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Biomedical subjects

Johan Svensson

Publications and source records attributed to Johan Svensson.

28 records · Page 2Linked to original sources
PubMed2004

Intrauterine exposure to maternal enterovirus infection as a risk factor for development of autoimmune thyroiditis during childhood and adolescence.

Maternal intrauterine enterovirus infection during pregnancy increases the risk for the offspring to develop type 1 diabetes mellitus. Type 1 diabetes mellitus and autoimmune thyroiditits (AIT) are closely linked. A common pathogenetic factor is possible. The objective of this study was to investigate a possible association between maternal enterovirus infection during pregnancy and the development of AIT in the offspring. Sera taken at delivery from 31 mothers whose children subsequently developed AIT was analyzed for immunoglobulin (Ig)A, IgG, and IgM antibodies against enterovirus, and compared to a control group comprising 233 randomly selected maternal sera. Of the mothers whose children developed AIT, 5 of 31 (16%) were enterovirus IgM-positive, compared to 17 of 233 (7%) in the control group (p = 0.16). The age at diagnosis of AIT was significantly lower in the group of children with IgM-positive mothers compared to children with IgM-negative mothers (p < 0.05). In addition, 3 children (60%) in the IgM-positive group were overtly hypothyroid at diagnosis of AIT, compared to no child (0%) in the IgM-negative group (p < 0.01). No significant differences were found in IgA and IgG antibody titers between the mothers whose children developed AIT and the control group. Although this study did not have enough power to reveal intrauterine exposure to maternal enterovirus infection during pregnancy as a risk factor for development of AIT during childhood and adolescence, it suggested an association with earlier onset of clinical disease in children to enterovirus IgM-seropositive mothers.

Adolescent↗
PubMed2004

Baseline characteristics and the effects of two years of growth hormone replacement therapy in adults with growth hormone deficiency previously treated for Cushing's disease.

OBJECTIVE: To determine baseline characteristics and the effects of 2 years of GH replacement therapy on body composition, muscle strength, bone mass, and metabolic indices in GH-deficient (GHD) adults previously treated for pituitary-dependent Cushing's disease. DESIGN: A single-centre, open-labelled, prospective study. PATIENTS: Fifteen consecutive GHD adults previously treated for pituitary-dependent Cushing's disease (CD group) and 15 closely matched GHD adults with previous nonfunctioning hypopituitary disease (NF group) were included. All patients had adult-onset GH deficiency. RESULTS: The mean dose of GH was similar in both study groups during the 2-year treatment. At baseline, diastolic blood pressure was higher, and lumbar (L2-L4) bone mineral density (BMD) was lower, in the CD group than in the NF group. The increase in lean mass in response to GH therapy, as measured by dual-energy X-ray absorptiometry (DEXA), was less marked in the CD group. GH replacement therapy reduced diastolic blood pressure only in the CD group. The patients in the CD group had greater treatment response in lumbar (L2-L4) spine BMD and in isometric and isokinetic knee extension strength than the patients in the NF group. At study end, no difference remained between the two study groups. CONCLUSIONS: This study revealed differences in the baseline characteristics between GHD patients previously treated for Cushing's disease as compared with closely matched GHD patients with previous nonfunctioning hypopituitary disease. The 2-year GH replacement therapy eliminated all the differences between the two study groups.

Absorptiometry, Photon↗
PubMed2003

Five years of growth hormone replacement therapy in adults: age- and gender-related changes in isometric and isokinetic muscle strength.

GH replacement therapy in adults with adult-onset GH deficiency (GHD) has been shown to increase isometric and isokinetic muscle strength in a few trials with limited numbers of patients. In this single center, prospective, open-label study, the effects of 5-yr GH replacement therapy on muscle function were determined in 109 consecutive adults (61 men and 48 women) with adult-onset GHD. The mean initial GH dose was 0.88 mg/d. The dose was gradually lowered, and after 5 yr the mean dose was 0.46 mg/d. The mean IGF-I SD score increased from -1.54 at baseline to 1.53 at study end. A sustained increase in lean body mass and decrease in body fat was observed. The GH treatment induced persistent increases in isometric knee flexor strength, concentric knee flexor strength at an angular velocity of 60 degrees/sec, and right-hand peak grip strength. After correction for age and gender using observed/predicted value ratios, a sustained increase was also observed in isometric (60 degrees) and concentric (180 degrees/sec) knee extensor strength, average right-hand grip strength for 10 sec, and left-hand grip strength. At study end, knee flexor and extensor strength was 96-104% of predicted and hand grip strength was 84-90% of predicted values. The local muscle endurance was transiently decreased after correction for age and gender. No gender difference was found in the treatment responses in muscle strength. However, muscle strength (also after correction for age and gender) was lower in women than men throughout the study period. In conclusion, GH replacement therapy in adults with adult-onset GHD normalized isometric and isokinetic knee flexor and extensor strength. Hand grip strength increased but was not fully normalized.

Adipose Tissue↗
PubMed2003

Long-term efficacy and safety of somatropin for adult growth hormone deficiency.

