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PubMedDate not supplied

A study of relapse in non lepromatous and intermediate groups of leprosy.

Dapsone has been used as a monotherapy and in well organised control units, the prevalence of leprosy has come down. The relapse rates presented in this communication are quite low compared with those reported by various authors quoted in this paper. Relapse rates appear to remain steady at about 5/1000 for each following year after R.F.C. for 7 years. This relapse rate does not appear to be related to regularity of treatment. The relapse rate appears that longer the duration of treatment, the earlier relapse due to severity of the disease of those who had longer treatment. Health education for R.F.C. cases on signs of relapse is a must before they are declared R.F.C. The levels of Sulphone in the blood remain above MIC for as much as ten days after the last dose and therefore Dapsone allows self-administration. It is expected that with the introduction of bacteriocidal drugs in the treatment of paucibacillary leprosy, the relapse rates would go down. As observed from a study conducted in Jalma, maintenance treatment as advocated by the NLCP (1964) and WHO (1970) does not seem to be necessary. The necessity of such maintenance treatment may be obviated with the use of multi-drug regimen in paucibacillary leprosy. This would enable a large number of cases to be released from control thereby reducing patient load considerably and making the supervised treatment of multibacillary cases more easy.

Female↗

PubMed1968

Dates of onset of relapses and the duration of infection in induced tertian malaria with short and long incubation periods.

The course of induced tertian malaria has been studied in patients in psychoneurological hospitals in Moscow over a long period. Various strains of P. vivax were used to infect patients; the sporozoites were transmitted by Anopheles maculipennis atroparvus bred under laboratory conditions. There are marked differences between the dates of onset of relapses, reckoned from the primary manifestations of the disease, in patients developing malaria after long and short incubation periods. P. vivax strains which have a short incubation period are characterized by producing in patients a series of relapses following a long latent period; strains with a long incubation period are characterized by the occurrence of relapses during the first 3 months after the end of the primary series of attacks. However, some P. vivax strains give rise to both types of relapse, depending on the incubation period. In any event, the duration of the disease does not, as a rule, exceed 2 years, including the incubation period. The number of mosquitos (and hence the number of sporozoites) used to infect a patient does not have any noticeable effect on the number and frequency of relapses. In short-incubation tertian malaria, the use of quinocide during the period of treatment of the primary manifestations greatly reduced the number of relapses; in long-incubation tertian malaria similarly treated with quinocide, no relapses occurred.

Anopheles↗

PubMed1983

[Treatment of relapsing acute leukemia].

Responses of multicombination chemotherapy with BH-AC . DMP regimen in relapse in adult acute leukemia showed significant decrease in terms of remission rate, duration of remission and survival time, in comparison to that in previously untreated cases. This strongly imply that clinical resistance to the drug previously used had developed in patients with relapsing acute leukemia. Therefore, antileukemic agents which have no cross resistance to those used previously should be selected for relapsing cases with much more intensive fashion of treatment than that used in the prior treatment. Ninety per cent of the long-term survivors in acute leukemia who had a single relapse had survived at 7 years, whereas only 30% of the patients who had multiple relapses had survived so. In other words, when the first relapse was treated successfully, the patients still have a good change to be cured. This results suggest that total care system has to be developed for relapsing acute leukemia.

Acute Disease↗

PubMed1995

Prolonged persistence of PCR-detectable minimal residual disease after diagnosis or first relapse predicts poor outcome in childhood B-precursor acute lymphoblastic leukemia.

The follow up of minimal residual disease (MRD) in childhood B-precursor ALL by polymerase chain reaction (PCR) may be of help for further stratification of treatment protocols, to improve outcome. However, the clinical relevance of this approach has yet to be defined. We report the retrospective follow-up of MRD in bone marrow (BM) samples from 50 childhood B-precursor ALL patients by IgH/TCR delta PCR. Twenty-two patients remained in continuous complete remission (median follow-up 61 months), and 28 experienced relapse (median follow-up 75 months). Initial regression of MRD on therapy correlated with outcome. At the end of induction therapy 2/18 (11.1%) patients from the CCR group were PCR positive vs 10/16 (62.5%) from the 'relapse' group (P = 0.005). The presence of PCR detectable MRD predicted event-free survival independent of standard clinical and cytogenetical parameters. Also subsequent to first BM relapse, a correlation between MRD regression and outcome was observed. Six of eight patients who became PCR negative in the time period between relapse and bone marrow transplantation are in CCR, whereas 7/7 patients who remained PCR positive in this time period died (P = 0.006). In approximately 70% of evaluable patients, clinical relapse was preceded by recurrence of detectable MRD at time intervals of 3-18 months earlier and the recurrence of PCR positivity after a period of negativity was always followed by overt relapse. At relapse, the combined use of IgH and TCR delta probes reduced false negativity caused by clonal evolution to approximately 10%. This study shows that the evolution of PCR detectable MRD is an independent predictor of outcome.

