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U. Larsson-Cohn, B. Tengström and L. Wide

ABSTRACT

Intravenous glucose tolerance tests and insulin determinations were performed on 37 women at different stages of the menstrual cycle and after one, three and twelve months of daily continuous treatment with 0.5 mg of norethindrone or 0.5 mg of chlormadinone acetate. The fasting blood glucose concentration, the k-values (percentage disappearance rate of glucose per minute) and the insulin response to glucose administration were compared. No statistically significant differences were found between the values obtained on two occasions before treatment, and during treatment.

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T. Bergh, S. J. Nillius, S.-G. Larsson and L. Wide

Abstract.

Twenty-eight women with hyperprolactinaemia and amenorrhoea received bromocriptine treatment which resulted in 31 term pregnancies. Bromocriptine treatment was stopped as soon as pregnancy was established. Nineteen of the women had radiological signs of a pituitary tumour. The pregnancies were clinically un-eventful in all cases except one who developed headache. Post-partum sellar X-ray showed pregnancy-induced enlargement of the pituitary fossa in 4 of the 28 women. Regression of the radiological changes occurred in 3 of the 4 women within 2 years after the delivery. The women with abnormal sellar X-rays had no difference in the mean prolactin levels before treatment and after pregnancy and lactation while all the women with normal sellae had lower prolactin levels after pregnancy than before. Three women resumed regular spontaneous menstruations after pregnancy and lactation but only one conceived again.

Thus, serious pituitary tumour complications are rare in hyperprolactinaemic women with bromocriptine-induced pregnancies. The pregnancy does not worsen the condition. Resolution of hyperprolactinaemia after bromocriptine-induced pregnancy is an unfrequent finding.

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K. Fuxe, K. Andersson, L.F. Agnati, L. Ferland and K. Larsson

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U. Larsson-Cohn, E. D. B. Johansson, L. Wide and C. Gemzell

ABSTRACT

Daily determinations of the plasma level of progesterone and the urinary excretion of luteinizing hormone (LH) and total oestrogens were performed in 6 subjects during one control cycle, immediately followed by three cycles of daily treatment with 0.5 mg of chlormadinone acetate continuously.

The control cycles were ovulatory according to the parameters investigated. Two of the women showed a normal LH excretion pattern in all treatment cycles. The four other subjects also had periodical variations in the LH excretion but no distinct midcycle peaks occurred. The mean oestrogen excretion was increased in all three treatment cycles but the difference was satistically significant only in the last two cycles.

Compared with the treatment cycles, the sum of progesterone values was significantly decreased in the first two cycles.

Chlormadinone acetate in this dose had no thermogenic effect. Three of the subjects showed bleeding irregularities which had no clear connection with the hormone variations measured in the study.

It is suggested that the low levels of progesterone might be due to a defective corpus luteum function.

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L Forsberg, A Villablanca, S Valimaki, F Farnebo, LO Farnebo, S Lagercrantz and C Larsson

BACKGROUND: Most patients who have been surgically treated for secondary hyperparathyroidism (HPT) harbor at least one pathological parathyroid gland with a tumor of monoclonal origin. OBJECTIVE: To elucidate the underlying genetic mechanisms behind secondary HPT, by studying a panel of such tumors for numerical alterations. METHODS: Sixteen parathyroid glands from eight patients (median age 58 years, range 31-74 years), were screened for numerical chromosomal imbalances, using comparative genomic hybridization (CGH). Mutation analysis of the multiple endocrine neoplasia type 1 gene (MEN1) was also performed by sequencing of the coding region. RESULTS: The results show that gross chromosomal alterations occur rarely in secondary HPT. In one of the three glands analyzed from one patient, a complete loss of chromosome 11 was detected. This gland also had an inactivating nonsense mutation, E469X, of the MEN1 gene. The mutation was present neither in the other two glands, nor in the constitutional tissue of the same patient, thus confirming its somatic origin. CONCLUSIONS: The relative lack of numerical chromosomal alterations would suggest that more discrete genetic alterations are responsible for the monoclonal growth in the majority of cases of secondary HPT. Furthermore, somatic inactivation of the MEN1 tumor suppressor gene contributes to the tumorigenesis in a small proportion of the cases.

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U. Larsson-Cohn, E. D. B. Johansson, L. Wide and C. Gemzell

ABSTRACT

Daily determinations of the plasma level of progesterone and the urinary excretion of LH, total oestrogens and pregnanediol were performed in 4 subjects during one control cycle, immediately followed for 2 or 3 months of daily treatment with 0.5 mg of norethindrone continuously.

