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PubMed2001

[Survival and disease progression in 251 patients with HIV-1 infection. Study of p24 antigen and viral burden as prognosis makers. Their value at 4 years of follow-up].

BACKGROUND: Prospective study of survival and AIDS or death progression in a cohort of 251 HIV infected patients whose seroconversion time is unknown, with a main objective: To analyse p24 antigen plasmatic levels and viral load as surrogate markers. PATIENTS: 251 patients were included, most of them undergoing antiretroviral therapy, and were followed-up consecutively in the HIV/AIDS Unity of Internal Medicine Service of the Hospital Universitario Arnau de Vilanova in Lleida. METHODS: We made clinical and analytical baseline studies and every 3 months thereafter. Related to p24 antigen 3 group were established: group I, < 20 pg/mL, group 2, 20-39 pg/mL, group 3, 40 or more pg/mL. We studied survival and progression according to baseline levels over 4 year period. Regard to viral load, we just compared this with p24 antigen in the last phase of the study (third and fourth year) for technical reasons. Survival analysis was made by Kaplan-Meier estimation. Relative risk was calculated by Cox's proportional hazards model. RESULTS: During the 48 months of follow-up 55 patients died. AIDS progression risk or death was 4.8 times higher for the p24 antigen > = 40 pg/mL group than for the p24 antigen < 20 pg/mL one; the relative risk of patients with p24 antigen between 20-39 pg/mL was 2.5 times higher than those included in the group of p24 antigen < 20 pg/mL. Related to progression study, 34 patients progressed. AIDS progression risk or death for p24 antigen > = 40 pg/mL group was 7.69 times higher compared with group 2 (p24 antigen levels between 20-39 pg/mL). The comparison with viral load by PCR determination shows controversial results. CONCLUSIONS: p24 antigen plasma level is a good survival and AIDS progress or death surrogate markers in HIV infected patients, and it is useful for 4 years or more. An isolated value < 20 pg/mL is a sign of good prognosis. Parallelism between p24 antigen plasmatic level and viral load has not been observed.

Adult↗
PubMed2002

The CC chemokine RANTES in breast carcinoma progression: regulation of expression and potential mechanisms of promalignant activity.

Breast cancer progression may be affected by various cellular components expressed by the tumor cells and/or by microenvironmental factors. Many studies report the correlation between breast cancer progression and monocyte infiltration into the tumor site. We have identified recently the CC chemokine regulated on activation, normal T cell expressed and secreted (RANTES), a major monocyte chemoattractant expressed by breast tumor cells, as a potential contributor to breast cancer progression. In the present study, analysis of the regulation of RANTES expression demonstrates that the expression of RANTES in breast tumor cells is elevated significantly and in a synergistic manner by IFN-gamma and tumor necrosis factor-alpha. Identification of the mechanisms by which RANTES may contribute to breast cancer progression included the analysis of the potential ability of RANTES to act in paracrine and indirect mechanisms, as well as directly on the tumor cells, to promote disease progression. Our results suggest that breast tumor cell-derived RANTES may promote breast cancer progression by its partial contribution to monocyte migration into breast tumor sites. Moreover, RANTES promotes the expression of matrix metalloproteinase (MMP) 9 by THP-1 monocytic cells and elevates vascularity in chick chorioallantoic membrane assays. Tumor necrosis factor-alpha, a major monocyte-derived cytokine, was found to promote the expression of MMP9 and MMP2 by MCF-7 and T47D breast adenocarcinoma cells, respectively, and to induce the de novo expression of an additional proteolytic enzyme by T47D cells, presumably MMP9. The possibility that RANTES may act directly on breast tumor cells was supported by detection of the expression of the CCR5 RANTES receptor in biopsy sections of breast cancer patients and by the ability of RANTES to promote the expression of MMP9 by MCF-7 cells. In all, our study suggests that the expression of RANTES by breast tumor cells results not only in monocyte migration to the tumor site but also in protumorigenic activities of RANTES and of proinflammatory cytokines that may facilitate metastasis formation and contribute to disease progression.

Animals↗
PubMed2002

[Main grade of Gleason's 7 score of the surgical sample correlated with biologic progression in patients treated for total prostatectomy].

