LVDA), obtained using a Coulter Counter Model S Plus IV, can be used to aid differentiation of chronic lymphoproliferative disorder (CLPD) subtypes. METHODS: Mean lymphocyte volume and lymphocyte distribution width were measured on each patient (n = 90) using a hard copy of an amplified LVDA histogram. The mean lymphocyte volume was taken as the mean of the values on either side of the peak at half maximum height. The lymphocyte distribution width was taken as the range of cell values between the two values used to calibrate the mean lymphocyte volume. A template showing typical histograms from commonly occurring CLPD was also produced on an acetate sheet. This was used to examine the histogram from each new patient to evaluate its usefulness as an alternative to the calculation of mean lymphocyte volume and lymphocyte distribution width. RESULTS: Mean lymphocyte volume and lymphocyte distribution width were significantly higher in B cell lymphocytic leukaemia of mixed cell type (B CLL/PL), B cell non-Hodgkin's lymphoma with peripheral blood spill, hairy cell leukaemia and T cell prolymphocytic leukaemia than in B cell chronic lymphocytic leukaemia (B CLL). The mean lymphocyte volume, but not the lymphocyte distribution width, was also significantly higher in T cell chronic lymphocytic leukaemia than in B CLL. The template gave an immediate preliminary indication of possible subtype(s) of disorder and could be used as an alternative to measurement of mean lymphocyte volume and lymphocyte distribution width. CONCLUSIONS: Electronic haematology analysers producing an LVDA provide a useful, cost effective cell sizing analysis which can aid the differentiation of subtypes of CLPD.

Cell Size↗
PubMed1991

Lactoferrin inducible monocyte cytotoxicity defective in esterase deficient monocytes.

We recently demonstrated a higher incidence of monocyte esterase deficiency in patients with lymphoproliferative neoplasia and gastrointestinal carcinoma than in the normal population. Using lactoferrin to stimulate monocyte cytotoxicity we have now compared the abilities of esterase positive and esterase deficient monocytes to lyse K562 cells. The esterase deficient monocytes were from normal subjects whose monocytes have consistently failed to show cytochemical esterase staining over 30-72 months and which lack specific monocyte isoenzymes. The esterase positive monocytes were from age and sex matched control subjects. Esterase positive monocytes responded to lactoferrin stimulation by a five-fold increase in cytotoxicity whereas deficient monocytes failed to produce any response. These results indicate a possible defect in cytotoxicity of esterase deficient monocytes and together with the epidemiological findings suggest a link between monocyte esterase deficiency and neoplasia.

Cells, Cultured↗
PubMed1990

Monocyte esterase deficiency in malignant neoplasia.

A survey of the incidence of monocyte esterase deficiency in 4000 inpatients (including 808 with malignant neoplastic disease) and 474 normal controls was performed using an automated esterase method. A highly significant excess of patients with malignant disease and the deficiency was evident when compared with normal controls or all other patients. Within the group of patients with malignant disease the demonstrable excess occurred in B chronic lymphocytic leukaemia, non-Hodgkin's and Hodgkin's lymphoma, and carcinoma of the gastrointestinal tract. There was also a significant excess of patients with the deficiency attending the renal unit, both among patients who had had renal transplants and those who had not. A familial incidence of monocyte esterase deficiency was found in 19 (35%) of first degree relatives of those patients in whom family studies were done. It is suggested that the reason for the increased prevalence of the anomaly in these disorders might be that the diminution of esterase activity has a role in their development.

Esterases↗
PubMed1990

Tartrate resistant acid phosphatase positive splenic lymphoma: a relatively benign condition occurring in a time-space cluster?

Conventional light and electron microscopic studies, together with cytochemical and immunocytochemical staining procedures, were carried out to ascertain whether the lymphomata of four elderly female patients living within 10 kilometers of each other, who presented within a short space of time with massive splenomegaly and varying cytopenia, belonged to any particular subgroup of lymphoma. In each case the lymphoma had a diffuse pattern and mature B cell phenotype. The malignant cells were of uniform cell type, slightly larger than admixed polymorphonuclear leucocytes, and showed minimal nuclear irregularity and positivity for tartrate resistant acid phosphatase (TRAP) staining. Their clinical and morphological features were compared with those of other lymphoproliferative disorders, but while sharing some features in common with each condition, this small group of patients seemed to have a unique combination of findings. The cytopenias of all four responded well after removal of the spleen and their disease has not been aggressive. It is concluded that these patients have a distinct subgroup of lymphoma, which it is important to recognise so that inappropriate use of aggressive cytotoxic drugs can be avoided.

