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Biomedical subjects

M C Shen

Publications and source records attributed to M C Shen.

At least 55 records · Page 3Linked to original sources
PubMed1994

Cytogenetic studies, ras mutation, and clinical characteristics in primary myelodysplastic syndrome. A study on 68 Chinese patients in Taiwan.

Cytogenetics and clinical features were studied for 68 Chinese patients with primary myelodysplastic syndrome (MDS). Ras mutation was analyzed in 25 of them. Thirty-four patients (50%) had clonal chromosomal abnormalities at initial analysis. The most common cytogenetic aberrations were -7, +8, 5q-, and 20q-, which occurred in 11 (16.2%), seven (10.3%), five (7.4%) and three patients, respectively. The incidence of -7 was higher and that of 5q- lower in our patients than in patients from most other geographic areas. The 17 patients with multiple chromosomal abnormalities had a significantly shorter median survival (9 months) than the 34 patients with normal karyotype (33 months) and the 17 patients with patients with single anomalies (26 months). Evolution to acute leukemia occurred in 20 patients (29%) after a median interval of 8 months following the diagnosis. Patients with multiple cytogenetic changes at initial analysis or in subsequent studies had a significantly higher frequency of acute transformation than others (55% vs. 18.6%, p = 0.007); the same was not true if only the data of initial study were considered. Serial cytogenetic studies are important in patient follow-up. N-ras mutation was detected in 5 (20%) of 25 patients within the study. There was no correlation between the gene mutation and acute transformation. But combing the data of N-ras mutation and cytogenetics, patients with either the N-ras mutation or clonal chromosomal abnormalities were at significantly higher risk for developing acute leukemia than those with neither of the changes (77% vs. 25%).

Adolescent↗
PubMed1994

Use of retinoic acids in the treatment of peripheral T-cell lymphoma: a pilot study.

PURPOSE: We have systemically analyzed, both in vitro and in vivo, the effect of 13-cis-retinoic acids (RA) on non-Hodgkin's lymphoma (NHL). METHODS: The in vitro growth-inhibitory effect of 13-cis-RA was examined in 11 (T cell, five; B cell, six) lymphoma cell lines by a tetrazolium colorimetric assay. A pilot clinical trial with oral 13-cis-RA 1 mg/kg/d was conducted in a selected group of 18 lymphoma patients, of whom 16 had failed to respond to at least one regimen of intensive chemotherapy. The in vitro and in vivo effects of 13-cis-RA were correlated with immunophenotypes, RA-induced changes of morphology, and patterns of DNA fragmentation of the lymphoma cells. RESULTS: Four of five T-lymphoma cell lines and none of six B-lymphoma cell lines were sensitive (concentration of 50% growth inhibition [IC50] < 1.5 microns) to 13-cis-RA (P = .015). In the clinical trial, five (two Ki-1, one angioinvasive type, one diffuse mixed cell, and one diffuse large cell) complete remissions and one (Ki1) partial remission were observed in 12 patients with peripheral T-cell lymphoma (PTCL), while none of six patients with B-cell lymphoma responded to 13-cis-RA. 13-cis-RA-induced cellular differentiation and apoptosis, as evidenced by the more mature morphology, characteristic nuclear condensation, and DNA ladder pattern signifying internucleosomal fragmentation, were demonstrated in the sensitive cell lines, as well as in the remitting lymphoma tissues. CONCLUSION: The 13-cis-RA appears to be active on lymphomas of T-lineage and their therapeutic indication may be extended to include some subtypes of PTCL. The mechanisms of action are related to differentiation and apoptosis of lymphoma cells. There appears to be no cross-resistance between 13-cis-RA and conventional chemotherapy.

Adult↗
PubMed1994

Analysis of human platelet glycoprotein IIb-IIIa by fluorescein isothiocyanate-conjugated disintegrins with flow cytometry.