OBJECTIVES: To analyse the influence of the main grade of Gleason score 7 of the operative specimen correlated with the blood PSA level on the laboratory progression-free survival of patients treated by radical prostatectomy. MATERIALS AND METHODS: 331 patients consecutively treated by radical prostatectomy and presenting a Gleason score 7 were analysed. Exclusion criteria were the use of radiotherapy and/or preoperative and/or postoperative endocrine therapy. The main grade (3 or 4), histological stage, and blood PSA level were analysed for their predictive value of laboratory progression-free survival. The mean follow-up was 3.5 years (range: 13.6 to 72.8 months). Laboratory recurrence was defined by a PSA > 0.4 ng/ml. RESULTS: The main grade of Gleason score 7 was 3 in 199 (60%) patients and 4 in 132 (40%) patients with a mean follow-up of 3.6 years. Laboratory progression-free survival rates were 89% and 72% for main grades 3 and 4, respectively (p = 0.03). When the cancer was confined to the prostate, the progression-free survival rates were 96% and 88% for main grades 3 and 4, respectively (p = 0.01). For a PSA < 10 ng/ml, main grade 3 was associated with a better laboratory progression-free survival rate than main grade 4 (p = 0.0007). No difference in terms of laboratory progression was observed in the presence of extraprostatic extension or PSA > 10 ng/ml. CONCLUSION: A high correlation was observed between the main grade of Gleason score 7 and laboratory progression-free survival. Main grade 3 constituted a factor of better prognosis than main grade 4.

Disease Progression↗
PubMed2002

The natural history of ankylosing spondylitis as defined by radiological progression.

OBJECTIVE: Radiological status is an important objective endpoint in the assessment of ankylosing spondylitis (AS). We investigated the disease development of AS using radiological change. METHODS: The existing radiographs (n = 2,284) of 571 AS patients attending the Royal National Hospital for Rheumatic Diseases were scored retrospectively using the Bath Ankylosing Spondylitis Radiology Index. (1) Progression of disease was initially examined cross sectionally. Univariate analysis was used to examine factors associated with joint involvement. (2) Progression of disease was then examined longitudinally for patients with films at time of symptom onset. (3) Rate of progression of radiological change was calculated using longitudinal data of 2 sets of radiographs taken 10 years apart (patient number = 54). The results from this were used to extrapolate backwards to age at first radiological change. RESULTS: (1) Progression to cervical spine disease was a function of: disease duration, severity of hip and lumbar involvement, and a history of iritis (p < 0.001). Lumbar involvement was associated with disease duration, age now, and severity of cervical and hip involvement (p < 0.001). Hip involvement was a marker for cervical disease and associated with disease duration (p < 0.001). (2) Longitudinal analysis revealed marked variation among patients with a slow general rate of progression. (3) The progression of AS over any 10 year period is linear [first 10 years = 30% (SD 0.3) of potential change, 10-20 yrs = 40% (SD 0.3) change, 20-30 yrs = 35% (SD 0.4) change (p = 0.5)]. Backward extrapolation suggests that the approximate time of first radiological change is at the age of 8 years. CONCLUSION. (1) AS is a linearly progressive disease with about 35% change every 10 years. Spinal involvement is largely an expression of disease duration while the hips become involved in about 25% of individuals and may predict a more severe outcome for the cervical spine. (2) Backward extrapolation shows that the disease process may start as young as 8 years of age. However, the time interval between the disease trigger and radiological change remains unknown.

Adolescent↗
PubMed2002

HLA and cytokine gene polymorphisms in relation to occurrence of palindromic rheumatism and its progression to rheumatoid arthritis.

