Cyclosporin and serum lipids in renal transplant recipients.
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Cyclosporine↗
Biomedical subjects
F Kronenberg
Publications and source records attributed to F Kronenberg.
Wegener's granulomatosis and Henoch-Schönlein purpura in a family with hereditary C4 deficiency.
Described here is a family in which the father with partial C4 deficiency had Wegener's granulomatosis and a son with complete C4 deficiency presented with Henoch-Schönlein Purpura. The possible role of C4 deficiency in the pathogenesis of both vasculitic disorders is discussed.
Adolescent↗
Women's health: new frontiers in rehabilitation medicine.
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Female↗
Elevated plasma concentrations of lipoprotein(a) in patients with end-stage renal disease are not related to the size polymorphism of apolipoprotein(a).
Patients with terminal renal insufficiency suffer from an increased incidence of atherosclerotic diseases. Elevated plasma concentrations of lipoprotein(a) [Lp(a)] have been established as a genetically controlled risk factor for these diseases. Variable alleles at the apo(a) gene locus determine to a large extent the Lp(a) concentration in the general population. In addition, other genetic and nongenetic factors also contribute to the plasma concentrations of Lp(a). We therefore investigated Apo(a) phenotypes and Lp(a) plasma concentrations in a large group of patients with end-stage renal disease (ESRD) and in a control group. Lp(a) concentrations were significantly elevated in ESRD patients (20.1 +/- 20.3 mg/dl) as compared with the controls (12.1 +/- 15.5 mg/dl, P < 0.001). However, no difference was found in apo(a) isoform frequency between the ESRD group and the controls. Interestingly, only patients with large size apo(a) isoforms exhibited two- to fourfold elevated levels of Lp(a), whereas the small-size isoforms had similar concentrations in ESRD patients and controls. Beside elevated Lp(a) concentrations, ESRD patients had lower levels of plasma cholesterol and apolipoprotein B. These results show that elevated Lp(a) plasma levels might significantly contribute to the risk for atherosclerotic diseases in ESRD. They further indicate that nongenetic factors related to renal insufficiency or other genes beside the apo(a) structural gene locus must be responsible for the high Lp(a) levels.
Adult↗
Hereditary complete deficiency of the fourth component of complement: effects on the kidney.
Hereditary complete C4 deficiency has until now been detected in 18 patients. A disturbed clearance of immune complexes probably predisposes these individuals to systemic lupus erythematosus and other immune complex diseases. Renal involvement of hereditary complete C4 deficiency is described in seven patients from three families. Three patients of one family suffered from SLE and a severe mesangial and endocapillary proliferative glomerulonephritis which required immunosuppressive treatment. In two patients from a second family a mild focal and segmental mesangioproliferative glomerulonephritis was present which, except for an episode of acute renal failure in one patient, did not cause serious clinical problems. One additional child died without renal involvement. The patient from a third family developed Henoch-Schoenlein purpura, mesangioproliferative glomerulonephritis with segmental scarring and terminal renal failure. Immunofluorescence studies showed deposition of immunoglobulins and complement C3 in the glomeruli. Severity of renal disease is probably determined by activation of the alternative pathway of complement in the kidney.
Adolescent↗
Effect of fever on menopausal hot flashes.
Some women report that they have fewer hot flashes when they have a fever. This is the first case of physiological monitoring of hot flashes during fever in a subject with a well documented pattern of frequent hot flashes when afebrile. During fever, there were fewer hot flashes than during afebrile periods, and these hot flashes also tended to be less intense. For most of the period of reduced hot flashes, internal (core) temperature was elevated, above 37.5 degrees C. When the fever broke, hot flashes resumed in a pattern similar to that of afebrile periods. Possible explanations for the reduction in hot flashes during a fever include: (1) a hot flash is triggered, but the characteristic physiological changes do not occur due to competing thermoregulatory drives, (2) the febrile core temperature inhibits whatever it is that triggers a hot flash; or (3) some product of the fever process inhibits the hot flash trigger or masks the physiological changes that occur during hot flashes.