Acid Phosphatase↗
PubMed1989

Immunoglobulin light chains in common acute lymphoblastic leukaemia.

A single immunoglobulin light chain lambda was identified in the blast cells of two out of 12 patients with common acute lymphoblastic leukaemia (C-ALL) using the alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique. Inhibition at the cell surface proved that the reaction was a genuine anti-lambda reaction. Immunoglobulin mu chain was not identified in these patients. Results of immunoglobulin typing in 103 patients with B chronic lymphocytic leukaemia (B-CLL) are cited to show the increased sensitivity of the APAAP technique as compared to the indirect immunoperoxidase technique for cellular immunoglobulin identification.

Female↗
PubMed1987

T-lymphocyte colony formation by lymphocytes from patients with aplastic anaemia.

T-lymphocyte colonies were cultured using lymphocytes from patients with aplastic anaemia and normal donors to assess their respective proliferative activities. Colony numbers from aplastic patient's cells were lower than from normal donors', though this was not significant. When lymphocytes from patients were co-cultured with normal lymphocytes, inhibition of T-colony formation was observed in 8 out of 12 experiments. As the degree of inhibition was greater than if patient cells grew no colonies, then, clearly, normal T-colony formation was inhibited. This ability of patients' lymphocytes to suppress lymphopoiesis might account for the low levels of patient T-colony formation, as well as low in vivo numbers of lymphocytes found in patients with aplastic anaemia. The role of patients' lymphocytes in causing marrow aplasia was investigated. Although the incorporation of patients' lymphocytes in normal granulocyte-macrophage (GM) colony-forming systems inhibited colony growth, in only 1 out of 8 patients was this inhibition significantly greater than that caused by the addition of normal lymphocytes to GM colony systems. Therefore, lymphocytes may not be the primary cause of aplastic anaemia, except for a few rare cases.

Adolescent↗
PubMed1987

Monocyte esterase? A factor involved in the pathogenesis of lymphoproliferative neoplasia.

Monocyte esterase activity was studied in 1,000 doctor-attending patients with normal hematological indices and in 56 patients with non-Hodgkin's lymphoma (NHL) or B chronic lymphocytic leukemia (CLL). The incidence of esterase deficiency was significantly greater in the NHL-CLL patients (7.1%) than in the population group (1.7%; p less than 0.05). In the NHL-CLL group, study of the families showed the esterase deficiency to be a familial characteristic. We postulate that the presence of the anomaly may be either a factor predisposing to the development of the NHL or CLL or a factor indicating a predisposition to these disorders.

Esterases↗
PubMed1986

Enumeration of absolute numbers of T lymphocyte subsets in B-chronic lymphocytic leukaemia using an immunoperoxidase technique: relation to clinical stage.

An immunoperoxidase technique has been used to identify and enumerate helper and suppressor T-cell subsets, as defined by reactivity with Coulter T4 and OKT8 monoclonal antibodies in 54 patients with B chronic lymphocytic leukaemia (B-CLL) and in the same number of matched controls. The ratio of T4+ to T8+ cells was significantly reduced in the B-CLL group as a whole (P less than 0.001) and in each stage of the three clinical staging systems. There was an increase in the median absolute level of T8+ cells in the whole CLL group (P less than 0.001). However, subdivision of the CLL group by clinical staging systems revealed a large group (28 patients) in which median T8+ cell levels were not raised and median T4+ cell levels were low (P less than 0.01). There was no significant decrease in T4+:T8+ ratio, increase in T8+ cells or decrease in T4+ cells with progression of clinical stage. Absolute numbers of E+ cells were significantly raised in all staging systems as were E+ T4- T8- cells (P less than 0.001). A significant alteration in either of these populations with progression of clinical stage was not present.

Adult↗
PubMed1986

Hereditary monocyte esterase deficiency.