OBJECTIVE: Palindromic rheumatism (PR) is an episodic arthropathy that may precede typical rheumatoid arthritis (RA), although pathogenetic relationships between these disorders remain unclear. The predictive value for those immunogenetic risk factors implicated in RA for disease progression in PR remains to be established. A previous retrospective analysis from our group has implicated rheumatoid factor in disease progression. Our objective was to determine the contribution of HLA and cytokine gene polymorphisms implicated in RA to predisposition to PR and to progression of PR to chronic joint inflammation. METHODS: We studied 147 patients with PR seen in a tertiary referral center; 87 were selected retrospectively from the period 1986-96 using a structured selection process and 60 were selected prospectively in the period 1997-2001. Comparison groups included 149 patients with RA and 149 ethnically matched controls. Typing for HLA-DRB1 alleles and HLA-DRB1-04 subtypes was performed following polymerase chain reaction (PCR) amplification using sequence-specific primers (SSP). Cytokine genotypes were ascertained following PCR-SSP with and without digestion with restriction enzymes. Time-adjusted survival analysis (Kaplan-Meier) and multivariate logistic regression were used to assess the independent contribution of immunogenetic markers in assessing progression of PR to chronic joint inflammation. RESULTS: Thirty-one percent of patients progressed to connective tissue disease after a mean of 10.6 (retrospective group) and 3.9 (prospective group) years. A significantly increased prevalence of the shared epitope (SE) allele was noted in patients with PR (65%) versus controls (39%) (OR 2.9, 95% CI 1.8-4.6, p < 0.001). This primarily reflected increased prevalence of the DRB1-0401 and 0404 and not DRB1-01 alleles. A weak contribution to disease susceptibility was also noted with carriage of the IL4 promoter -590T (OR 1.8, 95% CI 1.1-3.0, p = 0.02) and IL4 intron 3 RP1 (OR 1.7, 95% CI 1.1-2.9, p = 0.03) alleles. The TNFa +489A allele was associated with RA (OR = 2.7, 95% CI 1.5-5.1, p = 0.001) in both SE+ and SE- patients, but not with PR. Time-adjusted and multivariate Cox regression analysis revealed that only homozygosity for SE alleles was a significant independent risk factor for disease progression to chronicity in PR (hazard ratio 2.9, 95% CI 1.2-6.9, p = 0.02). However, none of 8 patients homozygous for SE- DRB1 XP4n alleles developed chronic disease after 10 years of followup (p = 0.07). CONCLUSION: The immunogenetic risk profile for PR resembles that for RA, indicating that PR is likely not an independent entity. A significant gene dose effect for SE alleles is operative in determining risk for progression from PR to RA.

Adult↗
PubMed2002

Progression of visual field loss in untreated glaucoma patients and suspects in St Lucia, West Indies.

PURPOSE: A 1986-1987 survey found an 8.8% prevalence of open-angle glaucoma in the black population of St Lucia, West Indies. This follow-up study assessed progression of visual field loss in untreated glaucoma patients and persons with suspected glaucoma 10 years later. METHODS: Subjects were 205 patients with or suspected of having glaucoma. The 1987 data included age, sex, visual acuity, and visual fields measured by automated threshold perimetry (Humphrey C-30-2 test). The 1997 data included intraocular pressure, visual acuity, and visual fields measured by the same test. Exclusion criteria included field unreliability, field improvement due to vision improvement, nonglaucomatous vision deterioration, glaucoma treatment since 1988, and scoring of a field as end-stage in 1987. Visual fields were scored by algorithms for the Advanced Glaucoma Intervention Study (AGIS) and Collaborative Initial Glaucoma Treatment Study (CIGTS). RESULTS: By AGIS criteria, 55% of 146 right eyes and 52% of 141 left eyes progressed. In linear regressions, progression severity was unassociated with male or female sex, intraocular pressure, or baseline visual field score, but was positively associated with age (P < .001, right; P = .002, left). By CIGTS criteria, more eyes progressed. The cumulative probability of reaching end-stage disease in 10 years in at least on eye was about 16% by AGIS criteria and was 35% by CIGTS criteria. CONCLUSIONS: These data provide a unique opportunity to study progression of untreated glaucoma. A considerably larger percentage of eyes showed progression of visual field loss, and the rate of progression was greater than in studies of visual field loss in treated eyes.

Adult↗
PubMed2003

An update on 'progression promoters' in renal diseases.