Body Temperature↗
Gamma delta T lymphocytes in human glomerulonephritis.
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Glomerulonephritis↗
Recurrent abdominal pain caused by a toothpick in a CAPD patient.
A 27-year-old patient on CAPD presented with febrile illness and abdominal pain suggestive of peritonitis. Dialysis fluid culture yielded Enterococcus. Response to treatment was slow, with pain persisting. Laparotomy revealed a toothpick, which was causing peritoneal irritation. It was unclear how the foreign object entered the peritoneum.
Abdominal Pain↗
CAPD: a successful treatment in patients suffering from therapy-resistant congestive heart failure.
During the last six years 13 patients suffering from congestive heart failure (CHF), refractory to conventional medical treatment and classified class IV as defined by the New York Heart Association (NYHA), were treated with continuous ambulatory peritoneal dialysis (CAPD) (1) at Innsbruck University Hospital, Department of Internal Medicine. All patients required intensive care and were end-stage. The minimum observation period was six weeks, maximum 67 months. Cardiac recompensation was effected in all patients, who were stabilized in class II after NYHA. The patient with the shortest observation period of six weeks received an orthotopic heart transplant. None of the patients died of a CAPD-associated complication. All patients were restored to a normal life style without major dependence on outside help. The occurrence and treatment of the prerenal kidney failure that causes life-threatening problems in end-stage CHF should be subject to further study with regard to its clinical course and the determination of plasma-ANF, plasma-renin and plasma-aldosterone concentration.
Aldosterone↗
Hot flashes: epidemiology and physiology.
A review of the literature illustrates the many questions about hot flashes that remain unanswered. My survey addresses some of these questions. The prospective and retrospective descriptions of hot flashes provide a more detailed profile of the hot flash than has previously been available. Further, data from this survey demonstrate that while the patterns of hot flashes may be varied, there are commonalities in hot flash physiology and subjective manifestation. The data indicate that hot flashes may start much earlier and continue far longer than is commonly recognized by physicians or acknowledged in textbooks of gynecology. Studies of hot flash duration must control for age or age at hot flash onset, since the older the subjects, the more potential years of hot flashes and the greater the probability of encompassing the entire period of hot flashes. Hot flashes are not static; patterns may change with time. For some women, hot flashes become less frequent and less intense; for others, hot flashes may continue at hourly intervals well into old age. How common these experiences are for women of all ages still needs to be discovered. As expounded by Kaufert, McKinlay, Goodman, and many others, a greater effort must be made to standardize definitions and question formats as well as to improve methodology in epidemiologic investigations to facilitate comparability between studies and insure that proffered conclusions indeed reflect the questions being asked. Physiological studies are critical counterparts to the epidemiology; yet such studies have been too few. My work, by examining the physiology and psychophysiology of hot flashes, has raised additional questions about central and peripheral inputs that may affect the subjective experience of hot flashes. A more complete understanding of the thermoregulatory, cardiovascular, and psychophysiology of women with hot flashes are compared to women without will facilitate the prediction of who is most likely to be affected and the identification of additional approaches to the management of hot flashes.
Adult↗
Thermoregulatory physiology of menopausal hot flashes: a review.
Hot flashes during the climacteric years have long been a frequent clinical complaint, generally considered within the realm of the internist, gynecologist, or endocrinologist. Yet the underlying mechanism of hot flashes remains unknown. Only within the past 10 years has there been significant research on hot flashes as a disturbance of thermoregulation. This paper focuses on thermoregulatory aspects of hot flashes, reviewing current knowledge of the thermoregulatory physiology and endocrinology of hot flashes and discussing future avenues for research. Hot flashes are compared with fever in terms of thermoregulatory changes and speculated mechanisms. Although several substances in the peripheral circulation are found in increased concentrations during hot flashes, none is a trigger for a hot flash. The pattern of hot flash occurrence is striking in its regularity, and the possibility of endogenous rhythmicity is discussed. Recently, investigators have begun to explore a primate model of menopausal hot flashes. These studies are summarized. Finally, the multiple effects of estrogen on various systems of the body and their interrelationships are discussed. An understanding of the mechanism of hot flashes would not only be of importance to women suffering with hot flashes but would further our knowledge of thermoregulatory function and the interactions between thermoregulatory and reproductive systems.