Adolescent↗

PubMed1995

Change in karyotype between diagnosis and first relapse in acute myelogenous leukemia.

We compared karyotype at first relapse with presenting karyotype in 212 patients with AML seen at MD Anderson Cancer Center (Houston, TX, USA) between 1975 and 1994. In 38% the karyotypes at diagnosis and relapse were identical. A stable karyotype was most frequent (70%) among patients who presented without cytogenetic abnormalities, suggesting that the finding of a normal karyotype is usually not due to sampling error. In contrast, a finding of insufficient metaphases at diagnosis was repeated at relapse in only 6% of cases. A change in karyotype occurred in 67% of 101 patients who presented with an abnormal karyotype and had sufficient metaphases for evaluation at relapse. The great majority of changes involved clonal evolution, clonal devolution (regression), or both; a purely normal karyotype and unrelated clones were seen in 11 and three of the 101, respectively. Change in karyotype between diagnosis and relapse and type of change were unrelated to remission duration. The only group in which karyotype at relapse vs that at diagnosis had a possible bearing on achievement of second CR were patients who presented with abnormalities other than inv(16), t(8;21) or t(15;17) and who at relapse had only normal metaphases; such patients had higher CR rates than comparable patients who retained their presenting abnormalities.

Chromosome Aberrations↗

PubMed1995

High-dose chemotherapy with or without total body irradiation followed by autologous bone marrow and/or peripheral blood stem cell transplantation for patients with relapsed and refractory Hodgkin's disease: results in 85 patients with analysis of prognostic factors.

Eight-five consecutive patients with relapsed or refractory Hodgkin's disease (HD) underwent high-dose chemotherapy or chemo/radiotherapy followed by autologous bone marrow (ABMT) and/or peripheral blood stem cell (PBSC) transplantation. Two preparative regimens were used. Twenty-two patients (26%) without prior radiation received fractionated total body irradiation (FTBI) 1,200 Gy in combination with high-dose etoposide (VP-16) 60 mg/kg and cyclophosphamide (CTX) 100 mg/kg. Sixty-three patients (74%) with prior radiotherapy received carmustine (BCNU) 450 mg/m2 instead of FTBI. The median age was 32 years (range, 16 to 56). The median number of prior chemotherapy regimens was three (range, 1 to 7). Forty-three patients (51%) received transplants in first relapse or second complete remission (CR), whereas 33 (39%) received transplants after second or subsequent relapse. All relapsed patients, except one, received conventional salvage chemotherapy and/or radiotherapy in an attempt to reduce tumor bulk before transplant. At the time of analysis in April 1994, fifty-seven patients (67%) are alive, including 44 (52%) in continuous CR, with a median follow-up for the surviving patients of 28 months (range, 7 to 66). Thirty patients (35%) relapsed at a median of 9 months (range, 1 to 43). Eleven patients (13%) died of transplant-related complications including veno-occlusive disease of the liver (VOD) in five, acute and late interstitial pneumonitis in three, graft failure in one, cerebral hemorrhage in one, and therapy-induced myelodysplasia (MDS)/acute leukemia in one patient. At a median follow-up of 25 months (range, 0.6 to 66), the cumulative probability of 2-year overall and disease-free survival (DFS) of all 85 patients is 75% (95% confidence interval [CI] 64% to 84%) and 58% (95% CI 47% to 69%), respectively. Three independent prognostic variables were identified by univariate analysis: number of prior chemotherapy regimens, prior radiotherapy, and extranodal disease at ABMT. Multivariate stepwise Cox regression identified the number of prior chemotherapy regimens as the only significant prognostic factor predicting for both relapse and DFS. There were no significant differences in the outcome of the treatment between the two preparative regimens. Our results confirm that high-dose therapy and ABMT is an effective therapy for patients with relapsed or refractory HD. Earlier transplantation is recommended before the development of drug resistance and end organ damage that results from repeated attempts of salvage therapy.

Actuarial Analysis↗

PubMed1994

Rate of relapse in multibacillary patients after cessation of long-course dapsone monotherapy supplemented by a final supervised single dose of 1500 mg of rifampin.

