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PubMed2006

Serum lipids and the progression of nephropathy in type 1 diabetes.

OBJECTIVE: Dyslipidemia contributes to the progression of microvascular disease in diabetes. However, different lipid variables may be important at different stages of nephropathy. This study examines the pattern of dyslipidemia associated with the progression of nephropathy in patients with type 1 diabetes. RESEARCH DESIGN AND METHODS: A total of 152 patients with type 1 diabetes were recruited in order to represent various phases of nephropathy. Patients were followed for 8-9 years, during which time they received standard care. Renal progression was defined a priori as a doubling in albumin excretion (in patients with normo- or microalbuminuria) or a decline in creatinine clearance (in those with macroalbuminuria). A panel of lipid variables was determined and correlated with indexes of progression. RESULTS: In patients with normoalbuminuria (n = 66), progression was associated with male sex (P < 0.05), borderline albuminuria (P = 0.02), and LDL-free cholesterol (P = 0.02). In patients with microalbuminuria (n = 51), progression was independently associated with triglyceride content of VLDL and intermediate-density lipoprotein (both P < 0.05). In patients with macroalbuminuria (n = 36), a significant decline in the renal function (>3 ml x min(-1) x year(-1)) was independently associated with poor glycemic control, hypertension, and LDL size (P < 0.05). When all patients with progressive nephropathy were analyzed together, only LDL cholesterol was predictive on multivariate analysis (P < 0.05), which masked the importance of triglyceride enrichment in microalbuminuria. CONCLUSIONS: Lipid variables are associated with progression of diabetic kidney disease, but the relationship is not the same at all stages. This finding has implications for the design of renoprotective strategies and the interpretation of clinical trials in type 1 diabetes.

Adult↗
PubMed1997

Lack of association between cystopathy and progression of diabetic nephropathy in insulin-dependent diabetes mellitus.

Whether an association exists between cystopathy and progression of diabetic nephropathy has never been clarified. The aim of the present study was to measure the degree of cystopathy in relation to the rate of progression of diabetic nephropathy. To that end, 17 insulin-dependent diabetic patients with diabetic nephropathy but without voiding symptoms were investigated urodynamically. The median age of the patients was 45 years (range 27-67 years), diabetes duration 23 years (range 14-44 years) and the serum creatinine level was 162 mumol/L (median, range 65-449 mumol/L) at the time of the study. The progression rate of diabetic nephropathy was analysed retrospectively by measuring changes in yearly mean values of Log10 serum creatinine for a period of 13 years (3-15 years) before the investigation. The progression rate was 0.028 mumol/L/year (median). Patients with a progression rate above and below the median rate were considered to be rapid (n = 8) and slow (n = 9) progressors, respectively. More women than men had a rapid progression rate of nephropathy. Rapid progressors were found to have smaller volume or residual urine (90 vs 165 ml; p < 0.05), larger volume voided (440 vs 270 ml; p < 0.05), lower opening pressure (18 vs 48 cm H2O; p < 0.05) and lower pressure at maximum flow (37 vs 64 cm H2O; p < 0.05) compared to slow progressors. However, these variables were not related to the progression rate of nephropathy (MANOVA). Furthermore, these results should be interpreted with caution because of the natural gender differences in pressure conditions. In conclusion, rapid progression of diabetic nephropathy does not seem to be associated with dysfunction of the urinary bladder measured with cystometry and pressure flow.

Adult↗
PubMed1999

[Clinical course of acute deep infarcts in carotid system--pathogenesis of progressing stroke].

