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Biomedical subjects

G Garewal

Publications and source records attributed to G Garewal.

At least 55 records · Page 3Linked to original sources
PubMed1990

Pure red cell aplasia associated with essential thrombocythemia (a case report).

A rare case of erythroblastopenia associated with essential thrombocythemia (ET) is described. The patient had markedly elevated platelet count (5200 x 10(9)/1) and significant platelet dysfunction leading to extensive soft tissue and gastrointestinal hemorrhage. There was paucity of erythroid precursors in the bone marrow - a feature hitherto undescribed in ET. The thrombocytosis responded to well busulphan therapy but patient succumbed to fulminant infection consequent upon drug induced neutropenia.

Female↗
PubMed1989

Pancytopenia in nutritional megaloblastic anaemia. A study from north-west India.

We have analysed 139 consecutive cases (71 males and 68 females) of nutritional megaloblastic anaemia over a period of four and a half years. The majority of these patients belonged to the low socio-economic class and many of them were strict vegetarians. Sixty one percent were in the second and third decades of life. At the time of presentation, 46% had mild hepatomegaly, 42% fever, 34% mild splenomegaly and 20% bleeding manifestations. Of 102 cases in whom the biochemical parameters were available, vitamin B12 deficiency was detected in 76%, folate deficiency in 6.8%, combined B12 and folate deficiency in 8.8%; the remaining 7.8% had normal vitamin levels at presentation. All 139 patients had severe anaemia, 80.5% had thrombocytopenia and 43.8% had neutropenia as well as thrombocytopenia. It appears that during progression (in terms of duration) of megaloblastosis, anaemia is followed by thrombocytopenia and then neutropenia. Infection and bleeding in these patients may be aggravated by impaired functions of neutrophils and platelets, respectively.

Adolescent↗
PubMed1988

Functional and ultrastructural changes of platelets in malarial infection.

This paper describes changes in the circulating platelets of 25 patients with acute malaria within 2 to 6 days of onset of illness. Thrombocytopenia was observed in 10 out of 15 patients with Plasmodium falciparum infection, and in 4 out of 9 patients with P. vivax infection. One patient with a mixed infection of both species had a disseminated intravascular coagulation. Platelet antibody was detected in the sera of 8 out of 11 cases by the complement lysis inhibition technique and indirect immunofluorescence. The mean platelet antibody concentrations in the sera of 11 patients and 53 control subjects were 122.70 +/- 80.25 ng/10(7) platelets and 36.69 +/- 18.72 ng/10(7) platelets, respectively. An inverse relationship between the platelet count and platelet antibody levels in serum supported the view that thrombocytopenia in malaria may be partly immune-mediated. Platelet aggregation responses to agonists such as ADP, adrenaline, collagen and ristocetin revealed hyperactivity. Ultrastructural study of unstimulated platelets from patients revealed several changes such as centralization of dense granules, glycogen depletion, and formation of pseudopods and microaggregates, indicating in vivo activation of the platelets, which may also lead to thrombocytopenia.

Adolescent↗
PubMed1987

Establishment and characterization of three new malignant lymphoid cell lines.

We have established 3 new EBV-negative cell lines, designated Sc-1, Ri-1 and Ci-1, from patients with B-cell lymphoma/leukemia. We characterized them by cytogenetics and by study of surface membrane antigens with a panel of monoclonal antibodies (MAbs), surface and cytoplasmic immunoglobulin (Ig) expression and Ig heavy- and light-chain genes. All 3 lines had a 14q+ abnormality. Ri-1 also had translocations involving chromosomes 2, 8 and 18. Ci-1 also had abnormalities involving chromosomes 2, 8 and 22 and its karyotype was 46, XX, t(2;8), t(14;22). The t(2;8) had the same breakpoints as those reported in some cases of Burkitt's lymphoma. We also studied a classical Ph1-positive cell line previously established by Pegoraro et al. (1983) and designated BV173. The phenotypes of these 4 lines based on Ig expression and marker studies correlated well with their respective genotypes. Our results are in keeping with the notion that leukaemic cell populations are clonal expansions of cells "frozen" at a particular stage in their differentiation. Specifically, BV173 cells are at an early stage of B-cell differentiation, Ri-1 and Ci-1 cells are at intermediate stages and Sc-1 cells are at a relatively late stage in the B-cell lineage.