AIM: This paper reviews progression in renal diseases. METHODS: An English language literature search using Medline (1980 January-2001 July) was done to assess research and review articles on progression in renal diseases. RESULTS: Factors that increase the risk of progression in renal diseases are hypertension, dyslipidaemia, underlying nephropathy, high dietary protein intake and proteinuria. Others are smoking, hyperglycemia, low birth weight, obesity, metabolic syndrome X, genetic factors such as angiotensin converting enzyme 'DD' genotype and chromosome 1q21, and exposure to lead. Hypertension induces arteriolar nephrosclerosis. The mechanisms whereby lipids contribute to vascular and renal injury are incompletely understood. Glomerular hyperperfusion and increased proteinuria may explain the adverse effects of increased protein intake on renal disease progression. Proteinuria contains numerous toxic/inflammatory systems that promote progression. Cigarette smoking has vasoconstrictive, thrombotic and direct toxic effects on the vascular epithelium. Hyperglycemia is strongly implicated in the progression of complications in diabetics. Oligonephropathy in low birth weight has been suggested to increase the risk for systemic and glomerular hypertension in adult life. In obesity, the combination of hyperfiltration, glomerular hypertrophy and glomerular hypertension is a primary initiating event for glomerular injury manifesting as glomerulomegally and focal and segmental glomerulosclerosis and proteinuria. Angiotensin I, with enzyme insertion/deletion polymorphism, especially the "DD" genotype, predisposes to a rapid decline in renal function. Finally, long-term exposure to low levels of environmental lead affects renal function. CONCLUSION: The control of hypertension, dyslipidaemia, proteinuria, obesity, avoidance of low birth weight, smoking and heavy metals such as lead are intervention strategies for preventing progression of renal diseases.

Angiotensin II↗
PubMed2002

[Surgical treatment of progressive and symptomatic retinal detachment in senile retinoschisis].

BACKGROUND: This is 23-years retrospective study of consecutive, non-selected patients with senile retinoschisis and rare progressive and symptomatic retinal detachment (RD). The presence of RD was manifested by spectrum of retinal pathology of inner and outer layers of senile retinoschisis, ranging from simple holes to giant tears with or without proliferative vitreoretinopathy. The goals of this study were: 1--to evaluate the characteristics of the progressive and symptomatic RD based on detail preoperative examination of the eye, 2--to evaluate the anatomic and functional results of RD surgery. PATIENTS AND METHODS: From 1978 to 1999, RD surgery was performed on 57 eyes of 55 patients (28 men and 27 women) with senile retinoschisis and progressive and symptomatic RD. On average, we observed the patients for approximately 11.3 years after surgery; the minimum follow-up period was 20 months. The patients were divided in two groups according to the preoperative findings and the surgical procedures. Based on the size and the location of the defects of the inner and outer layer of senile retinoschisis and the proliferative vitreoretinopathy these procedures were indicated: 1--Uncomplicated cases of progressive and symptomatic retinal detachment were operated on primary cryopexy and scleral buckling (CSB) with episcleral silicone implants in 45 eyes. 2--Complicated cases of progressive and symptomatic retinal detachment underwent a pars plana vitrectomy (PPV) in 12 eyes: a--primary PPV was used as the primary treatment method in 6 eyes, b--secondary PPV as a secondary treatment method after unsuccessfully primary CSB with episcleral silicone implants in next 6 eyes. RESULTS: Characteristics preoperative findings were: RD in two or more quadrants in 84.2% of the eyes, including macula region in 71.9% of the eyes. Defect of the outer layer of senile retinoschisis was located postequatorial in 80% of the eyes, large retinal tears were found in 53.3% of the eyes and single defect was diagnosed in 68.8% of the eyes. Defect the of inner layer of senile retinoschisis was located equatorial in 69.5% of the eyes, small defects were found in 78.2% of the eyes and multiple defects were diagnosed in 58.6% of the eyes. Defects of the outer and the inner layer of senile retinoschisis were diagnosed in the equal quadrant in 61.4% of the eyes. The results of surgery varied, depending on the size and location of the defects of the inner and outer layer of senile retinoschisis and proliferative vitreoretinopathy: 1--The complete retinal reattachment in group treated with CSB was achieved in 43 eyes (95.5%), the average visual acuity was 0.34-2--The complete retinal reattachment in group treated with PPV was achieved by: a--primary PPV in six eyes, the average visual acuity was 0.37, b--secondary PPV four eyes, the average visual acuity was 0.16. CONCLUSIONS: Characteristic of senile retinoschisis, especially its defects of inner and outer layers is important preoperative finding for optimal indication of primary surgical treatment of progressive and symptomatic retinal detachment. According to our clinical experiences we created the syllabus of the care about the senile retinoschisis and syllabus of surgical treatment of progressive and symptomatic RD. Standard surgical procedures are the CSB and in the last period also primary PPV.