The control cycles were ovulatory according to all the parameters investigated. During treatment the mid-cycle LH peak disappeared in all cases while the basal LH excretion showed considerable day to day variations. The excretion of total oestrogens was increased in all subjects but did not show the normal biphasic pattern. Periods of increased oestrogen excretion also appeared in the subjects with consistently low progesterone and pregnanediol levels during the treatment.

In two cases, all signs of luteal activity immediately disappeared after the commencement of treatment. The other cases had one and three periods of increased progesterone and pregnanediol levels respectively. However, these periods were shorter than those of the control cycles.

One of the subjects had regular menstrual bleeding while the other three had more or less irregular vaginal flows, often appearing during elevated but declining oestrogen excretion.

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UH Jansson, B Kristiansson, P Magnusson, L Larsson, K Albertsson-Wikland and R Bjarnason

OBJECTIVE: In children with coeliac disease, the ingestion of gluten causes small intestinal inflammation and a clinical picture of malabsorption, weight reduction and short stature. Decreased alkaline phosphatase (ALP) during gluten challenge was found in a previous study. ALP is a marker of bone formation and ALP activities are correlated with growth velocity. The aim of this study was to characterise the previously observed decrease of total ALP by investigating three specific bone ALP isoforms (bone/intestinal, B1 and B2) and three specific liver ALP isoforms (L1, L2 and L3) and, moreover, to correlate these ALP isoforms with other growth factors and growth markers. In addition, we also studied the association with possible weight changes, small intestinal mucosa inflammation, sex, age and gluten dose during gluten challenge. MATERIALS AND METHODS: Bone and liver ALP isoforms, IGF-I, IGF-binding protein (IGFBP)-3 and serum cross-linked carboxy-terminal telopeptide of type I collagen (ICTP) were measured together with change in weight and small intestinal mucosa histopathology in 54 children with earlier enteropathy who participated in a 4-week gluten challenge. RESULTS: We observed a decreased total ALP activity after 4 weeks of gluten challenge, 7.8+/-1.8 to 6.5+/-1.7 microkat/l (means +/- s.d.), which was mainly due to a reduction of the bone ALP isoforms. The sum of all three bone ALP isoforms decreased from 6.3+/-1.7 to 5.1+/-1.6 microkat/l. The decreased activities of the bone ALP isoforms correlated with the observed reductions of IGF-I (r=0.74, P<0.001), IGFBP-3 (r=0.51, P<0.001) and ICTP (r=0.57, P<0.001). The decrease of the growth factors and growth markers correlated with weight reduction, but when influences from the change in weight were adjusted for, the partial correlation of the small intestinal mucosa inflammation was significant for IGF-I (r=-0.56, P<0.001) and IGFBP-3 (r=-0.55, P<0.001). CONCLUSION: The decrease of total ALP was due to a reduction of bone ALP. The decrease of IGF-I and IGFBP-3 was independently correlated with weight change and small intestinal inflammation.

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T Frisk, F Farnebo, J Zedenius, L Grimelius, A Hoog, G Wallin and C Larsson

OBJECTIVE: Mutations in the RET proto-oncogene are found in about one third of sporadic medullary thyroid carcinomas (MTCs), mostly affecting codon 918. Glial cell line derived neurotropic factor (GDNF) and its membrane-bound GDNF family receptor alpha (GFRalpha-1), as well as neurturin (NTN) and its membrane-bound receptor GFRalpha-2 form a complex with the RET product, a receptor tyrosine kinase, resulting in downstream signaling to the nucleus. DESIGN: To elucidate the role of these RET ligands in MTC tumorigenesis, their expression was determined in 15 MTC samples, one papillary thyroid carcinoma (PTC) and three normal thyroid tissue specimens. METHODS: The mRNA expression of RET, GDNF, GFRalpha-1, NTN and GFRalpha-2 was investigated by mRNA in situ hybridization, and confirmed by reverse transcription-PCR analysis. RESULTS: None of the five genes was expressed in the normal thyroids or in the PTC. All MTCs showed expression of RET, 13 expressed GDNF, 12 expressed GFRalpha-1 and 9 expressed NTN and GFRalpha-2. In 7 of the tumors RET, GDNF and GFRalpha-1 were expressed at high levels, and in five of these seven tumors NTN and GFRalpha-2 genes were also expressed at high levels. The high level of expression was preferentially seen in tumor cells adjacent to stroma and connective tissue. All MTCs without expression of the RET ligands harbored the RET codon 918 mutation. CONCLUSIONS: The results suggest that this signaling pathway is important for MTC development, and that it may be activated by expression of the RET ligand complexes by the tumor cells themselves.