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Biomedical subjects

J Orav

Publications and source records attributed to J Orav.

10 recordsLinked to original sources
PubMed1992

Both hyper- and hypogonadotropic hypogonadism occur transiently in acute illness: bio- and immunoactive gonadotropins.

Previous reports of hypogonadotropic hypogonadism in critically ill men may not reflect the complexity of changes in the hypothalamic-pituitary-gonadal (HPG) axis during acute illness. We sampled blood throughout hospitalization in 55 men admitted to acute care units to delineate the spectrum of changes in circulating gonadotropin and sex steroid levels at the onset and during recovery from acute illness. Bioactive LH and FSH were measured in a subset of patients. Percent free testosterone was measured to assess changes in binding to sex hormone binding globulin. Medications and serum estrogen and prolactin levels were monitored as potential causes of hypogonadotropism. Sustained suppression of serum testosterone levels below the normal range occurred in 62% of men with varying diagnoses and disease severity. Percent free testosterone remained constant. Hypogonadotropism was observed in most men (60%) and occurred independently from head injury, surgery, medications, or hyperprolactinemia. In a subset of men (n = 16), LH and/or FSH rose transiently above the normal range. Bioactivity of both LH and FSH remained constant while serum testosterone levels decreased. In contrast to serum testosterone levels, mean serum levels of E1, E2 and androstenedione were not less than control values. We conclude that both primary and secondary hypogonadism occur transiently in acutely ill men and cannot be explained solely by medications, hyperprolactinemia, or hyperestrogenemia. Neither biopotency of gonadotropins nor binding of testosterone to SHBG change across the course of acute illness. The hypogonadism, often severe and prolonged, may contribute to the persistent catabolic state observed in many critically ill patients.

Acute Disease↗
PubMed1991

Immunologic effects of cyclophosphamide/ACTH in patients with chronic progressive multiple sclerosis.

We examined immune function and changes in T cell populations over a 1-year period in a series of progressive multiple sclerosis (MS) patients treated with different regimens of cyclophosphamide/ACTH as part of the Northeast Multiple Sclerosis Treatment Group. Our studies were designed to determine the effect of different cyclophosphamide/ACTH regimens on T cell populations and functional immune assays and to determine whether immune measures could be identified to predict which patients responded favorably to treatment. Cyclophosphamide/ACTH infusions significantly decreased the proportion of peripheral blood CD4+ T cells at 2, 6 and 12 months following treatment while there was a tendency for increased CD8 expression. This was associated with significant decreases of CD4/CD8 ratios at 2, 6 and 12 months following treatment compared to pretreatment. No changes in CD3+ T cells were observed while there were increased percentages of CDw26 (Ta1) positive and IL-2 positive T cells following treatment. The only T cell populations predictive of improvement were percentages of either CD3+ or CD4+ cells where increased percentages of either these populations at 2 months following cyclophosphamide/ACTH infusions were associated with improvement at both 6 and 12 months. In terms of functional immune measures, we found that cyclophosphamide/ACTH treatment decreased the level of proliferation in the allogeneic mixed lymphocyte reaction (MLR) at 2 months and of spontaneous proliferation of mononuclear cells at 12 months following therapy. Changes in spontaneous proliferation were predictive of clinical improvement at 12 months in that subjects with improved scores on the disability status scale (DSS) had decreases in spontaneous proliferation at 12 months as compared to pretreatment, whereas those stable or worse did not change significantly. Thus, our studies have demonstrated specific alterations in immune function following immunosuppression with cyclophosphamide/ACTH and suggest that certain immune measures may be linked to a positive clinical response and thus associated with disease progression in MS.

Adrenocorticotropic Hormone↗
PubMed1991

Effects of asymptomatic ischemia on long-term prognosis in chronic stable coronary disease.