We attempted to clarify the temporal profile and the predisposing factors for progressing neurological disorders in the patients with acute cerebral infarction in the territory of the deep perforators of the carotid system. The subjects were 19 patients with mild hemiparesis admitted to our hospital within 24 hours of stoke onset, and their mean age was 59.9 +/- 9.1. Six of those patients (about 32%) had gradual neurological deterioration after admission (progressive cases), and they had poor outcome compared with non-progressing patients. The mean progressing period was 3.7 +/- 1.0 days. Our examination suggest that both the changes in systemic hemodynamics and the risk factors for cerebrovascular disease (hypertension, diabetes mellitus, hyperlipidemia) do not always provide a correlation with the development of progressing stroke. However, we speculate that the impairment of the microcirculation plays a major role in progressing stroke in the territory of penetrating arteries because of the result that the mean infarct size of progressive patients had a tendency to be larger than that of non-progressive patients in the chronic stage.

Aged↗
PubMed2000

[Progression of silent cerebral infarction in Japanese: a hospital-based study].

Little is known about the risk factors for progression of silent cerebral infarction (SCI). We evaluated the 5-year change in high signal intensity on T2-weighted MR images of the brain in 50 asymptomatic patients with SCI. SCI progression was evaluated by the sum of the high intensity score (HIS) and the number of new lesions found on reexamination. Progression of SCI was seen in 19 patients (38%) on the 5-year follow-up examination. The baseline HIS in the whole brain was 8.02 +/- 6.93 and the follow-up HIS was 8.7 +/- 7.16 (p < 0.001). SCI progression was frequently seen in the corona radiata (p < 0.02 or < 0.05) or posterior periventricular white matter (p < 0.05). Patients with poor control of hypertension (> 160/95 mmHg) have a higher prevalence of SCI progression (9/12 (75%) vs. 10/38 (26.3%); OR = 8.4, p < 0.005) than the patients with effective control of BP (< or = 160/95 mmHg). The progression group showed a significantly higher baseline-HIS in the whole brain than the nonprogressing group (9.7 +/- 5.6 vs. 7 +/- 7.5; p < 0.05). Neither age percentages of alcohol drinkers, male sex, current smokers, hypertensives, hyperuricemia, hypercholesterolemia, diabetes, obesity, left ventricular hypertrophy, ischemic heart disease, nor differences in the controls of diabetes and hypercholesterolemia during the study were different between the progressing and the nonprogressing groups. Our data showed that poor control of high blood pressure and the degree of T2 high intensity in the baseline were strong predictors of SCI progression.

Aged↗
PubMed2004

Malignant progression in meningioma: documentation of a series and analysis of cytogenetic findings.

OBJECT: The malignant progression of benign tumors is well documented in gliomas and other systemic lesions. It is also well known that some meningiomas become progressively aggressive despite their original benign status. The theory of clonal evolution is widely believed to explain malignant progression in meningioma; however, the data used to explain stepwise progression have typically been derived from the cytogenetic analysis of different types of tumors of different grades and in different patients. In this study, the authors examined the data obtained in a group of patients with meningiomas that showed clear histopathological progression toward a higher grade of malignancy and then analyzed the underlying cytogenetic findings. METHODS: Among 175 patients with recurrent meningiomas, 11 tumors showed a histopathological progression toward a higher grade that was associated with an aggressive clinical course. Six tumors progressed to malignancy and five to the atypical category over a period averaging 112 months. Tests for MIB-1 and p53 and cytogenetic studies with the fluorescence in situ hybridization (FISH) method were performed in successive specimens obtained in four patients. The MIB-1 value increased in subsequent samples of tumors. Cytogenetic analysis with FISH showed deletions of 22, 1p, and 14q. In all but one case, these aberrations were also present in the previous specimen despite its lower hispathological grade. CONCLUSIONS: The authors documented the progression of meningiomas from benign to a higher histological grade. These tumors were associated with a complex karyotype that was present ab initio in a histologically lower-grade tumor, contradicting the stepwise clonal evolution model. Although it was limited to the tested probes, the FISH method appears to be more accurate than the standard cytogenetic one in detecting these alterations. Tumors that present with complex genetic alterations, even those with a benign histological grade, are potentially aggressive and require closer follow up.