Body Temperature↗
Changes in neurotensin-like immunoreactivity during menopausal hot flashes.
An elevation of plasma immunoreactive neurotensin (iNT) was found during menopausal hot flashes. The flash-associated increases in iNT were concomitant with several physiological changes, including increased heart rate, finger blood flow, and finger temperature. Plasma iNT during hot flashes increased 245 +/- 65% (+/- SEM; n = 41), peaking 3.6 +/- 0.4 min after the onset of the hot flash. Immunochemical and chromatographic analyses indicated that the components of iNT elevated during a hot flash consisted primarily of C-terminal-related variants of NT, but not NT itself or any of its known metabolites. The three major substances identified using high pressure liquid chromatography and a C-terminal-directed RIA that appeared in women with hot flashes were also present in plasma of women without hot flashes and men. Since NT is a vasoactive and cardioactive peptide that can also affect temperature regulation, our results suggest the active involvement of these variants of NT in hot flashes.
Adult↗
Menopausal hot flashes: thermoregulatory, cardiovascular, and circulating catecholamine and LH changes.
Thermoregulatory, cardiovascular and endocrine changes were simultaneously monitored in 11 post-menopausal women with frequent hot flashes (catecholamine and LH levels were measured in 5 and 6 subjects respectively). Plasma samples were obtained at 1- and 5-min intervals. Hot flashes were accompanied by abrupt increases in plasma epinephrine (about 150%) and concomitant decreases in norepinephrine (about 40%). Increased luteinizing hormone was associated with most hot flashes. A detailed sequence of hot flash-associated changes was established. An aura preceded the onset of the hot flash by several seconds. HR and FBF increased just before the onset of the flash and reached peak levels of 10-20 beats/min and 30-fold respectively. Coincident with vasodilation and sweating, finger temperature increased an average of 3.9 degrees C and esophageal temperature fell 0.2-0.6 degrees C. Flashes of both discrete and prolonged intervals were observed. Sensation was a reliable index of flash occurrence and intensity as measured physiologically. Our observations are consistent with the hypothesis that hot flashes are due to a change in the thermoregulatory set point. Furthermore, the changes in catecholamine levels are consistent with the cardiovascular changes accompanying hot flashes.
Body Temperature Regulation↗
Hot flashes: phenomenology, quality of life, and search for treatment options.
Menopausal hot flashes are a significant problem for women. Hot flashes can impact on daily functioning, particularly when they disrupt sleep, leading to fatigue and irritability during the day. However, our knowledge about this primary complaint of menopausal women is far from complete. It is known that a hot flash is associated with thermoregulatory, cardiovascular, and endocrine changes. However, much is unknown about the phenomenology of hot flashes, such as the range of variability in the pattern and longitudinal course of hot flashes. Although estrogen plays a role in the etiology of hot flashes, the mechanism by which its withdrawal precipitates hot flashes and its replacement relieves them is not understood. Nor do we know what it is that triggers individual hot flash episodes. We are beginning to learn about factors, such as ambient temperature, that modulate the frequency of severity of hot flashes. And very new data suggest that the ingestion of certain foods may influence hot flashes via estrogenic substances present in the food plants. Although there is much anecdotal information about herbs and other nonconventional remedies, little or no research had been done to assess the efficacy or safety of these methods for the treatment of hot flashes. An immediate focus on some of the most promising of these therapies could broaden the available treatment options and should provide new insights into the mechanism underlying hot flashes.
Behavior Therapy↗