Disintegrins are a group of snake venom peptides which inhibit human platelet aggregation by acting as glycoprotein IIb-IIIa (GPIIb-IIIa) antagonists. They are cysteine-rich, Arg-Gly-Asp (RGD)-containing peptides, and bind to GPIIb-IIIa complex on platelet membrane with a very high affinity (Kd, 10(-7)-10(-8) M). In this study, we analyzed GPIIb-IIIa complex on platelet membrane by flow cytometry using fluorescein isothiocyanate (FITC)-conjugated disintegrins as probes. Of these FITC-conjugated disintegrins, FITC-Rhodostomin is the most sensitive probe because Rhodostomin was conjugated with more FITC molecules than Trigramin and Halysin were. The binding fluorescence intensity of FITC-Trigramin (FITC-Tg), FITC-Halysin (FITC-Hy) and FITC-Rhodostomin (FITC-Rn) was measured in both resting and ADP-activated platelets of diluted human platelet-rich plasma. The binding fluorescence of FITC-disintegrins was abolished by EDTA and 7E3, a monoclonal antibody against GPIIb-IIIa. ADP markedly increased the fluorescence intensity of FITC-Tg and FITC-Hy bound on platelets especially when lower doses of these probes were used, whereas it had little effect on that of FITC-Rn. Therefore, FITC-Tg and FITC-Hy can be used for the detection of the activated platelets as noted by a higher ratio of fluorescence intensity (approx. 2-4) between ADP-activated and resting platelets as compared with that (approx. 1-1.3) in the case of FITC-Rn as the probe. The platelets from three patients with Glanzmann's thrombasthenia were probed with FITC-disintegrins.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Hematophagic histiocytosis: a clinicopathologic analysis of 23 cases with special reference to the association with peripheral T-cell lymphoma.

The clinicopathologic features of 23 patients with hematophagic histiocytosis (HH) are described. All of them exhibited increased histiocytes associated with hemophagocytosis in the marrow. The patients usually presented with fever, hepatosplenomegaly, lymphadenopathy, and cytopenia. The underlying illnesses were heterogeneous, including non-Hodgkin's lymphoma in 17, systemic lupus erythematosus in one, diabetes mellitus in one, acute myelomonocytic leukemia in one, myelodysplastic syndrome in one, and unknown cause in two. Among 17 non-Hodgkin's lymphoma, 14 were peripheral T-cell lymphoma, two were B-cell lymphoma, and one was an undefined phenotype. Among 14 patients with peripheral T-cell lymphoma, six of the patients had nasal T-cell lymphoma. Five of these 14 patients initially diagnosed as malignant histiocytosis turned out to be T-lineage lymphoma after immunophenotypic studies. Active infections, most of viral origin, were documented in eight patients, including Epstein-Barr virus in three, cytomegalovirus in three, herpes simplex virus in three, Pseudomonas aeruginosa in one, Bacteroides vulgatus in one, and mycoplasma in one. Some of them had mixed virus and bacteria infection. Sixteen (70%) of our patients died of their acute illness within 10 weeks of the diagnosis of HH. In the past, the clinical and histologic differentiation between hematophagic histiocytosis and true histiocytic neoplasm (histiocytic medullary reticulosis/malignant histiocytosis) has proved difficult, but now these can be distinguished with immunohistologic, immunogenetic, and cytogenetic studies, especially in the cases of peripheral T-cell lymphoma with hemophagocytic syndrome.

Acute Disease↗
PubMed1994

Non-spinal psoas abscess due to Mycobacterium tuberculosis in a patient with acquired immunodeficiency syndrome: report of a case.

Of the 36 patients with human immunodeficiency virus (HIV) infection admitted to our institution since 1985, one had a non-spinal psoas abscess due to Mycobacterium tuberculosis without pulmonary involvement. A 32-year-old male homosexual had prolonged fever and weight loss for two months. Serologic tests for antibodies against HIV were positive. A characteristic hypodense lesion within the right psoas muscle was noted by computerized tomographic (CT) scanning. Diagnosis of psoas abscess was confirmed by ultrasound-guided needle aspiration. The smear of the aspirated pus showed numerous acid-fast bacilli and cultures grew M. tuberculosis. The lesion responded rapidly to antituberculous therapy and a follow-up CT scan 10 months later showed improvement.

AIDS-Related Opportunistic Infections↗
PubMed1993

Genetic basis and carrier detection of hemophilia B of Chinese origin.

We have characterized the genetic defects of 17 hemophilia B patients of Chinese origin by means of the polymerase chain reaction (PCR) and direct sequencing. The single-strand conformation polymorphism (SSCP) was used as an initial screening method to analyze the entire coding region and the flanking introns of each individual's factor IX gene. The abnormal exons were subsequently amplified and the nucleotide sequence determined. Of the 17 patients studied, 16 had single point mutations and one had a gross gene deletion of exons VII and VIII of factor IX. Among these 16 factor IX variants with point mutations 13 were missense and two were nonsense mutations. The remaining one had a nucleotide deleted, resulting in frame shifting at amino acid residue 97. A total of ten novel mutations, including the one with gross gene deletion, are reported in this study which have not been described previously. Five of the remaining seven variants were missense mutations with novel amino acids substituted for residues 127, 132, 180, 207, and 215, respectively. Mutations containing different amino acid residues at those positions have been reported. The last two are variants that have already been described to contain mutations at amino acid residues 333 and 365, respectively. To evaluate the efficiency of SSCP analysis in assessing the mutated exons and to further confirm our results we sequenced the entire exons of all 17 factor IX genes. The mutations detected by SSCP method were indeed the only mutation identified in each factor IX variant.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1993