Adult↗
PubMedDate not supplied

Serum matrix metalloproteinase 3 levels in comparison to C-reactive protein in periods with and without progression of radiological damage in patients with early rheumatoid arthritis.

OBJECTIVE: To evaluate serum matrix metalloproteinase 3 (MMP-3) levels in comparison to C-reactive protein (CRP) in periods with and without progression of radiological damage in patients with early rheumatoid arthritis (RA). METHODS: Thirty-two patients with RA and radiological progression (> or = 5 points according to the Sharp/van der Heijde method) during 6 months followed by a 6-month period without radiological progression (< or = 1 point) were selected from a prospective follow-up study of early RA patients. Serum MMP-3 levels, CRP, the erythrocyte sedimentation rate (ESR), disease activity index (DAS), swollen joint count (SJC), tender joint count (TJC), and Ritchie articular index (RAI) were measured monthly and results were transformed into mean values for the 6-month periods. RESULTS: During the period with radiological progression the mean serum MMP-3 correlated significantly with the mean CRP (r = 0.68, p < 0.001), ESR (r = 0.54, p = 0.001) and swollen joint count (r = 0.48, p = 0.006). In the period without radiological progression the mean serum MMP-3 only correlated with the mean CRP (r = 0.44, p = 0.012). Individual changes--expressed in percentages (%)--between the two periods showed a decrease in both the mean serum MMP-3 and CRP in 19 and an increase in 3 patients, in parallel with other markers of disease activity in these patients (69% of cases). The individual change (%) in mean serum MMP-3 or CRP did not correlate with the difference in radiological progression between the two periods. CONCLUSIONS: Serum MMP-3 and CRP are closely related and there seems to be no difference between serum MMP-3 and CRP with regard to the monitoring of the progression of radiological damage.

Adult↗
PubMed2004

Radiological progression in established rheumatoid arthritis.

Radiographic progression in established rheumatoid arthritis (RA) gives an objective measure of anatomical damage that defines the course of the disease and the longterm effects of treatment. This review defines the rate of joint damage, progression in individual joints, and predictive factors. Six longitudinal prospective studies of 103-378 RA patients followed for up to 20 years show that initially patients had less than 3% maximum possible damage, this rose to 11% maximal damage by 5 years and over 40% by 20 years. The rate of progression changed from an initial rate of 1.6% maximal progression annually to a later rate of 2.0% annually. Between 1977 and 1998 5 prospective studies of 40-147 hospital-based RA cases seen within 12 months of developing RA showed 60-73% of cases developed one or more erosions in the hands and wrists. However a community-based cohort of early RA patients reported, more recently showed 41% of 335 cases developed erosions. There are marked differences between joints. The wrists show most damage and in one series of 103 cases, by 20 years 18% of wrists were completely destroyed and only 25% were nonerosive. The same series showed ankle joints are rarely involved; at 20 years only 7 patients had major abnormalities with minor changes in 17 cases. Rheumatoid factor (RF) positivity is the dominant predictor of erosive damage. In one survey of 439 cases who presented with inflammatory polyarthritis, patients with an initial high RF had over twice the radiographic progression of seronegative cases. A further 8 studies, which enrolled 1395 patients, all show a strong link between radiolographic damage and RF status. The other key clinical predictor is disease activity indicated by surrogate measures such as the C-reactive protein (CRP) level. Suppressing disease activity judged by CRP levels not only decreases the progression of joint damage, but also may reduce new joint involvement to a greater extent than progression in already damaged joints. New potential markers of damage such as anticyclic citrullinated peptide ELISA tests may further improve the identification of those RA patients most at risk of erosive damage and, by implication, most in need of suppressive therapy.

Arthritis, Rheumatoid↗
PubMed2005

Race-ethnic differences in the extent, prevalence, and progression of coronary calcium.