Adult↗
PubMed1986

Antigenic determinants on myeloid leukaemia colony-forming cells resemble those of normal myeloid progenitor cells and differ from those of circulating blast cells.

We studied the antigenic characteristics of leukaemic colony-forming cells (CFU-L) from the blood of patients with chronic granulocytic leukaemia (CGL) in blastic transformation (BT) and acute myeloid leukaemia (AML) by in vitro culture techniques after complement-mediated lysis with one anti-DR and 10 selected myeloid monoclonal antibodies (McAbs), all of which were cytotoxic in the presence of complement. At the same time we studied the antigenic characteristics of the circulating blast cells from the same patients using in addition one non-complement fixing antibody (BI.3C5) with standard immunofluorescence and immunoalkaline phosphatase techniques. We also used myeloid progenitor cell assays in conjunction with cytotoxic McAbs to investigate the antigenic determinants on Day 7 CFU-GM, Day 14 CFU-GM and BFU-E from the blood of patients with CGL in chronic phase (CP) and from normal bone marrow. We found that two of the McAbs, S4-7 and WGHS29.1, recognized a higher proportion of CFU-L from the blood of AML patients than from patients with CGL-BT. However, the patterns of reactivity for CFU-L from CGL-BT and AML patients with the other McAbs quite closely resembled those observed in CFU-GM and BFU-E from normal individuals and patients with CGL in CP. A McAb with DR specificity and one of the myeloid McAbs, 54/39, recognized both CFU-L from CGL-BT and AML and reacted also with circulating blast cells from the same patients. In contrast, six of the other myeloid McAbs that recognized CFU-L failed to label the corresponding blast cells. We conclude that the antigenic properties of CFU-L in CGL-BT and AML are very similar to, but perhaps not identical with, those of normal CFU-GM and BFU-E. There was a major discrepancy in the antigenic profiles of CFU-L and of the blast cells predominating in the blood.

Antibodies, Monoclonal↗
PubMed1986

Cytogenetics in nutritional megaloblastic anaemia: prolonged persistence of chromosomal abnormalities in lymphocytes after remission.

Chromosomal studies were performed in phytohaemagglutinin-stimulated cultures of lymphocytes and in bone marrow cells without culture from 115 patients with megaloblastic anaemia resulting from nutritional deficiency of folate and vitamin B12. Essentially similar chromosomal abnormalities were observed in the two cell lines. These were characterized by striking morphological aberrations such as elongation and despiralization (uncoiling or incomplete contraction), increased frequency of chromosome breakage and centromere spreading. Numerical abnormalities, chromatid exchanges and translocations were virtually absent. Autoradiographic studies of chromosomes after pulse-labelling with 3H-thymidine during the terminal 6 h of phytohaemagglutinin-stimulated lymphocyte cultures revealed a differential pattern of distribution of the radionucleotide in the chromosome of megaloblastic lymphocytes as compared to those from normal lymphocytes. Repeated chromosomal studies were done in 65 of these patients at various intervals after starting therapy with the deficient vitamins. After 48 h of therapy, chromosomal abnormalities were remarkably reduced in the bone marrow; but many of these morphological chromosomal changes (i.e. despiralization and breaks) persisted in the lymphocytes of a significant proportion of patients for variable periods up to 6-12 months after haematological remission resulting from therapy with the deficient vitamins. These abnormalities did not, however, persist after remission in those patients who had repeated episodes of infections.

Adolescent↗
PubMed1986

Plasma transcobalamins in haematological disorders.

Plasma UBBC-B12 and transcobalamins were measured in 112 patients suffering from different haematological disorders. The data showed different patterns of changes in plasma transcobalamin profile in different haematological disorders. Plasma UBBC-B12 and transcobalamins were significantly higher than normal in untreated chronic myeloid leukaemia, acute promyelocytic leukaemia, nutritional megaloblastic anaemia and in refractory anaemias with hypercellular marrow. Normal levels of these proteins were noted in chronic lymphatic leukaemias, in primary and secondary hypereosinophilic states and in multiple myeloma. Subnormal levels of these proteins were observed in hypoplastic anaemia and acute lymphoblastic leukaemia. Chronic myeloid leukaemia patients during blast crisis and acute myeloid leukaemia patients except those suffering from acute promyelocytic leukaemia showed varying pattern of plasma transcobalamins depending on type of blast crisis or FAB subtype of AML. The significance of these changes in plasma transcobalamins have been discussed along with the experience of other workers in this field.

Anemia↗