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Dive into the research topics where Birgitta Bülow is active.

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Featured researches published by Birgitta Bülow.


Clinical Endocrinology | 1997

Increased cerebrovascular mortality in patients with hypopituitarism

Birgitta Bülow; Lars Hagmar; Zoli Mikoczy; Carl-Henrik Nordström; Eva Marie Erfurth

OBJECTIVE An increased prevalence of atherosclerosis has been shown among patients with hypopituitarism. The aim of the present study was to assess whether patients with hypopituitarism experience increased cardiovascular, in particular cerebrovascular, mortality.


Journal of Internal Medicine | 2002

Adrenal incidentaloma - experience of a standardized diagnostic programme in the Swedish prospective study.

Birgitta Bülow; Bo Ahrén

Abstract  Bülow B, Ahrén B (Lund University, Lund, Sweden) on behalf of the Swedish Research Council Study Group of Endocrine Abdominal Tumours. Adrenal incidentaloma – experience of a standardized diagnostic programme in the Swedish prospective study. J Intern Med 2002; 252: 239–246.


Clinical Endocrinology | 2002

High incidence of mental disorders, reduced mental well-being and cognitive function in hypopituitary women with GH deficiency treated for pituitary disease

Birgitta Bülow; Lars Hagmar; Palle Örbaek; Kai Österberg; Eva Marie Erfurth

objective Previous studies have shown possible neuroendocrine effects of GH. In the present study we investigated the incidence of mental disorders and the prevalence of mental distress and cognitive dysfunction in hypopituitary women with untreated GH deficiency compared to population‐based controls.


Clinical Endocrinology | 2001

Is there an increase in second brain tumours after surgery and irradiation for a pituitary tumour

Eva Marie Erfurth; Birgitta Bülow; Zoli Mikoczy; Gudrun Svahn-Tapper; Lars Hagmar

OBJECTIVE To assess the incidence of second brain tumours in patients operated and irradiated for pituitary tumours.


Clinical Endocrinology | 1999

A low individualized GH dose in young patients with childhood onset GH deficiency normalized serum IGF‐I without significant deterioration in glucose tolerance

Birgitta Bülow; Eva Marie Erfurth

Many GH deficient (GHD) patients have impaired glucose tolerance and GH substitution in these patients has caused deleterious effects on glucose tolerance with hyperinsulinaemia. This further impairment of glucose tolerance might be due to an unphysiologically high dose of GH. Whether such a deterioration can be avoided by an optimal GH replacement dose is not known. In most previous studies, the GH dose was calculated according to body weight or body surface area and not adjusted according to the serum IGF‐I response.


Clinical Endocrinology | 2004

Survivors of childhood acute lymphoblastic leukaemia, with radiation‐induced GH deficiency, exhibit hyperleptinaemia and impaired insulin sensitivity, unaffected by 12 months of GH treatment

Birgitta Bülow; Katarina Link; Bo Ahrén; Ann-Sofie Nilsson; Eva Marie Erfurth

OBJECTIVE  Adult survivors of childhood acute lymphoblastic leukaemia (ALL) often exhibit GH deficiency (GHD), due to prophylactic cranial radiotherapy (CRT). It is not known whether the observed risk for adiposity in these patients is associated with impaired insulin sensitivity and whether the insulin sensitivity is affected by GH replacement therapy.


Clinical Endocrinology | 2001

Low individualized growth hormone (GH) dose increased renal and cardiac growth in young adults with childhood onset GH deficiency

Katarina Link; Birgitta Bülow; Kerstin Westman; Eva Cecilia Salmonsson; Jan Eskilsson; Eva Marie Erfurth

OBJECTIVE In childhood onset GH deficiency (GHD) a reduction in left ventricular mass (LV‐mass) and impairment of systolic function as well an impairment in glomerular filtration rate (GFR) has been shown. The aim of the present study was to assess if a low GH dose resulted in an improvement in morphological and functional parameters of these organs.


The Lancet | 2001

Premature mortality and hypopituitarism

Eva Marie Erfurth; Bengt Åke Bengtsson; Jens Sandahl Christiansen; Birgitta Bülow; Lars Hagmar

thereafter allocate observation time to the latter category. Tomlinson and colleagues emphasise that a drawback with the previous cohort studies is that they compare small numbers of patients. We think that they have misunderstood this issue. They have based their analyses on 181 dead patients (18% of the cohort), whereas the analysis in one of the Swedish cohorts 3 was based on 188 (55%) dead patients. Thus, the statistical power was similar in the two studies. The discrepancy in proportion of diseased patients is due to differences in calendar year for start of observation and length of follow-up. Moreover, we are surprised that Tomlinson and colleagues discuss their finding that patients with craniopharyngioma have an especially poor survival prognosis without mentioning the original finding made in one of the Swedish cohorts.


Clinical Endocrinology | 2003

The gender differences in growth hormone-binding protein and leptin persist in 80-year-old men and women and is not caused by sex hormones.

Birgitta Bülow; Bo Ahrén; S Fisker; Ove Dehlin; Elmo Jensen; Torbjörn Svensson; Gillis Samuelsson; Eva Marie Erfurth

objective  Leptin and growth hormone‐binding protein (GHBP) both show gender differences that might be explained by sex hormones. To study the potential relevance of oestradiol and testosterone, we have examined 80‐year‐old subjects in whom oestradiol is higher in men than in women. The interrelationships between leptin, insulin, GHBP and fat mass in this age group were also investigated.


Metabolism-clinical and Experimental | 1999

Individualized low-dose growth hormone (GH) treatment in GH-deficient adults with childhood-onset disease: Metabolic effects during fasting and hypoglycemia

Birgitta Bülow; Carl-David Agardh; Bodil Eckert; Eva Marie Erfurth

Growth hormone (GH) has insulin-antagonistic effects, and GH secretion is augmented during fasting and hypoglycemia. In the present study, 10 patients aged 21 to 28 years with childhood-onset GH deficiency (GHD) were studied during a 24-hour fast and a hypoglycemic glucose clamp before and after 9 months of GH replacement. During the 24-hour fast, blood glucose, serum insulin, and serum free fatty acid (FFA) levels were measured. In the hypoglycemic clamp, the counterregulatory hormones (plasma catecholamines, serum glucagon, and serum cortisol), serum insulin-like growth factor (IGF) binding protein-1 (IGFBP-1), serum FFA, and glucose uptake were measured. The GH dose was adjusted to the response of serum IGF-I, and the median GH dose was 0.14 IU/kg/wk (range, 0.08 to 0.19). At the end of the study, serum IGF-I levels were normalized in all but one patient, in whom serum IGF-I was above the normal range. Nine months of GH treatment did not cause any significant changes in the blood glucose level, insulin to glucose ratio, or serum FFA level during the 24-hour fast, and none of the patients experienced hypoglycemia either before or after GH treatment. However, GH therapy resulted in increased insulin resistance during hypoglycemia, without changes in the counterregulatory hormonal responses, serum IGFBP-1, or serum FFA.

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Bo Wängberg

University of Gothenburg

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