When multidrug therapy was implemented in Senegal, 406 multibacillary (MB) patients who had been treated for more than 10 years by dapsone alone, and who had become clinically inactive and skin-smear negative, were released from treatment. Of these 406 patients, 298 were given a supervised single dose of 1500 mg of rifampin. Subsequently, 302 of them (229 who had been given rifampin and 73 who had not) were followed up by means of annual clinical and bacteriological examinations. Of the former 229 followed up for a mean period of 4.9 years, 34 patients relapsed (22 males and 12 females), giving a crude relapse rate of 15% and an overall risk of relapse of 3.1 per 100 patient-years. Of the latter 73 followed up for a mean period of 2.4 years, 5 relapsed (4 males and 1 female), giving a crude relapse rate of 6.8% and an overall risk of relapse of 2.9 per 100 patient-years. Such results, which are in agreement with those of a similar study conducted recently in Mali, indicate that the intake of a single dose of 1500 mg of rifampin by MB patients when they are released from long-course dapsone monotherapy does not result in a decrease of the relapse rate. Therefore, MB patients who have been treated with dapsone alone, even for long periods, should be put under multidrug therapy prior to their release from control.

Dapsone↗

PubMed1994

Analysis of Ig and T-cell receptor genes in 40 childhood acute lymphoblastic leukemias at diagnosis and subsequent relapse: implications for the detection of minimal residual disease by polymerase chain reaction analysis.

The rearrangement patterns of Ig and T-cell receptor (TcR) genes were studied by Southern blot analysis in 30 precursor B-cell acute lymphoblastic leukemias (B-ALLs) and 10 T-ALLs at diagnosis and subsequent relapse. Eight precursor B-ALLs appeared to contain biclonal/oligoclonal Ig heavy-chain (IgH) gene rearrangements at diagnosis. Differences in rearrangement patterns between diagnosis and relapse were found in 67% (20 cases) of precursor B-ALLs (including all eight biclonal/oligoclonal cases) and 50% (five cases) of T-ALLs. In precursor B-ALLs, especially changes in IgH and/or TcR-delta gene rearrangements were found (17 cases), but also changes in TcR-beta, TcR-gamma, Ig kappa, and/or Ig lambda genes (11 cases) occurred. The changes in T-ALLs concerned the TcR-beta, TcR-gamma, TcR-delta, and/or IgH genes. Two precursor B-ALLs showed completely different Ig and TcR gene rearrangement patterns at relapse, suggesting the absence of a clonal relation between the leukemic cells at diagnosis and relapse and the development of a secondary leukemia. The clonal evolution in the other 23 ALL patients was based on continuing rearrangement processes and selection of subclones. The development of changes in Ig and TcR gene rearrangement patterns was related to remission duration, suggesting an increasing chance of continuing rearrangement processes with time. These immunogenotypic changes at relapse occurred in a hierarchical order, with changes in IgH and TcR-delta genes occurring after only 6 months of remission duration, whereas changes in other Ig and TcR genes were generally detectable after 1 to 2 years of remission duration. The heterogeneity reported here in Ig and/or TcR gene rearrangement patterns at diagnosis and relapse might hamper polymerase chain reaction (PCR)-mediated detection of minimal residual disease (MRD) using junctional regions of rearranged Ig or TcR genes as PCR targets. However, our data also indicate that in 75% to 90% of ALLs, at least one major rearranged IgH, TcR-gamma, or TcR-delta band (allele) remained stable at relapse. We conclude that two or more junctional regions of different genes (IgH, TcR-gamma, and/or TcR-delta) should be monitored during follow-up of ALL patients for MRD detection by use of PCR techniques. Especially in biclonal/oligoclonal precursor B-ALL cases, the monitoring should not be restricted to rearranged IgH genes, but TcR-gamma and/or TcR-delta genes should be monitored as well, because of the extensive changes in IgH gene rearrangement patterns in this ALL subgroup.

Adolescent↗

PubMed1994

Nonhereditary p53 mutations in T-cell acute lymphoblastic leukemia are associated with the relapse phase.