The beneficial effects of somatropin (growth hormone [GH] replacement therapy) in adults are now established. Long-term somatropin administration in GH-deficient adults improves body composition, muscle strength, quality of life, bone mass and density, and lipoprotein pattern. The extent to which somatropin therapy can also reduce cardiovascular morbidity and mortality in GH-deficient adults remains to be determined. By starting with a low dose of somatropin, which is gradually increased based on clinical response (body composition, well-being, and serum insulin-like growth factor-1 concentration), effective treatment can be achieved with a minimum of fluid-related adverse effects. Thorough long-term monitoring of glucose metabolism, cardiovascular measurements, and underlying pituitary disease, is, however, mandatory.

Adult↗
PubMed2002

Effects of seven years of GH-replacement therapy on insulin sensitivity in GH-deficient adults.

The few trials in GH-deficient (GHD) adults that have investigated the long-term effects of GH-replacement therapy on insulin sensitivity have shown conflicting results. In this study, insulin sensitivity was determined using the hyperinsulinemic, euglycemic clamp technique in 11 GHD adults at baseline and after 6 months, 1 yr, 2 yr, and 7 yr of GH-replacement therapy. Furthermore, insulin sensitivity in the GHD patients was compared with that in 11 matched control subjects at baseline and with that in 11 other matched controls at study end. The mean initial GH dose was 1.10 mg/d. The dose was gradually lowered; and after 7 yr, the mean dose was 0.61 mg/d. A sustained reduction in body fat and a sustained increase in fat-free mass were observed. Serum high-density lipoprotein-cholesterol (HDL-C) increased, and serum low-density lipoprotein-cholesterol (LDL-C) decreased, after 7 yr of treatment. Fasting blood glucose was transiently increased during the first year of GH replacement. The glucose infusion rate/body weight (GIR/BW), as measured using the hyperinsulinemic, euglycemic clamp technique, was unaltered during GH-replacement therapy. The comparisons with the control subjects revealed that GIR/BW in the GHD patients was 45% of that in the control subjects at baseline; whereas, at study end, the GIR/BW was 71% of that in the control subjects (P = 0.06 vs. baseline). This could suggest that GH-replacement therapy may prevent the age-related decline in insulin sensitivity in GHD patients.

Adult↗
PubMed2002

Increased orderliness of growth hormone (GH) secretion in GH-deficient adults with low serum insulin-like growth factor I.

Available studies suggest that a proportion of GH-deficient (GHD) adults maintain serum IGF-I concentrations within the age- and sex-matched normal range. The basis for this distinction is not known. In this study 24-h GH profiles (sampling every 30 min) were appraised in five GHD adults with low serum IGF-I concentrations (<2 SD of the age- and sex-matched normal range), five GHD adults with normal serum IGF-I levels (within +/-2 SD), and five healthy subjects. Serial GH concentrations, measured using a chemiluminescence assay, were analyzed by deconvolution and approximate entropy (ApEn; regularity) analyses. The apparent half-duration of GH secretory bursts was longer in both GHD groups than in the healthy controls, as determined by deconvolution analysis (P < 0.05 each). The GH burst frequency was higher, the interburst interval was shorter, and the GH burst amplitude was lower in GHD adults with normal serum IGF-I than in healthy controls (P < 0.05, P < 0.05, and P < 0.01, respectively). The percentage of total daily GH secretion that was pulsatile was also reduced in the GHD adults with normal serum IGF-I compared with the other two groups (P < 0.05 and P < 0.05, respectively). In contrast, ApEn ratios were lower in the GHD adults with low serum IGF-I than in the GHD adults with normal IGF-I and controls (P < 0.01 and P < 0.05, respectively). Serum IGF-I concentrations correlated positively with ApEn ratios in the total study population (n = 15) and in the GHD adults (n = 10). In conclusion, 24-h patterns of GH release differed in GHD adults with low vs. normal serum IGF-I concentrations. GHD adults with low IGF-I levels maintain low ApEn ratios (denoting greater relative orderliness of GH secretion), whereas GHD patients with normal IGF-I values generate a high frequency, low amplitude GH output. The foregoing contrasts point to distinct neuroendocrine features of the GH-deficient state of adults, which can be related to concurrent IGF-I production.

Adult↗
PubMed2002

The importance of growth hormone (GH) and GH secretagogues for bone mass and density.

Potent antiresorptive agents have been developed for the treatment of osteoporosis and bone disorders. There are few agents available that stimulate bone formation. Recently, treatment with parathyroid hormone was found to induce a potent increase in hip and lumbar bone mineral density (BMD). The present review focus on growth hormone (GH)/ growth hormone secretagogues (GHSs). GH/GHSs stimulates bone turnover, thereby increasing bone mass and density.

Acromegaly↗
PubMedDate not supplied

Association between mutations in a thyroid hormone transporter and severe X-linked psychomotor retardation.

Monocarboxylate transporter 8 (MCT8) is a thyroid hormone transporter, the gene of which is located on the X chromosome. We tested whether mutations in MCT8 cause severe psychomotor retardation and high serum triiodothyronine (T3) concentrations in five unrelated young boys. The coding sequence of MCT8 was analysed by PCR and direct sequencing of its six exons. In two patients, gene deletions of 2.4 kb and 24 kb were recorded and in three patients missense mutations Ala150Val, Arg171 stop, and Leu397Pro were identified. We suggest that this novel syndrome of X-linked psychomotor retardation is due to a defect in T3 entry into neurons through MCT8, resulting in impaired T3 action and metabolism.

Child↗