Comparison of clinical and biologic features between myeloid and lymphoid transformation of Philadelphia chromosome positive chronic myeloid leukemia.

Analysis of clinical and biologic features of chronic myeloid leukemia (CML) in blast crisis (BC) was performed on 36 patients: 25 had myeloid and 11 had lymphoid transformation. The median duration from diagnosis to onset of BC was significantly shorter in patients with lymphoid BC (6 months) than in those with myeloid BC (41 months). Patients in lymphoid transformation showed better response to therapy and had a significantly longer median survival time after BC than patients with myeloid transformation (56% vs 0% and 10 months vs 4 months, respectively). The leukemic cells from all the patients with lymphoid BC showed B-cell immunophenotype, confirmed by the presence of immunoglobulin (Ig) heavy chain gene rearrangements in the five patients studied. Two of the eight patients with complete marker study expressed myeloid-associated antigens on the blasts. A high incidence of CD7 expression (7/17 or 41%) was found in patients with myeloid BC, but none of the patients who had DNA analysis showed rearrangement of T-cell receptor beta chain gene. Chromosomal abnormalities +8, +19, +21, and i(17q) were detected only in the patients with myeloid BC but not in those with lymphoid BC. Combined analysis of the patients in this series and those reported previously has revealed a statistically significant difference in the distribution of bcr breakpoints between myeloid and lymphoid BC: the bcr breakpoints in more than half of the patients with myeloid crisis were mapped to Zone 2 while those in patients with lymphoid crisis occurred most frequently in Zone 3.

Adolescent↗
PubMed1993

Characterization of genetic defects of hemophilia A in patients of Chinese origin.

The molecular characterization of hemophilia A of Chinese origin was carried out by the polymerase chain reaction (PCR) and direct sequencing of patients' factor VIII genes. Single-strand conformation polymorphism (SSCP) and dideoxy fingerprinting (ddF) were used as screening methods to detect mutated DNAs. A total of 102 individuals from 87 different families, including 10 patients (10 families) with mild-to-moderate and 92 patients (77 families) with severe hemophilia A, were analyzed by PCR-SSCP and PCR-ddF. Of the 87 independent cases, 40 revealed a single mutation in the coding regions of their factor VIII genes. These mutations include 21 with single base changes resulting in 8 nonsense and 13 missense codons, 16 with deletion or insertion of 1-11 nucleotides, and 3 with deletion of large DNA fragments. The frequency of 8 of the identified factor VIII polymorphisms or silent mutations was also determined among Chinese. The frequencies for codons 1241, 1269, and 2223 (the numbering system follows J. Gitschier et al., 1984, Nature 312: 326-330) were found to be different from those reported for other populations. As for the 47 severe cases whose mutational events were not readily detected by PCR-SSCP and PCR-ddF, the reverse transcriptase PCR method was applied. In 24 such cases analyzed, 17 were found to be of the "intron 22 mutations" as described by Naylor et al. (1992, The Lancet, 342: 1066-1067), accounting for 39% of Chinese patients with hemophilia A.

Amino Acid Sequence↗
PubMed1993

Characterization of acute myeloid leukemia (AML) coexpressing lymphoid markers: different biologic features between T-cell antigen positive and B-cell antigen positive AML.