We have previously reported that greater than 60% of human leukemic T-cell lines possess mutations in the p53 tumor suppressor gene. To determine whether T-cell acute lymphoblastic leukemia (T-ALL) patient samples possess p53 mutations, we screened peripheral blood-and bone marrow-derived leukemia samples, taken at diagnosis and at relapse, for p53 mutations. Exons 4 through 9 and selected intron regions of the p53 gene were analyzed using polymerase chain reaction-single-strand conformation polymorphism and direct sequencing. p53 mutations were found in 0 of 15 T-ALL diagnosis samples, as compared with 10 of 36 (28%) T-ALL relapse samples. To determine whether p53 mutations play a role in the recurrence (relapse) of T-ALL, two special groups of T-ALL patients were studied: (1) a group of 8 relapse patients whose disease was refractory to chemotherapeutic treatment, and (2) a group of 6 "paired" T-ALL cell samples from patients for whom we possess both diagnosis and relapse samples. Three of 8 relapsed patients (37.5%) whose disease was refractory to the reinduction of remission by chemotherapy possessed missense mutations of the p53 gene. All 3 cases had mutations in exon 5. Among the paired samples, 3 of 6 patients harbored p53 mutations at disease recurrence, but possessed only wild-type p53 alleles at diagnosis. One case had mutation on exon 4, 1 case in exon 5, and 1 case in exon 8 with loss of heterozygosity. These data clearly indicate that recurrence of T-ALL is associated with missense mutations in p53. Our results indicate that (1) mutations of p53 do occur in T-ALL in vivo, and such mutations are associated with the relapse phase of the disease; and (2) p53 mutation is involved in the progression of T-ALL. This conclusion is supported by our observation that the introduction of T-ALL-derived mutant p53 expression constructs into T-ALL cell lines further increases their growth rate in culture, enhances cell cloning in methylcellulose, and increases tumor formation in nude mice.

Base Sequence↗

PubMed1994

Molecular evidence for minimal residual bone marrow disease in children with 'isolated' extra-medullary relapse of T-cell acute lymphoblastic leukemia.

Central nervous system (CNS) relapse confers a poor prognosis in children with acute lymphoblastic leukemia (ALL). It is uncertain whether morphologically undetectable leukemia is present in the bone marrow at the time of CNS relapse, or whether the CNS acts as a 'sanctuary' site to allow reseeding of the marrow at a later time. We examined DNA from bone marrow samples from six patients with T-cell ALL with isolated CNS relapse using sensitive polymerase chain reaction (PCR) assays to detect minimal residual disease. One of these PCR assays was based on amplification of leukemia-specific TCR-delta gene rearrangements, while the other assay relied upon detection of the c-tal deletion. In four patients, where bone marrow samples were taken at the time of CNS relapse, residual disease was detectable in every sample at a level below morphological detection. In addition, three patients had residual disease detected in their subsequent bone marrow when CNS disease was not evident. Our findings, although preliminary, suggest that relapse of leukemia in the CNS reflects resurgence of the disease in the bone marrow that is first detected clinically in the CNS. The concomitant molecular detection of bone marrow leukemia at time of 'isolated' CNS relapse in children with T-cell ALL explains subsequent bone marrow relapse in some of these children, and argues for intensive systemic therapy of these patients.

Adolescent↗

PubMed1993

[Time-dependent interrelationships between pathological prognostic factors and relapse rate in breast cancer patients].

Eleven pathological factors among 462 patients with primary breast carcinoma (1960-1968) were analysed paying a special attention to changes of the influence on relapse. Factors were included; tumor size (T), extent of nodal involvement (N), nuclear grade (NG), fat infiltration (F), tumor infiltrating lymphocyte (TIL), tumor necrosis (NEC), lymphatic & vessel permeation (LY) and others. Cox regression analysis on 3 non-overlapping intervals (within 2 years, 2-5 years and after 5 years) using the seven factors selected by Cox analysis in the whole periods under the condition of p < 0.10 showed that significant factors were N, NG and T within 2 years, N, TIL, NG and NEC in 2-5 years, F, N, TIL and T after 5 years, respectively (p < 0.05), in the following order. TIL means the relapse suppressing factor and others mean relapse factors. As for the changes of beta value, it decreased with time for N and NG, but contrarily increased with time for F. This means that N and NG participate mainly in an early relapse and F mainly in a delayed relapse. TIL showed a significant relapse suppressing factor only after 2 years. These results revealed that prognostic factors have its altered influence on relapse with time, namely a distinct time-dependency.

Breast Neoplasms↗

PubMed1993

[Treatment and prognosis after late relapse in childhood acute lymphoblastic leukemia].