Adult↗
PubMed2003

Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient-level meta-analysis.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure and urine protein excretion and slow the progression of chronic kidney disease. PURPOSE: To determine the levels of blood pressure and urine protein excretion associated with the lowest risk for progression of chronic kidney disease during antihypertensive therapy with and without ACE inhibitors. DATA SOURCES: 11 randomized, controlled trials comparing the efficacy of antihypertensive regimens with or without ACE inhibitors for patients with predominantly nondiabetic kidney disease. STUDY SELECTION: MEDLINE database search for English-language studies published between 1977 and 1999. DATA EXTRACTION: Data on 1860 nondiabetic patients were pooled in a patient-level meta-analysis. Progression of kidney disease was defined as a doubling of baseline serum creatinine level or onset of kidney failure. Multivariable regression analysis was performed to assess the association of systolic and diastolic blood pressure and urine protein excretion with kidney disease progression at 22 610 patient visits. DATA SYNTHESIS: Mean duration of follow-up was 2.2 years. Kidney disease progression was documented in 311 patients. Systolic blood pressure of 110 to 129 mm Hg and urine protein excretion less than 2.0 g/d were associated with the lowest risk for kidney disease progression. Angiotensin-converting enzyme inhibitors remained beneficial after adjustment for blood pressure and urine protein excretion (relative risk, 0.67 [95% CI, 0.53 to 0.84]). The increased risk for kidney progression at higher systolic blood pressure levels was greater in patients with urine protein excretion greater than 1.0 g/d (P < 0.006). CONCLUSION: Although reverse causation cannot be excluded with certainty, a systolic blood pressure goal between 110 and 129 mm Hg may be beneficial in patients with urine protein excretion greater than 1.0 g/d. Systolic blood pressure less than 110 mm Hg may be associated with a higher risk for kidney disease progression.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Dietary therapy in uremia: the impact on nutrition and progressive renal failure.

BACKGROUND: In rats with experimental chronic renal failure (CRF), low-protein diets protect against histologic damage and improve mortality. In CRF patients, low-protein diets ameliorate uremic symptoms and certain CRF complications. Fortunately, low-protein diets are nutritionally sound in CRF patients because they activate compensatory mechanisms that conserve protein with a low-protein diet. These results do not determine if dietary protein restriction can slow the rate of progression of CRF or the time to dialysis. METHODS: Reports evaluating low-protein diets and changes in nutritional status and/or progression of CRF are analyzed for efficacy. The MDRD Study is reviewed in depth. RESULTS: When dietary compliance was achieved, the nutritional status was unimpaired and progression was slowed. Studies with limited dietary compliance failed to find any beneficial effect on progression. Problems in study design suggest caution before accepting the initial MDRD Study conclusion that dietary restriction does not slow progression. Subsequent analyses of MDRD results indicate that protein restriction can slow progression of CRF. CONCLUSION: Evidence that dietary protein spontaneously decreases in progressively uremic patients should not be construed as an argument against the use of dietary therapy. Rather, it is a persuasive argument to restrict dietary protein intake in order to minimize CRF complications while preserving nutritional status. In patients with uremia or progression despite other measures, dietary therapy should be started along with monitoring for dietary compliance and nutritional adequacy.

Diet, Protein-Restricted↗
PubMed2001

Stage progression in Ta papillary urothelial tumors: relationship to grade, immunohistochemical expression of tumor markers, mitotic frequency and DNA ploidy.