The clinical and biologic characteristics of acute myeloid leukemia (AML) with coexpression of lymphoid-associated antigens (Lym+ AML) were studied from 39 cases who represented 24% of 161 newly diagnosed de novo AML. Twenty-seven cases (16.8%) were positive for the expression of T-cell markers (T+ AML) and 12 (7.5%) for B-cell markers (B+ AML). Chromosomal abnormalities t(9;22)(q34;q11) and t/del(11)(q23), which were considered to be associated with acute leukemia coexpressing markers of more than one cell lineage, were detected in five and in four patients, respectively. There was no prognostic significance of B-cell or T-cell antigen expression in AML. Of 12 T+ AML cases in which cells were available for gene analysis, all showed germline configuration of immunoglobulin heavy chain and T-cell receptor beta chain genes, while seven of nine B+ AML showed rearrangements of either or both of the genes. Double labeling of the cells with myeloperoxidase and lymphoid markers demonstrated that individual blasts in all the five T+ AML tested were simultaneously expressing myeloperoxidase activity and CD7; however, most blasts in the three B+ AML studied expressed either myeloperoxidase activity or CD10, but not both. In eight of the nine T+ AML tested, the T-cell antigen-positive leukemic blasts were significantly decreased to less than 10%, after in vitro culture with the differentiation-inducing agent phorbol ester. B-cell markers remained positive (> or = 20%) on the cells in the two B+ AML who had the same study. These findings suggested that T+ AML and B+ AML might have different biologic features. Further studies on more patients are needed to clarify this point.

Acute Disease↗
PubMed1992

Hodgkin's disease and non-Hodgkin's lymphoma containing Reed-Sternberg-like giant cells in Taiwan. A clinicopathologic analysis of 50 cases.

Hodgkin's disease (HD) is uncommon in Taiwan. In reviewing the clinicopathologic features of 50 cases, the authors found that the diagnosis of HD was complicated with non-Hodgkin's lymphoma (NHL). Fourteen cases were reclassified as NHL containing Reed-Sternberg (RS) giant cells, mostly peripheral T-cell lymphoma (PTL), and 34 cases as classic HD, which included 8 cases of lymphocyte predominance, 10 of nodular sclerosis, 12 of mixed cellularity, and 4 of lymphocyte depletion. For cases of HD, there was a bimodal age-incidence distribution with peaks at the third and fifth decades; 61.8% manifested Stage B symptoms and 80.6% had Stage III/IV disease. The group of patients with NHL, compared with those with classic HD, was found to be older (mean age, 41.4 years versus 33.1 years; P less than 0.05), to have more extranodal disease (35.7% versus 8.8%, P less than 0.05), less complete remission rate (25% versus 67.9%, P less than 0.05), and shorter median survival (29 months versus 90 months). Most of the NHL patients originally were diagnosed as having atypical or unclassified HD. Thus, the authors conclude that the previous observation of a predominance of mixed cellularity HD in Asian regions may be attributable to the inclusion of PTL, which may mimic HD in histology. Because there is a marked difference in clinical behavior and prognosis, it is important to distinguish between HD and NHL containing RS giant cells in an area with a high incidence of PTL.

Adult↗
PubMed1992

Cytogenetic study of acute lymphoblastic leukemia and its correlation with immunophenotype and genotype.

Among 72 Chinese patients with acute lymphoblastic leukemia (ALL), 50 had clonal chromosomal abnormalities. Structural abnormalities were detected in 42 patients: these included t(9;22) in 9, t(1;19) in 6, t(4;11) in 5, del(11)(q23) in 4, and del(6q) in 4. Adults had a higher incidence of t(9;22) and t(1;19) but a lower incidence of t(4;11) and hyperdiploid greater than 50 karyotype than children. A significant difference was also noted in white blood cell (WBC) count among various karyotypic groups. Patients with chromosomal abnormalities t(9;22), t(1;19), t(4;11) and del(11) (q23) had a shorter complete remission duration as compared with patients free of these abnormalities. Immunophenotyping was performed on 69 patients. All patients with t(9;22), t(1;19), and t(4;11) had B-lineage ALL restricted to certain stages of maturation: groups III and IV, groups IV and V, and group II, respectively (according to the classification of Foon and Tood). Among patients with t(9;22), t(4;11), and del(11)(q23), which have been considered to be associated with acute mixed-lineage leukemia, one each, respectively, showed myeloid antigen expression on the leukemic blasts (My+ ALL). No cross-lineage rearrangements of immunoglobulin (Ig) or T-cell receptor (TCR) genes were detected in these karyotypic subgroups of patients who underwent gene analysis.

Adolescent↗
PubMed1992

Characterization of Philadelphia-chromosome-positive acute leukemia by clinical, immunocytochemical, and gene analysis.

