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At least 181 records · Page 10Linked to original sources
PubMed1988

Chronic progressive myelopathy: its relation to the spinal progressive form of multiple sclerosis.

The causes and clinical features of chronic progressive myelopathy (CPM) were evaluated in a retrospective study of 107 patients. A special emphasis was put on those in whom no underlying cause for the myelopathy could be determined. Of 76 such, 39 (51%) had oligoclonal immunoglobulins (Ig) in the CSF and were therefore considered as possible MS, while the remainder, without oligoclonal Ig, were designated "myelopathy of unknown origin" (MUO). Our "possible MS" group was similar clinically to reported series of proven spinal MS, and it seems therefore, that the presence of oligoclonal Ig permits the recognition of a group of patients with myelopathy who might be at a greater risk for MS. Patients with MUO differed from possible MS patients in several clinical characteristics, but most significantly in disease course and levels of functional disability which were more benign in the former. Myelopathy in possible MS patients was also of a primary pyramidal and asymmetrical nature. It is therefore suggested that the segregation of patients with CPM of undetermined origin into 2 separate groups based on the presence or absence of oligoclonal Ig might be of prognostic significance.

Adult↗
PubMed1988

T cell subsets and disease progression after total lymphoid irradiation in chronic progressive multiple sclerosis.

T lymphocyte subset percentages were determined in 16 total lymphoid irradiation (TLI) treated and 18 sham treated control patients with chronic progressive multiple sclerosis. During the first year after treatment, the ratio of T helper/inducer to T suppressor/cytotoxic cells (Th/Ts ratio) was significantly higher in sham treated multiple sclerosis patients who worsened clinically compared with TLI treated and sham treated multiple sclerosis patients who remained clinically stable. TLI caused a fall in the percentage of T helper cells in treated patients, while the percentage of T suppressor cells remained stable during the first year after treatment. In contrast, the percentage of T suppressor cells fell in sham treated multiple sclerosis patients who worsened clinically.

Follow-Up Studies↗
PubMed1986

Progression of membranous nephropathy to acute crescentic rapidly progressive glomerulonephritis and response to pulse methylprednisolone.

There have been only sporadic reports of membranous nephropathy (MN) evolving into acute crescentic rapidly progressive glomerulonephritis (AC-RPGN). A patient with MN developed acute oliguric renal failure with a serum creatinine (SCr) of 8.4 mg/dl after 5 years of normal renal function. Biopsy now revealed epithelial crescent formation superimposed on MN. Pulse methylprednisolone resulted in significant improvement in renal function, with a SCr of 2.2 mg/dl at 6 months. No other favorable outcomes occurred in the 4 previous case reports of MN evolving into RPGN. AC-RPGN should be considered a treatable etiology of acute renal failure in the setting of MN.

Acute Kidney Injury↗
PubMed1978

Scleroderma (progressive systemic sclerosis): progress and course based on a personal series of 118 cases.

A follow-up study has been made of a personal series of 118 cases of patients with scleroderma (progressive systemic sclerosis) followed for periods up to 25 years. These were classified according to the early distribution of skin changes as Type 1 (skin changes in fingers only), 48 cases; Type 2 (skin changes beyond the fingers but mainly in extremities), 47 cases; and Type 3 (diffuse), 19 cases, and atypical, four cases. Eighty per cent of the total series have survived five years, and 68% have survived 10 years. Survival is related to the type of scleroderma, being much better for Types 1 and 2 (acrosclerotic) than for Type 3 (diffuse). Actual compared with expected survival rate was better for younger than for older patients and for females than for males. Although the disease type gives an indication of survival in general, the caution must be used in the individual cases, as the course of the disease is very variable even in patients of the same type, and is subject to remission and relapse.

Adolescent↗
PubMed1992

B cell deficiency progresses with lineage maturation in nude.X-linked immunodeficient mice B cell deficiency progresses with lineage maturation.

Previously we showed that unlike normal, nude, or X-linked immune deficient (xid) mice, nude.xid mice are deficient in bone marrow pre-B cell targets for Abelson murine leukemia virus transformation. We show that nude.xid bone marrow is deficient in both CD45(B220)+ and CD45(B220)- surface (s)IgM- progenitors that give rise to B cell colonies in Whitlock-Witte cultures. CD45(B220)+ precursors had normal differentiation potential in vitro. CD45(B220)- precursors differentiated into CD45(B220)+ cells at the same rate as normal controls, but acquired sIgM at a much slower rate. These results correlated with the observation that in nude.xid mice the severity of B lineage defects correlates with maturity: a profound (ninefold) deficit of sIgM+, CD45(B220)+ mature B cells, a fivefold deficit in the sIgM-, CD45(B220)+ precursors of short term B cell colonies (colonies forming within 4-5 days in Whitlock-Witte cultures), and a moderate (twofold) decrease in the frequency of sIgM-, CD45(B220)- (less mature) precursors of long term B cell colonies (colonies forming after 14 days of Whitlock-Witte culture. Thus the combination of the nude and xid mutations produces a deficiency in early B cell progenitors and the deficiency becomes more profound with further maturation. Therefore the lack of mature B cells is the result of a cascade effect. Inasmuch as bone marrow progenitors are affected, and these are the source of the vast majority of B cells, most B cells are affected by the xid mutation and the xid defect cannot be attributed to a loss of a fetal lineage of B cells. These results suggest that xid affected cells lack the capacity to progress efficiently through differentiation in the absence of an exogenous factor(s) that is dependent on the product of a normal allele at the nude locus. This product might be supplied in vivo by a T cell or T cell-dependent source and/or epithelial elements such as bone marrow stromal cells all of which are known to be affected by the nude mutation.