PURPOSE: We studied 363 patients with stage Ta bladder tumors during long-term followup who were classified according to the 1998 WHO and International Society of Urological Pathology consensus classifications. We determine whether various immunohistochemical and molecular markers could predict tumor progression. MATERIALS AND METHODS: A total of 680 patients in western Sweden with a first diagnosis of bladder carcinoma in 1987 and 1988 were registered and followed for at least 5 years. There were 363 (53%) tumors that were papillary stage pTa. The tumors were classified as papillary urothelial neoplasm of low malignant potential in 95 patients, low grade papillary urothelial carcinoma in 160 and high grade carcinoma in 108. Of the patients in the latter group 95 were subdivided into WHO grade 2 and 13 into WHO grade 3. Tissue from the primary tumors that progressed in stage during followup was further analyzed with immunohistochemical methods (p21, p53, Ki67 and pRb), DNA ploidy and mitotic frequency. The results were compared with those in matched controls (nonprogressors). RESULTS: Recurrence developed in 35% of patients with papillary urothelial neoplasm of low malignant potential compared to 71% with low grade urothelial carcinoma and 73% with high grade carcinoma (p <0.0001). No papillary urothelial neoplasm of low malignant potential progressed in stage. Disease progressed in 4% of patients with low grade compared to 23% with high grade carcinoma (p <0.0001). Of the patients with WHO grade 3 disease progressed in 45% compared to grade 2 in 20% (p <0.0011). At first diagnosis p53 score was significantly higher (p <0.0022) among patients with WHO grade 2 carcinoma which later progressed compared to that in matched controls but there was no significant difference regarding the other markers. In contrast to grade 2 most grade 3 carcinoma was aneuploid, had high mitosis frequency, high p53 and Ki67 scores as well as loss of retinoblastoma gene expression. CONCLUSIONS: The 1988 WHO and International Society of Urological Pathology consensus classifications divide noninvasive papillary bladder tumors into 3 subgroups with different clinical behavior, which seems to be an advantage compared with the 1973 WHO classification. A disadvantage is that the high grade carcinoma group contains 2 subgroups with different progression rates and immunohistochemical marker profiles, corresponding to the 1999 WHO grades 2 and 3. Grade 2 tumors in patients that progressed in stage years later seem to have different immunohistochemical and molecular marker profiles compared to those in matched controls.

Aged↗
PubMed2002

Feasibility study: watchful waiting for localized low to intermediate grade prostate carcinoma with selective delayed intervention based on prostate specific antigen, histological and/or clinical progression.

PURPOSE: We assessed the feasibility of a watchful waiting protocol with selective delayed intervention using clinical, prostate specific antigen (PSA) or histological progression as treatment indications for clinically localized prostate cancer. MATERIALS AND METHODS: In this prospective, single arm cohort study patients with favorable clinical parameters (stage T1b to T2b N0M0, Gleason score 7 or less and PSA 15 ng./ml. or less) are conservatively treated with watchful waiting. When a patient meets disease progression criteria, arbitrarily defined by the 3 parameters of the rate of PSA increase, clinical progression or histological upgrade on repeat prostate biopsy, appropriate treatment is implemented. Patients are followed every 3 months for the first 2 years and every 6 months thereafter. Serum PSA measurement and digital rectal examination are done at each visit and repeat prostate biopsy is performed 18 months after study enrollment. RESULTS: Since November 1995, the study has accrued 206 patients with a median followup of 29 months (range 2 to 66). Of these men 137 remain on the surveillance protocol with no disease progression, while 69 were withdrawn from study for various reasons. There was clinical, PSA and histological progression in 16, 15 and 5 cases, respectively. The estimated actuarial probability of remaining on the surveillance protocol was 67% at 2 years and 48% at 4. The probability of remaining progression-free was 81% and 67% at 2 and 4 years, respectively. CONCLUSIONS: A policy of watchful waiting with selectively delayed intervention based on predefined criteria of disease progression is feasible. This strategy offers the benefit of an individualized approach based on the demonstrated risk of clinical or biochemical progression with time and, thus, it may decrease the burden of therapy in patients with indolent disease, while providing definitive therapy for those with biologically active disease.

Aged↗
PubMed2003

Fibroblast growth factor 2 promotes tumor progression in an autochthonous mouse model of prostate cancer.