BACKGROUND: Ischemia on ambulatory electrocardiographic monitoring has been shown to adversely affect short-term prognoses in patients with unstable angina, after myocardial infarction, and with chronic stable angina. METHODS AND RESULTS: In this long-term study, we followed 138 patients (mean age, 59 +/- 9 years) with chronic stable angina and positive exercise tests for cardiac events (e.g. death, myocardial infarction, percutaneous transluminal coronary angioplasty, or coronary artery bypass graft surgery). In 105 patients, ambulatory electrocardiographic monitoring was performed after all antianginal medication was withheld for 48 hours. In 26 patients, the diagnostic tests were repeated while on their usual medication. In addition to the 105 patients, 33 patients had their monitoring performed only while on their usual medication. During 37 +/- 17 months of follow-up, there were nine deaths, nine myocardial infarctions, and 35 revascularization procedures. In patients monitored off medication, Cox survival analysis showed that the occurrence of ischemia on electrocardiographic monitoring was the most significant predictor of death and myocardial infarction in the subsequent 2 years (p = 0.02) and all adverse events for 5 years (p = 0.009). Patients who were monitored on medication and did not have ischemia (n = 18) appeared to have more adverse events than patients who had no ischemia while being monitored off medication (n = 43). CONCLUSIONS: Asymptomatic ischemia on ambulatory electrocardiographic monitoring in patients with stable angina predicts death and myocardial infarction for 2 years and all adverse events for 5 years. Monitoring performed while on medication may show no ischemia; however, this may not indicate low risk of future coronary events.

Actuarial Analysis↗
PubMed1990

Memory impairment in multiple sclerosis.

We compared the performance of 50 multiple sclerosis (MS) patients and 35 normal controls on a variety of memory tasks to determine the nature and severity of memory deficits in the MS patients and the proportion of patients affected. We also determined the relationship between memory and other cognitive functions, demographic factors, disease characteristics, depression, and psychoactive medication. We found significant differences between patients and controls on almost all memory tests. Patterns of learning, effects of interference, and improvement with cuing were similar for both groups. Thirty percent of patients showed severe memory impairment, 30% were moderately impaired, and 40% were mildly or not impaired. Memory dysfunction was related to impairment of other cognitive functions, lower socioeconomic status, chronic progressive type of MS, and use of antianxiety medication, but not to severity of disability, duration of MS symptoms or depression.

Adult↗
PubMed1988

Hypomanic reactions to ACTH and prednisone treatment for multiple sclerosis.

Nine of 50 MS patients became hypomanic or manic during treatment with ACTH or prednisone. Symptoms did not occur with every drug exposure and were more common with ACTH. Patients at risk were identified by episodes of major depression before and after the onset of MS and by family histories of depression or alcoholism.

Adrenocorticotropic Hormone↗
PubMed1988

Immunosuppression with high-dose i.v. cyclophosphamide and ACTH in progressive multiple sclerosis: cumulative 6-year experience in 164 patients.

One hundred sixty-four patients with chronic progressive multiple sclerosis (MS) have been treated with a regimen of high-dose IV cyclophosphamide and ACTH over the past 6 years. Their status was reviewed to determine complications associated with treatment, dosage of medication used to induce a remission, factors which may predict a response to therapy, and subsequent course following treatment. One year following initial treatment, 81% of patients were improved or stabilized. Reprogression occurred in 69% of patients at a mean time of 17.6 months. Fifty-eight patients who initially stabilized after treatment and then reprogressed were treated a second time. One year after retreatment, 70% of these patients were improved or stabilized. Alopecia, nausea and vomiting, and minor infections were the most frequent complications. There were no deaths associated with treatment, the complication rate did not change with multiple treatments, and no late complications have yet been observed. Improvement tended to occur in younger patients with shorter disease duration. Although this treatment regimen is generally well tolerated and can favorably affect the course of chronic progressive MS in a majority of patients, a single treatment does not induce a permanent remission, and some form of maintenance treatment or retreatment is required. Current treatment programs involve testing a modified induction regimen and periodic outpatient booster injections to maintain remission.

Adrenocorticotropic Hormone↗
PubMed1987

Depression in multiple sclerosis.

Standardized interview techniques, diagnostic criteria, and rating scales were used to assess 50 moderately disabled multiple sclerosis (MS) patients. Fifty-four percent met lifetime Research Diagnostic Criteria for major depression, with a significant increase in the rate from before to after the onset of MS symptoms. The MS patients were significantly more depressed than other medical patients described in the literature. Major depressions were associated with steroid-treated exacerbations and a history of major depression. Symptoms of depression may be easily confused with those of MS, resulting in inadequate diagnosis and treatment.

Adult↗