OBJECTIVE: To compare across four race-ethnic groups the baseline prevalence and extent of coronary calcium and the 7-year rate of progression in the extent of coronary calcium. DESIGN: The South Bay Heart Watch is a prospective cohort study designed to appraise the value of coronary calcium for predicting cardiovascular outcomes in asymptomatic adults with cardiac risk factors. Statistical analyses were conducted to evaluate ethnic differences in the prevalence, extent, and progression of coronary calcium among Caucasian, African-American, Hispanic, and Asian participants. SETTING: Population-based study. PATIENTS OR PARTICIPANTS: Between December 1990 and December 1992, 1289 participants without coronary heart disease underwent baseline risk factor screening and computed tomography for coronary calcification (Cohort 1). Seven years later, 828 (64%) participants returned for follow-up evaluation and re-scanning (Cohort 2). MAIN OUTCOME MEASURES: Prevalence, extent, and progression of coronary artery calcium. RESULTS: In Cohort 2, compared to Whites, African Americans had a lower prevalence of coronary calcium at baseline (P=.012) and follow-up (P=.005), smaller calcium scores at baseline (P=.005) and follow-up (P=.0004), and less progression (P=.001); Hispanics had a lower prevalence of coronary calcium at follow-up (P=.04) with smaller calcium scores (P=.011), and less progression (P=.009). In contrast, no differences were seen between Whites and Asian/Pacific Islanders. Race-ethnic differences in progression persisted after adjusting for risk factors and participation bias (P<.05). CONCLUSIONS: The present results lend further credence to the notion that race-ethnic differences exist in the prevalence and rate of progression of coronary calcification. The relationship between calcification and the incidence of coronary heart disease in these race-ethnic groups needs further exploration.

Aged↗
PubMed2005

Progression to renal failure.

Chronic renal failure is characterized by a persistently abnormal glomerular filtration rate. It represents a developing process that is initiated by various causes, all with the common end result of persistent and usually progressive damage of varying severity to the kidneys. Although the causes and the locations of renal insult may vary, many features are common in progression to renal failure, and the final histological picture is one of glomerulosclerosis, interstitial fibrosis and loss of renal cells, mainly by apoptosis. The rate of progression varies significantly. However, individual genetic variations and disease-specific mechanisms contribute to the variability in rates of progression and response to therapy. Possible mechanisms of progressive renal damage include hemodynamic factors, hypertension, proteinuria, angiotensin II, and other chemical mediators such as cytokines and growth factors. Processes and predictive factors of progression to renal failure are discussed here along with clinical practice guidelines: Evaluation, Classification and Stratification. Prevention of the progression is also briefly mentioned.

Adolescent↗
PubMedDate not supplied

[Diabetic retinopathy: twelve-year incidence and progression].

INTRODUCTION: Diabetic retinopathy (DR) it is the main cause of preventable blindness in productive-age adults. The rate of progression to blindness from DR differs among countries and populations. MATERIAL AND METHODS: In order to report the incidence and progression of DR after 12 years of follow-up in a cohort (n = 100) of adult patients with diabetes mellitus type 2 (DM2) in Leon, Guanajuato, Mexico, we designed an open population cohort study from April 1992 to July 2004. Main variables studied longitudinally were incidence and progression of DR, fasting blood glucose, glycated hemoglobin and associated clinical parameters. RESULTS: Mean age was 54 +/- (SD) 9.2 years and the time since DM2 diagnosis was 9 +/- 6 years. Incidence rates at 3, 6 and 12 years were 23, 48 and 71%, respectively; and for progression were 56, 70 and 74%, respectively. The 12-year proliferative DR incidence and progression were 14.3 and 32%, respectively. Mean fasting blood glucose levels were 193 mg/dL and for glycated hemoglobin 11%. Mortality was 45%, half attributable to acute myocardial infarction. DISCUSSION: Diabetic retinopathy in our population has a high incidence that doubled in 3 years, and has an accelerated progression toward more severe forms. Incidence and progression are higher than that reported in white non-Hispanics. It should be high priority in our country to (a) prevent diabetes mellitus, (b) improve its metabolic control, (c) establish RD diagnostic programs and (d) give appropriate treatment.

Adult↗
PubMed2006

[Clinical and radiological (PET, MRI) correlations depending on disease progression in patients with multiple sclerosis].