Fibroblast growth factor (FGF) 2 (or basic FGF) is expressed at increased levels in human prostate cancer. FGF2 can promote cell motility and proliferation, increase tumor angiogenesis, and inhibit apoptosis, all of which play an important role in tumor progression. To determine whether FGF2 plays a critical role in prostate cancer progression, we have used the transgenic adenocarcinoma of the mouse prostate (TRAMP) model system. A high percentage of TRAMP mice develop metastatic prostate cancer, and thus the TRAMP model is useful for evaluating cancer progression. TRAMP mice were crossed with FGF2 knockout (FGF2(-/-)) mice, and tumor progression in TRAMP mice that were either hemi- or homozygous for inactivation of the FGF2 allele was compared with progression in wild-type TRAMP mice. Inactivation of even one FGF2 allele resulted in increased survival, a decrease in metastasis, and inhibition of progression to the poorly differentiated phenotype in primary prostatic tumors. When compared with wild-type mice, poorly differentiated tumors arising in FGF(+/-) and FGF(-/-) mice expressed higher levels of vascular endothelial growth factor and, in some cases, increased levels of acidic FGF intracellular binding protein, a nuclear FGF1-binding protein. These findings suggest that both FGF2-mediated angiogenesis and intranuclear FGF2 activities may promote tumor progression and support the hypothesis that FGF2 plays a significant role in prostate cancer progression in vivo.

Alleles↗
PubMed2003

Progression of diabetic retinopathy after phacoemulsification in diabetic patients: a three-year analysis.

BACKGROUND: This retrospective study was conducted to analyze the progression rates of diabetic retinopathy (DR) after phacoemulsification in diabetic patients and to determine whether phacoemulsification causes the progression of DR. METHODS: The medical charts of diabetic patients who had undergone cataract surgery using phacoemulsification techniques during a 3-year period and had completed 3 years of follow-up were retrospectively reviewed. Data were collected to evaluate the visual outcomes and progression of DR postoperatively. The retinopathy progression rates of operated and nonoperated eyes were compared. RESULTS: Thirty-seven diabetic patients were enrolled. Binocular cataract surgeries were performed in 14 patients. Monocular cataract surgeries were performed in the remaining 23 patients whose nonoperated fellow eyes served as the control group. The postoperative retinopathy progression rates of eyes with preoperative mild to moderate nonproliferative diabetic retinopathy (NPDR) were significantly greater than eyes without preoperative retinopathy whether at postoperative 1 year or postoperative 3 years. No statistical significance was found for the rate of retinopathy progression between operated and nonoperated eyes at 1 year and 3 years postoperatively. Of 51 operated eyes, 33 (64.7%) achieved an uncorrected visual acuity of 20/40 at 1 year postoperatively, and 47 (92.1%) had improvement of visual acuity of more than two lines. CONCLUSION: Uncomplicated phocoemulsificaton had no significant influence on the postoperative progression of DR. Patients with preoperative NPDR had greater chances to show postoperative retinopathy progression. The majority of diabetic patients who had no DR or had mild to moderate NPDR achieved visual improvement after phacoemulsification.

Aged↗
PubMed2006

Multistate and multifactorial progression of gastric cancer: results from community-based mass screening for gastric cancer.

Although multistate progression models for gastric cancer have been proposed, estimation of quantitative parameters of such models is yet to be done. The present study was conducted to elucidate risk factors for gastric cancer and its precursors, and to model the progression rates from superficial gastritis to gastric cancer. Data were derived from a community-based screening programme for gastric cancer in the Matzu region of Taiwan. A total of 2184 residents participated in a two-stage screening project. Subjects testing positive for Helicobacter pylori infection or pepsinogen (PGI or PII/PGII ratio) and immunoglobulin G (IgG), and subjects with a history of peptic ulcer or other upper gastrointestinal disease or with a family history of gastric cancer were referred to endoscopy. We identified 325 biopsy-proven precursors and gastric cancers, including 148 superficial gastritis (SG), 42 atrophic gastritis (AG), 117 intestinal metaplasia (IM) and two gastric cancers. Three further cancers were diagnosed on endoscopy alone and 14 were later diagnosed in those who did not comply with referral to endoscopy. A Markov process model was used to estimate the progression rates from superficial gastritis through to gastric cancer, with exponential regression to assess the effect of covariates on progression rates. The annual progression rate from SG to AG was 0.0670 (95% confidence interval [CI] 0.0446-0.0895). Annual progression rates from AG to IM and from IM to gastric cancer were 0.2775 (0.1665-0.3884) and 0.2265 (0.1315-0.3214), respectively. This gives average dwelling times in AG and IM of 3.60 years and 4.42 years, respectively. Progression from no disease to SG was significantly accelerated in those testing positive for H. pylori, those testing positive for PGI and in subjects with a family history of gastric cancer or a personal history of upper gastrointestinal disease. Further progression to AG and IM was significantly accelerated in those testing positive for PGI and in those with a history of upper gastrointestinal disease.