We evaluated the clinical courses and laboratory features in 13 late-relapse cases of 55 children with acute lymphoblastic leukemia who had been in complete remission for longer than their years. In 8 of 13 cases, leukemia relapsed in bone marrow; 2 with testicular, 1 with central nervous system and one with ovarian involvement. Further, extramedullary relapse not involving bone marrow occurred in 5 cases (4 testicular and 1 CNS). Late-relapse was more frequently observed in boys (37.5%) than in girls (4.4%). Initial age and leukocyte counts were of no value in predicting late-relapse. The relapse rate in cases initially treated by the VPL regimen was twice that of those by a multi-drug regimen. A second prolonged remission was achieved in 5 of 10 cases by combinations of intensive chemotherapy (modified HEX) and irradiation to the testes or CNS. On the contrary, all late relapse patients initially treated by the multi-drug chemotherapy had a poor outcome. More intensive chemotherapy, including high-dose chemoradiotherapy and bone marrow transplantation, should be employed in this group of patients.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1993

Characterization of mixed chimerism in patients with chronic myeloid leukemia transplanted with T-cell-depleted bone marrow: involvement of different hematologic lineages before and after relapse.

We have characterized mixed chimerism (MC) in five patients with chronic myeloid leukemia (CML) who received transplants with T-cell-depleted bone marrow (BM) and who relapsed within 4 years after transplantation. To study the possible relation of MC with relapse, we purified different populations of leukocytes and analyzed their donor/recipient origin by a method based on polymerase chain reaction amplification of minisatellite DNA regions. Our results show that before relapse, all hematopoietic recipient cells are T cells, whereas monocytes, B, and natural killer (NK) cells are of donor origin. This observation does not appear to be specific for CML as similar results were found in two control patients with acute myeloid leukemia (AML). At the time of (CML) relapse, recipient granulocytes, monocytes, and erythrocytes appeared and progressively replaced the respective lineages of donor origin. No other lineages seemed to be involved as B cells and NK cells remained of donor origin and no significant changes in the number of recipient T cells were detected. In this respect relapse of CML after BM transplantation (BMT) seems not to be very different from the primary disease in chronic phase before transplantation. Furthermore, we conclude that after BMT, an association between mixed chimerism before relapse and the (CML) relapse does exist because both phenomena are consequences of T-cell depletion of the BM graft. However, this correlation might well be indirect as the MC caused by the recipient T cells appears to be independent of the one caused by the recurrent disease.

Adult↗

PubMed1995

Detection of minimal residual disease in patients with childhood common acute lymphoblastic leukemia after autologous bone marrow transplantation with ex vivo purging and systemic IL-2 infusion: unsuccessful prediction of subsequent relapse.

We sequentially analyzed minimal residual disease (MRD) in 7 children with common acute lymphoblastic leukemia (cALL) after autologous bone marrow transplantation (ABMT) with ex vivo purging followed by systemic interleukin-2 infusion. After ABMT, 3 of the 7 patients remained in complete remission (CR) for more than 1 year, and 4 subsequently relapsed. MRD was estimated by polymerase chain reaction amplification to detect the leukemia clone-specific immunoglobulin heavy chain third complementarity determining region (IgH CDR-III). The IgH CDR-III sequences from the relapsed patients were identical with those determined at each respective initial diagnosis. In 2 patients, the levels of MRD were 10(-2) and 10(-5) in the harvested bone marrow (BM) cells, and even after purging the levels were 10(-4) and 10(-5) cells, respectively. One of the 2 patients relapsed 3 months after ABMT, while the other remained in CR for 33 months after ABMT. Among the 4 patients who subsequently relapsed after ABMT, MRD was not detected in the BM samples even 1 month before relapse. Our results suggest that PCR-negativity does not necessarily indicate a lower risk of subsequent relapse. Detection of MRD tends to favor the assessment of the therapeutic effects rather than prediction of relapse.

Base Sequence↗

PubMed1996

Polymerase chain reaction is highly predictive of relapse in patients following T cell-depleted allogeneic bone marrow transplantation for chronic myeloid leukemia.