Philadelphia chromosome (Ph') was detected at presentation in 10 out of 110 patients with acute lymphoblastic leukemia (ALL) and five of 168 patients with acute myelogenous leukemia (AML). Two other ALL patients who had studies at relapse were also included in the analyses. One of the 12 Ph'-positive (Ph+) ALL patients had simultaneous expression of myeloid-associated antigen on the leukemic blasts, while all the five AML patients coexpressed markers of lymphoid cells. Double labeling of the cells with myeloperoxidase and CD10 on three Ph+ AML cases showed that most leukemic blasts expressed either myeloperoxidase activity or CD10 but not both. Cross-lineage gene rearrangements of T-cell receptor (TCR) beta-chain gene were detected in three of the eight Ph+ ALL patients tested. All the four Ph+ AML cases studied showed immunoglobulin heavy chain gene rearrangements, and three of them also had simultaneous rearrangements of TCR beta-chain gene. The results revealed that Ph+ acute leukemia in this study belonged either to ALL or mixed lineage leukemia, and none was pure AML. This finding is contrary to that of acute blast crisis of chronic myelogenous leukemia in which the majority of patients had myeloid transformation. Rearrangements of bcr were detected in four of the 10 Ph+ ALL and three of the four Ph+ AML patients tested. No significant difference was noted in the clinical or hematologic manifestations among Ph+ leukemia with or without bcr rearrangements.

Adult↗
PubMed1992

Experience of desmopressin (DDAVP) administration in patients with congenital and acquired bleeding disorders.

Desmopressin (DDAVP) 0.3 micrograms/kg was administered intravenously to three normal volunteers and 12 patients with von Willebrand's disease (vWD), congenital or acquired platelet function defect, or uremic bleeding to assess its effects and side effects. DDAVP significantly shortened the bleeding time as compared with basal values. The mean peak post-DDAVP level of factor VIII coagulant activity increased 5.9 +/- 0.5 (mean +/- SEM) fold, von Willebrand factor antigen increased 3.7 +/- 0.3 fold, von Willebrand factor ristocetin cofactor activity increased 4.6 +/- 0.6 fold and the tissue-type plasminogen activator antigen increased 3.4 +/- 0.6 fold. Analysis of the multimeric structure of the von Willebrand factor revealed that type I vWD had complete correction after DDAVP infusion transiently. Except for a mild drop in both systolic and diastolic blood pressures, few side effects were noted. By concomitant intravenous infusion of DDAVP and oral administration of tranexamic acid, we successfully treated two cases of type I vWD undergoing tooth extraction, and one case of acquired bleeding disorder undergoing a biopsy of a mandibular mass, and a uremic patient complicated by intractable traumatic hematuria. Our experiences confirmed that most patients with vWD and some patients with congenital or acquired bleeding disorders can be treated effectively by DDAVP infusion without the need for plasma product replacement. In this study we found that a patient with a variant form of type I vWD had prolongation of the bleeding time, thrombocytopenia and platelet aggregation after DDAVP infusion.

Adolescent↗
PubMed1991

Characterization of genetic defects of hemophilia B of Chinese origin.

To define the precise genetic defects of hemophilia B of Chinese origin, we have used the polymerase chain reaction (PCR) combined with direct sequencing to analyze the amplified DNA fragments containing the entire coding regions and their flanking introns of the factor IX gene from 6 affected individuals. Among these patients, two are siblings with normal factor IX antigen level (CRM+) yet reduced factor IX clotting activity (28%). Analysis of their factor IX genes revealed a G to A transition at nucleotide residue 10394, which causes substitution of an arginine for a glycine at amino acid residue 48. This is a novel mutation which resides in the first EGF-like domain of factor IX. Studies of two other hemophilia B patients with CRMr phenotypes (factor IX antigen level less than 35%, and clotting activity less than 1%), demonstrated a distinct mutation in each individual's factor IX gene. In one case, a guanine to adenine (residue 6365) transition results in replacement of arginine by glutamine at the -4 codon of the propeptide of factor IX. In the other, thymine at 6442 was mutated to cytosine which causes an arginine for cysteine substitution at residue 23. We have also characterized 2 discrete CRM- patients. Both exhibited an identical mutation at nucleotide residue 6460 which generates a translation termination codon (CGA to TGA) at the 29th amino acid. The mutation created a new NlaIII restriction enzyme site which could be used to identify this variant.

Amino Acids↗
PubMed1991

Immunoglobulin and T-cell receptor gene rearrangements in acute lymphoblastic leukemia--a higher incidence of double rearrangements in patients with myeloid antigen expression.