Adult↗
PubMed1995

[The quantification of human immunodeficiency virus viremia in patients with rapid and slow progression of the disease].

BACKGROUND: The natural course of the human immunodeficiency virus type 1 (HIV-1) infection is very variable. The factors which appear to determine the speed of immunodeficiency progression are multiple, although the virulence of the predominant viral strain seems to be one the main factors. The plasmatic viremia in individuals with rapid and slow HIV-1 progression was analyzed in an attempt to establish the degree of correlation between HIV-1 replication and the natural course of the disease. METHODS: Forty-two samples from 34 seropositive patients, 11 with rapid progression criteria (< 5 years from acute infection and CD4+ lymphocytes < 0.2 x 10(9)/l) and 23 with slow progression (> 7 years from demonstrated infection and > 0.5 x 10(9) CD4+ lymphocytes/l) were studied. The plasmatic viremia was quantified by a new method of plasma DNA genetic amplification, denominated the branched DNA (bDNA) technique. As a reference circulating p24 was determined and the presence of several proviral regions were studied in peripheral blood lymphocytes by polymerase chain reaction (PCR). RESULTS: The presence of RNA molecules was detected in plasma of 7 (58.3%) out of 12 samples of rapid progression (RP) patients by bDNA. To the contrary, this was negative in 30 samples from slow progression (SP) patients. Four of the 5 negative RP samples corresponded to patients who had taken antiretroviral drugs at the time of the study. The p24 antigenemia was positive in 5 (41.6%) from the RP patients and in none of the SP patients. The presence of gag, pol and env sequences was positive by PCR in all RP patients and in most of the SP patients. However, repeatedly negative results by PCR were observed in 5 SP samples for all or some of the genomic regions studied. CONCLUSIONS: Patients with rapid progression of HIV-1 have higher plasmatic viremia than subjects with slow disease progression.

Adult↗
PubMed1996

Apoptosis in progressive crescentic glomerulonephritis.

Recent studies in the experimental proliferative glomerulonephritis (GN) indicate that apoptosis is the major mechanism that mediates the resolution of glomerular hypercellularity during the repair process of experimental GN. The role of apoptosis during progressive GN, however, has not yet been well understood. We have, therefore, examined the role of apoptosis during the progression of experimental crescentic GN to end-stage renal failure. A progressive model of antiglomerular basement membrane GN was induced in Wistar-Kyoto rats with a single injection of anti-rat glomerular basement membrane antibody. Renal function and histologic studies were performed chronologically from Day 0 to Week 8 after disease induction. The incidence of apoptosis in glomeruli as well as glomerular crescents was examined during the progression of crescentic GN to end-stage kidney disease. Many leukocytes infiltrated glomeruli from the early phase of GN, and severe necrotizing and mesangiolytic glomerular damage was observed from Day 5 to Week 3. After glomerular damage, mesangial hypercellularity with mesangial cell proliferation and extracellular matrix accumulation began with crescent formation. Thereafter, glomerular inflammation continued with marked extracellular matrix accumulation until Week 4, and the renal function deteriorated. The proliferative glomerular lesions subsequently progressed to sclerotic lesions and eventually to chronic renal failure in Week 8. Although the number of proliferating cells and infiltrating leukocytes slowly decreased, glomerular inflammation resolved with scar formation as mesangial sclerosis. Significant apoptosis was present from Day 7 (mean +/- SEM, 0.53 +/- 0.12 cells/glomerular cross-section) and gradually increased in number with the proliferating lesions as glomerular inflammation continued. Moreover, apoptosis increased during the resolution of the glomerular inflammation, and many apoptotic cells were present in the sclerotic lesions in Week 8 (1.97 +/- 0.27 cells/glomerular cross-section). As glomerular inflammation subsided, cellular crescents progressed to fibrous crescents with a reduction of cellularity by Week 8, and apoptosis increased significantly within these lesions. These findings indicate that apoptosis plays an essential role in the resolution of intra- and extraglomerular inflammation and in the elimination of glomerular cells within the scarring regions for progressive crescentic GN. The regulation of the apoptotic phenomenon during crescentic GN may be important in the progression of glomerular inflammation and the development of pathologic glomerular sclerosis.