An inherited cytochemical staining abnormality of monocytes is described, affecting members of three generations of one family. alpha-Naphthyl acetate and alpha-naphthyl butyrate esterase staining reactions have been consistently negative in 95% of the monocytes of the propositus and her son and in 60-70% of the monocytes in two of four grandchildren.

Aged↗
PubMed1986

Successful remission induction with deoxycoformycin in elderly patients with T-helper prolymphocytic leukaemia.

Two elderly patients with prolymphocytic leukaemia (PLL) of T helper phenotype were treated with the adenosine deaminase inhibitor--deoxycoformycin--and achieved remission. The first patient has remained in an unmaintained remission for over a year. The second patient, treated with a regime which produced less side effects, subsequently relapsed in skin and lymph nodes and died. In view of the rarity of this condition a multi-centre assessment of the effectiveness of deoxycoformycin is indicated. T-lymphocyte colony formation in both cases was found to be reduced. Co-culture of the patients' lymphocytes with nonadherent mononuclear cells from normal individuals also showed inhibition of T-colony formation indicating that lack of nutrients or accessory cells was not responsible for low T-colony forming capacity.

Aged↗
PubMed1985

Acid hydrolase activities in B cell chronic lymphocytic leukaemia lymphocytes: correlation of cytochemical reactions with immunological phenotype.

The cytochemical reactions of 5 acid hydrolases, alpha-naphthyl acetate esterase (ANAE), acid phosphatase (AP), beta-glucuronidase, beta-glucosaminidase and dipeptidylaminopeptidase IV (DAP IV) were investigated in lymphocytes from 30 patients with B cell chronic lymphocytic leukaemia (B-CLL). Based on ANAE and AP reactivities, 4 cytochemically distinctive subgroups were identified: Group 1: AP and ANAE less than 50% positive lymphocytes (5 cases); Group 2: AP greater than 50%, ANAE less than 50% positive lymphocytes (11 cases); Group 3: AP less than 50%, ANAE greater than 50% positive lymphocytes (7 cases); Group 4: AP and ANAE greater than 50% positive lymphocytes (7 cases). beta-Glucuronidase displayed similar patterns of reactivity to AP. beta-Glucosaminidase activity was observed in the majority of lymphocytes in most patients, whereas DAP IV activity was present in less than 20% of lymphoid cells. The study failed to establish any relationship between cytochemical grouping and patients' clinical status, peripheral lymphocyte counts, E or mouse rosette values, light or heavy chain cellular immunoglobulin (Ig) class. Attempts to correlate acid hydrolase and Ig heavy chain isotype expression, putative markers of B cell maturation, were unsuccessful and indicate that within the narrow spectrum of B cell differentiation seen in B-CLL these characteristics are unrelated.

Acid Phosphatase↗
PubMed1983

Stable E rosette-forming lymphocytes in the peripheral blood in non-Hodgkin's lymphoma.

The peripheral blood of 49 patients with non-Hodgkin's lymphoma and the same number of normal controls was examined for the presence of lymphocytes forming rosettes with sheep erythrocytes at 37 degrees C (stable E rosettes). Nineteen lymphoma patients but only five normal controls showed increased absolute levels. (P less than 0.01). There was no correlation between the occurrence of increased Stable E Rosette levels and the histological type of lymphoma but there appears to be a positive relationship with the presence of clinical stage III-IV disease at presentation (P = 0.011). It is suggested that stable E rosettes represent an immunological response to residual lymphoma in our patients. A longitudinal study in one patient is reported in detail to demonstrate the occurrence of fluctuations in stable E rosette levels coinciding with clinical changes.

Aged↗
PubMed1983

Identification of cellular immunoglobulins in chronic lymphocytic leukaemia by immunoperoxidase staining.

An indirect immunoperoxidase technique has been used for visualisation of cellular immunoglobulins in chronic lymphocytic leukaemia. Baker's formol calcium was used as fixative. Monoclonal light and heavy chain patterns were demonstrated in 24 out of 27 cases. Only one case did not have any demonstrable immunoglobulins. The presence of alpha or gamma heavy chain immunoglobulin isotypes in leukaemic lymphocytes was found to be related to low mouse rosetting capacity (p less than 0.05).

Adult↗