Among 160 patients who were diagnosed as having acute lymphoblastic leukemia (ALL) by French American British (FAB) criteria, 32 patients (20%) expressed myeloid-associated antigens on leukemic blasts (My+ALL). Correlation of immunophenotype with rearrangement of immunoglobulin (Ig) heavy chain and T-cell receptor (TCR) beta chain genes was performed on 73 of these patients (21 were My+ALL). Rearrangements of both Ig and TCR genes (double rearrangements) were detected in 24 patients, including three (19%) of 16 T-lineage ALL. 17 (33%) of 52 B-lineage ALL, and four of five ALL expressing both B and T-cell surface markers. Also a higher incidence of double rearrangements in My+ALL was found as compared with My-ALL (43% vs 29%). This difference was more evident when only B-lineage ALL was considered (50% in My+ patients vs 24% in My- patients). However the difference is not statistically significant yet possibly due to the small number of patients in the study. Further studies on more patients are needed to confirm this. In My-B-lineage ALL, rearrangements of TCR beta chain gene were restricted to certain subgroups (Groups III & IV) of patients who expressed CD10 surface antigens but lacked cytoplasmic Ig. In My+ B-lineage ALL, rearrangements of TCR beta chain gene could be found in various subgroups studied (Groups II through V). Cross-lineage gene rearrangement in My+ALL may involve mechanisms different from those in My-ALL.

Adolescent↗
PubMed1991

A subset of acute lymphoblastic leukemia with co-expression of myeloid antigens: prevalence and clinical significance.

In order to evaluate the biological features and clinical significance of myeloid antigen expression in acute lymphoblastic leukemia (ALL), immunophenotype analysis was performed on leukemic cells from 160 patients diagnosed as ALL by the French, American and British (FAB) criteria using a comprehensive panel of monoclonal antibodies to lymphoid and myeloid associated antigens. Expression of myeloid antigens was found in 32 cases (20%), including 11 out of 49 adults (22.4%) and 21 out of 111 children (18.9%). CD33 was positive in 18 patients (11.3% of the total cases), CD13 in 15 patients (9.4%), CD 11b in 12 patients (7.5%) and CD14 in 1 patient (0.6%). Nine patients expressed two or more myeloid antigens. There were no significant differences in clinical manifestations and hematological pictures between the ALL patients with myeloid antigen expression (My+ ALL) and those without (My- ALL). No consistent chromosomal abnormality was found in My+ ALL. Eighty percent of the childhood and 44.4% of the adult My+ ALL patients achieved complete remission, compared with 87% and 80%, respectively, for childhood and adult My- ALL, but the differences were not statistically significant. After a median follow-up of 2.1 years, there were also no statistically significant associations between myeloid antigen expression and shorter duration of remission or poorer survival rate for patients with both adult and childhood ALL.

Adult↗
PubMed1991

[A comparative study of antinuclear antibody measurement using different cells as nuclear substrates].

In an attempt to evaluate possible variations in the antinuclear antibody (ANA) titers resulting from nuclear substrate difference, we measured the ANA titer of 104 normal subjects using substrates from mouse liver cell (MLC) and HEp-2 cell (CSI, USA). We also performed similar experiments on 50 sera from 50 patients with rheumatic disease using mouse liver cell, HEp-2 cell (CSI), HEp-2 cell (AFT, Japan), and HEp-2 cell (AI, USA) as substrates. The ANA titer assay using HEp-2 cell (CSI), which is routinely used in our laboratory, was regarded as the reference method. The results showed that when HEp-2 (CSI) was used, 98.1% normal subjects had ANA titer lower than 1:320, therefore a cut-off value of 1:320 was used. While using the MLC method, 96.2% normal subjects had ANA titer lower than 1:80, and the cut-off value was set at 1:80 accordingly. The geometric mean ANA titers of the 50 sera from 50 rheumatic disease patients were 676 for HEp-2 cell (CSI), 503 for HEp-2 cell (AFT), 368 for HEp-2 cell (AI), and 265 for MLC, respectively. Although statistically significant difference (p less than 0.05) in geometric mean titer existed between reference method and the other 3 methods, the latter 3 methods still had good sensitivity (97.2% for HEp-2 cell (both AFT and AI); 91.7% for MLC), and specificity (100% for HEp-2 cell (both AFT and AI); 71.4% for MLC) for selecting out sera with abnormal ANA titer. We also evaluated the relationships between ANA titer and anti-double stranded DNA antibody (anti-dsDNA) concentration in another 210 sera from 151 patients with rheumatic disease. Statistically, there is no distinct correlation between anti-dsDNA and ANA of all fluorescence staining patterns except for peripheral pattern, in which case a significant correlation could be demonstrated.

Adolescent↗