Animals↗
PubMed1996

Progression of HIV: follow-up of Edinburgh injecting drug users with narrow seroconversion intervals in 1983-1985.

OBJECTIVE: To describe progression and survival of individuals infected with HIV by injecting drug use in Edinburgh. DESIGN AND METHODS: From 313 HIV-infected patients with retrospectively estimated narrow seroconversion intervals, 260 infected via injecting drug use in the years 1983-1985 were selected for the study group. MAIN OUTCOME MEASURES: The effects of gender, age, human leukocyte antigen (HLA) type and zidovudine (ZDV) treatment on progression and survival from seroconversion; Weibull estimates of the AIDS incubation distribution and the overall survival distribution; slopes of absolute CD4 lymphocyte loss (on the square root scale) and loss of CD4 percentage. RESULTS: The cumulative progression rates at 10 years were 68% to CDC stage IV and 31% to AIDS with a mortality rate of 25%. Three-year survival rates for AIDS and CDC stage IV cases were 25 and 72%, respectively. Gender and age effects on progression or overall survival were not found, although those aged over 30 years experienced poorer survival from AIDS. A strong HLA (A1, B8, DR3) association with faster progression and poorer survival was found. Median survival was estimated by Weibull distribution to be 12.6 years; median AIDS-free time was estimated to be 11.6 years. CD4 cell loss was approximately linear when transformed to the square root scale as was the decline in CD4 percentage. Only HLA effects on slopes were found: A1,B8, DR3 was significantly associated with faster loss of both absolute CD4 cells and CD4 percentage (P < 0.001) and B27 was significantly associated with slower loss of CD4 percentage (P = 0.01). CONCLUSIONS: Edinburgh IDU do not seem to progress more rapidly than other cohorts with predominantly different risk activities. Older age was associated with poorer survival from AIDS but no gender effect was found for progression or overall survival. The clearest significant association with AIDS progression, mortality and loss of CD4 cells was the phenotype HLA A1,B8,DR3. In contrast HLA B27 was associated with slower loss of CD4 cells.

Adult↗
PubMed1997

Do close but negative margins in radical prostatectomy specimens increase the risk of postoperative progression?

PURPOSE: When tumor extends close to the margin of resection yet does not extend to the inked edge of the gland, it is unclear whether patients have an adverse prognosis compared to cases with greater distance between the tumor and margin. MATERIALS AND METHODS: Among radical prostatectomy specimens with negative margins the distance between the most peripheral tumor and the surgical margin of resection was measured in 52 cases with and 49 without progression. All patients had clinically confined disease (stages T1 or T2) with subsequent progression or a minimum 5-year followup without evidence of disease. No patient received preoperative or postoperative radiotherapy or hormonal therapy until progression occurred. All men underwent a postoperative serum prostate specific antigen test to evaluate progression. Seminal vesicles and lymph nodes were pathologically free of tumor. All prostates were serially sectioned, completely embedded and assessable regarding margins of resection. RESULTS: Patients with progression were no more likely to have tumor close to the margin than those without progression. In a regression analysis analyzing the effect of Gleason score, distance between tumor and margin, location of closest margin and pathological stage as related to progression, only grade was predictive of progression (p < 0.00001). CONCLUSIONS: It is not necessary for pathologists to designate these margins as close, since biologically this finding has no significance. Furthermore, physicians who are involved in treatment of patients after radical prostatectomy for prostate cancer should not alter therapy depending on whether margins are reported as close.