The aim of the study was to investigate the structural-functional changes in the cerebral gray matter (cortical and subcortical areas) of patients with multiple sclerosis (MS) depending on the disease severity. One hundred and seven patients (107) with definite diagnosis of MS (Mc Donald's criteria), aged 16-60 years, illness duration 1-30 years, and 21 healthy age-matched controls have been studied. Neurological assessment including Kurtzke and EDSS scales (range 0-8) was performed in all the patients. The patients and controls underwent MRI with a 1,5 imager and PET using 18F-flurodeoxyglucose (FDG). A type of the disease course was determined as remitting in 63 patients, primarily-progressive in 8, remitting progressive in 6 and secondary-progressive in 30. To analyze pathogenesis of the disease progression, the patients were divided into 3 clinical groups: (1) remitting (RRMS, n=63); (2) progressive (PRMS) with EDSS < or =6 (n=34); 3) PRMS with EDSS >6 (n=11). Along with the progression of MS from RRMS to PRMS and increasing of EDSS, the rCMRglu reduction of the cerebral gray matter developed from the supplementary motor cortex of a dominant hemisphere to the marked global reduction of cerebral metabolic rate in the PRMS group (EDSS >6). In the PRMS group with EDSS56, there was functional reorganization of cortical and subcortical areas compensatorily developing with the disease progression. In the PRMS group with EDSS >6, the data obtained did not support the evidence for the regional compensatory increase of rCMRglu in the same brain areas. Decompensation of the functional cortical reorganization in the PRMS group with EDSS >6 correlated with diffuse brain atrophy as well as with atrophy of the gray matter of the regional basal ganglia, first of all of the thalamus.

Adolescent↗
PubMed1995

Pre-transplant hypertension: a major risk factor for chronic progressive renal allograft dysfunction?

Despite of advances in 1-year survival rates of renal allografts, no comparable achievements have been made in long-term graft survival. To identify risk factors for chronic progressive renal allograft dysfunction we conducted a retrospective study in 639 patients transplanted between 1983 and 1990. Graft function was assessed by the slope of individual 1/creatinine regression lines and chronic progressive graft dysfunction was defined as a slope of the 1/creatinine line of > 0.1 dl/mg/year, indicating a loss of glomerular filtration rate of > 10 ml/min/year regardless of the initial serum creatinine value. A number of possible risk factors were determined and analysed by linear regression analysis. One hundred and six patients (16.6%) showed chronic progressive graft dysfunction. No correlation was found between the rate of functional deterioration and the age and gender of the donor or the recipient, the blood group, the prevalence of hepatitis B or C, the number of blood transfusions, the total ischaemia time, or the number of kidneys from female donors grafted into male recipients. Chronic progressive graft dysfunction was associated with the number of HLA-B/DR mismatches (P = 0.04) and with a first acute rejection episode later than 60 days after transplantation (P < 0.001). Chronic progressive graft dysfunction also occurred in the absence of an acute rejection episode. Significantly (P < 0.001) more patients with chronic progressive graft dysfunction were hypertensive not only 12 months after transplantation, but also at the time of transplantation, indicating that hypertension may not only be secondary to deteriorating graft function, but that hypertension per se leads to graft damage and initiates chronic progressive graft dysfunction. All efforts should be made to control blood pressure adequately to improve long-term survival of renal allografts.

Adult↗
PubMed1996

[Relation between progression of atherosclerosis and the phenomenon of restenosis after coronary angioplasty].

The authors undertook a retrospective study of medium-term coronary angiographic controls of a group (Gr) of patients (pts) who had undergone coronary angioplasty for rapidly progressive lesions, to determine whether the rate of progression of a coronary stenosis before angioplasty affected the risk of restenosis. 89 pts underwent primary angioplasty with absence of restenosis at 6 months, but required another angioplasty for another lesion. Angiographic follow-up after the 2nd procedure was performed in 86 pts (96%). The coronary lesion dilated at the 2nd angioplasty procedure was analysed quantitatively with four measurements: one immediately before angioplasty, one after, one at the 6 months control, and finally, one measurement 6 months before the angioplasty during the procedure on the 1st site. Multivariate statistical analysis showed that the only predictive factor of post-angioplasty loss in the general population was the immediate gain (F = 11.82; p < 0.005). On the other hand, no correlation was found between progression of the lesion before angioplasty and loss. The rapidly progressive nature of the lesion was defined with a threshold of 0.4 mm, corresponding to the variability of the quantitative angiographic system. Analysis of the procedure parameters showed a lower inflation pressure in the Gr with rapidly progressive lesions (6.58 +/- 21 atm vs 7.63 +/- 1.96 atm; p < 0.05). The immediate gain was significantly greater in the rapidly progressive lesion Gr (0.82 +/- 0.34 vs 0.67 +/- 0.29 mm; p = 0.05). The loss at the 6 months control was identical in the two Gr (0.31 +/- 0.50 vs 0.31 +/- 0.42 mm; p < 0.05). The loss/gain ratio was also comparable (0.37 +/- 0.76 vs 0.45 +/- 0.52; p > 0.05). These results show that rapidly progressive atherosclerosis does not increase the risk of post-angioplasty restenosis.