Animals↗
PubMedDate not supplied

[Progressive pseudorheumatoid arthropathy in childhood (late spondylo-epiphysial dysplasia with progressive arthropathy). Description of a case].

The progressive pseudorheumatoid arthropathy of childhood is a very rare disorder that follows an autosomal recessive mode of inheritance, and which can be framed in the group of the spondyloepiphyseal dysplasia tarda. This affection is characterized by specific radiological anomalies and by clinical signs resembling an inflammatory disease, with the normality of the routine laboratory studies. The authors describe a case recently come to their attention.

Arthritis, Rheumatoid↗
PubMed1979

[Problem of progression in schizophrenia. I. Problem of progression of attack-like forms].

A total of 552 patients with attack-like schizophrenia, who attained old age were examined clinically. It was established that the development of negative changes in such patients occurs predominantly during the first half of life. Subsequently not all patients demonstrate a progressive development of the disease and even if it does occur it is seen in the form of more frequent or longer attacks and a complication of psychopathological disorders. At the same time there is a certain correlation between the clinical picture of the attacks and the severity of deficitary changes. A reverse development of some personality changes in long-term remissions in old age are described.

Adult↗
PubMed1995

PROGRESS (perindopril protection against recurrent stroke study): rationale and design. PROGRESS Management Committee [corrected].

RATIONALE: Patients with a history of cerebrovascular disease have a very high risk of stroke, and usual levels of both systolic and diastolic blood pressure are directly and continuously associated with this risk. Trials of blood pressure lowering in patients with transient ischaemic attacks or stroke have been too small to reliably detect the effects on stroke risk of the modest blood pressure reductions achieved. OBJECTIVES: The primary objective of PROGRESS is to determine precisely the effects of blood pressure reduction with an angiotensin converting enzyme (ACE) inhibitor-based regimen on the stroke risk in patients with a history of transient ischaemic attacks or minor stroke. DESIGN: The study is a randomized, double-blind, placebo-controlled clinical trial. Before randomization, there is a 4-week run-in phase on open-label ACE inhibitor treatment. The scheduled duration of treatment and follow-up is 4-5 years. SETTING: The study will be conducted in collaborating clinical centres in Australia, Belgium, the People's Republic of China, France, Italy, Japan, New Zealand, Sweden and the United Kingdom. PATIENTS: The study will involve 6000 patients with a history of transient ischaemic attacks or stroke (ischaemic or haemorrhagic) in the past 5 years. To be eligible patients should have no definite indication for or contra-indication to treatment with an ACE inhibitor and no disability likely to prevent regular attendance at study clinics. INTERVENTIONS: Study treatment will comprise perindopril and indapamide or matching placebos for patients without an indication for or contra-indication to treatment with a diuretic, perindopril alone or matching placebo for all other patients. STUDY OUTCOMES: The primary study outcome is total strokes and secondary outcomes include fatal or disabling strokes, total major cardiovascular events, cardiovascular deaths, cognitive function and dementia, and disability and dependency.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Effects of perindopril-based blood pressure lowering and of patient characteristics on the progression of silent brain infarct: the Perindopril Protection against Recurrent Stroke Study (PROGRESS) CT Substudy in Japan.

Controversy persists as to whether reducing the blood pressure of patients with a history of stroke leads to an increased risk of silent brain infarct (SBI) and dementia. A total of 667 patients were randomized to receive the angiotensin-converting enzyme (ACE) inhibitor perindopril (4 mg daily), with or without the diuretic indapamide (2 mg daily) or matching placebo(s). Brain CT scanning was performed annually over the mean follow-up period of 3.9 years. Active treatment reduced the blood pressure (systolic/diastolic) by 5.2/2.6 mmHg over the follow-up period. A total of 119 new SBI were detected and 92% of them were lacunar type small infarcts. The frequency of reaching the primary end-point (recurrent symptomatic stroke or new SBI) was similar in the placebo group (26.5%) and in the active treatment group (25.9%). There was no significant difference in brain atrophy indices between two groups. In the subgroup with a history of large artery infarction, 7 out of 55 patients from the placebo group developed new SBI, while none of the 40 patients from the active treatment group did so (p = 0.020). The baseline diastolic blood pressure was significantly associated with the risk of new SBI (p = 0.004), but the stroke subtype was not. In conclusion, blood pressure-lowering with a perindopril-based regimen did not increase the risk of SBI and brain atrophy in patients with a history of stroke. The baseline diastolic blood pressure was an independent predictor of new SBI, but the index stroke subtype did not influence the risk of SBI.

Aged↗
PubMed1995

Glomerular thrombosis predicts progression of glomerulonephritis: can we prevent progression?

The evidence for the important role of coagulation in the genesis and perpetuation of glomerular injury in diffuse proliferative lupus glomerulonephritis is reviewed. The importance of early detection is emphasized, so that treatment can be started before irreversible glomerular injury has occurred. Urinalysis and simple tests of renal function are effective means of early detection.

Biopsy↗