Disease Progression↗
PubMed1997

Long-term efficacy of intravesical bacillus Calmette-Guerin for carcinoma in situ: relationship of progression to histological response and p53 nuclear accumulation.

PURPOSE: We assessed the influence of the histological response to intravesical bacillus Calmette-Guerin (BCG) and the prevalence of p53 nuclear accumulation on the clinical behavior of patients with carcinoma in situ. MATERIALS AND METHODS: Of 60 patients with Bergquist grade 3 carcinoma in situ 13 had primary and 47 had secondary carcinoma in situ. Patients received 6 weekly instillations and nonresponders received an additional 6 instillations at 2-week intervals. No maintenance was administered. Median followup was 48 months. The p53 nuclear accumulation was detected by immunohistochemical analysis with antibody PAb 1801. RESULTS: The complete histological response rate to BCG therapy was 64%, which decreased to 52% at 4 years. BCG was more effective for treatment of primary than secondary carcinoma in situ (complete response rate 85 versus 57%, respectively). The 45% progression rate was related to the initial histological response occurring in 26% of patients with a complete versus 77% with a partial and no response. Consequently, the progression rate was only 8% for primary versus 57% for secondary carcinoma in situ. Of the patients receiving only 1 course of BCG 40% had progression compared to 62% of those who received 2 courses. Patients in whom both courses failed had a progression rate of 89%. Intravesical BCG converted the p53 nuclear immunoreactivity from positive to negative in 73% of the 26 patients expressing reactivity before treatment, of whom 68% also had a complete response. The progression rate was related to the prevalence of p53 nuclear reactivity after but not before treatment (90% of patients with versus 37% without p53 nuclear accumulation had progression). All 3 complete responders with p53 nuclear reactivity after BCG had progression, which suggests that molecular genetic change may precede histological change. Complete responders without p53 nuclear accumulation after BCG treatment experienced the lowest progression rate (21%). CONCLUSIONS: Our results suggest that patients with a persistent complete histological response and without p53 nuclear accumulation after BCG treatment can be followed conservatively. Cystectomy should be considered in all other patients.

Adjuvants, Immunologic↗
PubMed1996

Can bifocals slow myopia progression?

BACKGROUND: Retrospective studies have suggested that in children with near point esophoria, bifocals can slow myopia progression by about 50 percent. A prospective study was conducted to test this hypothesis. METHODS: Thirty-two children, all with near point esophoria, were randomly divided into either correction with single-vision or with bifocal lenses containing a +1.25 D and. Axial length and refraction were measured under cycloplegia every 6 months for 18 months. Twenty-eight children completed the study. RESULTS: Myopia progressed at an equal rate in both groups for the first 12 months. Progression was much faster during the first 6 months, which was during the school year, than during the second 6 months, which included all of the summer vacation (0.64 D/yr vs 0.29 D/yr). During the last 6 months, myopia progressed rapidly for children in single-vision lenses (0.80 D/yr) but slowly for those in bifocals (0.37 D/yr). A repeated-measure analysis of variance showed that season of the year had a significant effect on myopia progression (p > 0.002) and that the effect differed for the two treatment groups (p > 0.043). Over the whole 18-month study, myopia progressed at rate of 0.57 D/yr for those in single-vision lenses and 0.39 D/yr in those in bifocals (p = 0.26). CONCLUSIONS: Bifocals seemed to slow myopia progression in these children with near-point esophoria, although a longer-term study with more subjects is needed to confirm this finding. Myopia progressed more rapidly during the school year than during summer vacation.

Adolescent↗