Aged↗
PubMed1997

The effect of thyroid hormone therapy on angiographic coronary artery disease progression.

OBJECTIVE: To study the effect of adequacy of thyroid hormone replacement therapy on coronary atherosclerosis. DESIGN: Retrospective cohort study of elderly hypothyroid patients with coexisting coronary artery disease. The association between the adequacy of thyroid replacement and the progression of angiographic coronary artery disease was investigated. Fisher's exact test was used for statistical analysis. SETTING: Coronary angiographies were performed at the Cardiac Catheterization Laboratory of the Victoria General Hospital, Halifax, Nova Scotia, the only tertiary referral centre for Nova Scotia and Prince Edward Island. Information about the past and current thyroid status of the subjects was collected from their family physicians. PATIENTS: Of 4103 patients admitted for coronary angiography during 1992 and 1993, 25 were on thyroid replacement therapy to treat hypothyroidism. Ten patients who underwent more than one coronary arteriography were selected (seven females and three males, mean age 65 +/- 10 years). RESULTS: Of five patients inadequately treated for hypothyroidism, all demonstrated angiographic evidence of coronary atherosclerosis progression. However, five of seven who were treated adequately did not show atherosclerosis progression (P = 0.02, OR = 0.72, 95% CI 1.36 to infinity). Decreasing or maintaining the dose of L-thyroxine at 100 micrograms or less resulted in coronary atherosclerosis progression in six of six patients, whereas five of six patients taking fixed or increasing doses of L-thyroxine 150 micrograms or higher were spared from disease progression (P = 0.015, OR = 0.41, 95% CI 2.4 to infinity). CONCLUSIONS: Angiographic coronary artery disease progression may be prevented by adequate thyroid replacement in hypothyroidism. With the help of modern, sensitive thyroid stimulating hormone assays higher doses of L-thyroxine may be safer and more effective in the atherosclerosis management of this patient population. Thyroid hormones can protect against atherosclerosis, presumably due to their metabolic affects on plaque progression.

Aged↗
PubMed1997

Mechanisms of progression in autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) progresses to end-stage renal insufficiency before the age of 73 in approximately 48% of affected individuals. Why the disease, characterized by innumerable cysts arising in proximal and distal tubules, eliminates functioning non-cystic parenchyma in some patients and spares other is a mystery. The cysts initiate in early childhood in fewer than 1% of renal tubules as a consequence of the focal expression of mutated DNA. Tubule cells proliferate, causing segmental dilation, in association with the abnormal deposition of extracellular matrix proteins. Most of the cysts separate from the parent tubules and fill with fluid by cAMP-mediated chloride secretion. Risk factors associated with accelerated loss of renal function include: genotype (PKD Type 1 progresses more rapidly than PKD Type 2); gender (males progress more rapidly than females); race (black patients progress more rapidly than whites); hypertension; proteinuria. The relation between kidney size and progression to renal failure is debated. Progressive PKD is associated with the cellular expression of proto-oncogenes (fos, myc, ras, erb), growth factors (EGF, HGF, acid and basic FGF), chemokines (MCP-1. osteopontin), metalloproteinases, and apoptotic markers, and the interstitial accumulation of Types I and IV collagen, laminin, fibronectin, macrophages and fibroblasts, the magnitudes of which increase with age. Cyst activating factor (CAF), a neutral lipid identified in cyst fluid that stimulates fluid secretion and proliferation of renal epithelial cells and monocyte chemotaxis, has recently been identified as a potential progression factor. In those patients destined to develop renal failure there is loss of non-cystic parenchyma in association with mass replacement by fluid-filled cysts in a network of interstitial fibrosis. The decline in renal function is probably the consequence of processes leading to interstitial fibrosis, as in other nephropathies, rather than due to simple mechanical displacement of parenchyma by cysts.

Disease Progression↗