In chronic myeloid leukemia (CML) the polymerase chain reaction (PCR) can be used to detect minimal residual disease after bone marrow transplantation (BMT). Previous studies have shown that PCR positivity is common following BMT. However, the clinical significance of this finding for any given individual who is PCR positive remains unclear, as many of these patients remain long-term disease-free survivors after allogeneic BMT. In the present study, we used PCR to detect BCR-ABL mRNA in 144 blood or marrow samples from 36 patients who received a T cell-depleted BMT for CML in first chronic phase. Six patients had no evidence of PCR-detectable residual disease at any time following transplant. The other 30 patients had at least one positive PCR result post-BMT. Once PCR positivity was found, it was usually sustained, with only four patients having a subsequent PCR negative assay. No patient who had two consecutive PCR-positive assays had a return to PCR negativity. None of the six patients with exclusively PCR-negative assays have developed either cytogenetic or hematologic relapse at a median follow-up of 42 months. Of the 30 patients with at least one PCR-positive assay post-BMT, 28 were PCR positive at last follow-up, and 22 have progressed to cytogenetic or hematologic relapse. If the PCR-positive assay occurred within 24 months of the transplant then the estimated probability of progression to cytogenetic or hematologic relapse was 65% at 24 months. Twenty of the 26 patients who were studied early (< or = 6 months) after BMT had at least one positive PCR assay. Fifteen of the 20 patients who were PCR positive < or = 6 months following transplant have progressed to either cytogenetic or hematologic relapse resulting in an estimated probability of relapse of 84% at 24 months. These results indicate that following T cell-depleted BMT for CML in first chronic phase, PCR is highly predictive of relapse and may identify a cohort of patients in need of therapeutic intervention before the onset of overt clinical relapse.

Biomarkers, Tumor↗

PubMed1996

Relapse of leprosy after multidrug therapy.

Relapse of leprosy after multidrug therapy among leprosy patients treated at Mahasarakarm, Kalasin and Roi-et from 1984 to 1994 were analyzed. Twenty PB relapses (45.45%) and twenty four MB relapses (54.55%) were found among 5,298 originally classified PB patients and 5 MB relapses occurred in 2,624 originally classified MB patients. Mean relapse interval was between 3-4 years. The relapse rate within 10 years after stopping MDT was 0.83 per cent in PB and 0.19 per cent in MB. The estimated relapse rate per 1,000 patient-years was 1.55 for PB and 0.41 for MB respectively.

Drug Therapy, Combination↗

PubMed1996

Application of random-effects regression models in relapse research.

This article describes and illustrates use of random-effects regression models (RRM) in relapse research. RRM are useful in longitudinal analysis of relapse data since they allow for the presence of missing data, time-varying or invariant covariates, and subjects measured at different timepoints. Thus, RRM can deal with "unbalanced" longitudinal relapse data, where a sample of subjects are not all measured at each and every timepoint. Also, recent work has extended RRM to handle dichotomous and ordinal outcomes, which are common in relapse research. Two examples are presented from a smoking cessation study to illustrate analysis using RRM. The first illustrates use of a random-effects ordinal logistic regression model, examining longitudinal changes in smoking status, treating status as an ordinal outcome. The second example focuses on changes in motivation scores prior to and following a first relapse to smoking. This latter example illustrates how RRM can be used to examine predictors and consequences of relapse, where relapse can occur at any study timepoint.

Alcoholism↗

PubMed1997

Relapse of tuberculosis after treatment in human immunodeficiency virus-infected patients.

OBJECTIVES: To evaluate the relapse rate of tuberculosis after a complete course of antituberculous therapy in human immunodeficiency virus-infected patients and to identify the risk factors for relapse. PATIENTS AND METHODS: Historic cohort study of all adult patients who were diagnosed as having human immunodeficiency virus infection and a first episode of culture-proved tuberculosis at 2 university hospitals in Madrid, Spain, between 1986 and 1992, and who completed at least 6 months of treatment were included and followed up until September 1994. RESULTS: Of 276 patients with human immunodeficiency virus infection and tuberculosis, 87 could not be evaluated (6 died before treatment, 39 died during treatment, 36 did not complete the planned therapy, and 6 were unavailable during treatment). The remaining 189 received a standard regimen (ie, 3 or 4 drugs, always including rifampin and isoniazid, for > or = 6 months). The median duration of follow-up for these 189 patients was 31.5 months, with a total of 4668 patient-months of follow-up after treatment; 105 patients (56%) were followed up until death. The relapse rate was 7.9% (2.7/100 patient-years). With multivariate analysis, a shorter duration of treatment and a low CD4+ cell count were associated with a greater probability of relapse. Relapses occurred in 5 (3.4%) of 148 patients who were treated for 9 or more months (1.7/100 patient-years) and in 10 (24%) of 41 patients who were treated for less than 9 months (10.9/100 patient-years) (P < .001; relative hazard, 9.2; 95% confidence interval, 3.1-26.9). CONCLUSIONS: As standard antituberculous therapy for 9 months is associated with a low rate of relapse, maintenance therapy is not required. Duration of treatment for less than 9 months is associated with a high rate of relapse.

AIDS-Related Opportunistic Infections↗