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At least 361 records · Page 20Linked to original sources

Disordered growth hormone secretion in fibromyalgia: a review of recent findings and a hypothesized etiology.

Growth hormone (GH) deficiency occurs in about 30% of fibromyalgia patients. Treatment of GH deficient fibromyalgia patients with recombinant growth hormone improves several clinical features, including the tender point count. Defective GH secretion in these patients appears to be due to increased somatostatin tone in the hypothalamus. An hypothesis is presented which relates dysfunctional GH secretion to the effects of intermittent hypercortisolemia on upregulating the density of beta-adrenergic receptors in the hypothalamus. The resulting augmentation of beta-adrenergic tone stimulates the release of somatostatin, thus, impairing GH secretion.

Clinical Trials as Topic↗

Overproduction of protein kinase C causes disordered growth control in rat fibroblasts.

We have generated a series of rat fibroblast cell lines that stably overexpress a full-length cDNA encoding the beta 1 form of protein kinase C (PKC). These cell lines contain a 20- to 53-fold increase in PKC activity and exhibit dramatically enhanced morphologic changes following exposure to the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA). They grow to a high saturation density in monolayer cultures and, when maintained at postconfluence, develop small, dense foci. In contrast to control cells, which display complete anchorage dependence, PKC-overproducing cells form small colonies in soft agar in the absence of TPA and large colonies in the presence of TPA. Thus, the mere overproduction of a single form of PKC is sufficient to confer multiple growth abnormalities in rat fibroblasts. These results provide direct evidence that PKC plays a critical role in growth control and that it mediates several of the cellular effects of the phorbol ester tumor promoters. They also suggest that the activation of PKC may be of central importance in the process of multistage carcinogenesis.

Amino Acid Sequence↗

Nationwide age references for sitting height, leg length, and sitting height/height ratio, and their diagnostic value for disproportionate growth disorders.

AIMS: To obtain age references for sitting height (SH), leg length (LL), and SH/H ratio in the Netherlands; to evaluate how SH standard deviation score (SDS), LL SDS, SH/H SDS, and SH/LL SDS are related to height SDS; and to study the usefulness of height corrected SH/H cut-off lines to detect Marfan syndrome and hypochondroplasia. METHODS: Cross-sectional data on height and sitting height were collected from 14,500 children of Dutch origin in the age range 0-21 years. Reference SD charts were constructed by the LMS method. Correlations were analysed in three age groups. SH/H data from patients with Marfan syndrome and genetically confirmed hypochondroplasia were compared with height corrected SH/H references. RESULTS: A positive association was observed between H SDS, SH SDS, and LL SDS in all age groups. There was a negative correlation between SH/H SDS and height SDS. In short children with a height SDS <-2 SDS, a cut-off limit of +2.5 SD leads to a more acceptable percentage of false positive results. In exceptionally tall children, a cut-off limit of -2.2 SDS can be used. Alternatively, a nomogram of SH/H SDS versus H SDS can be helpful. The sensitivity of the height corrected cut-off lines for hypochondroplasia was 80% and for Marfan syndrome only 30%. CONCLUSIONS: In exceptionally short or tall children, the dependency of the SH/H ratio (SDS) on height SDS has to be taken into consideration in the evaluation of body proportions. The sensitivity of the cut-off lines for hypochondroplasia is fair.

Adolescent↗

Histopathological analysis of Leri-Weill dyschondrosteosis: disordered growth plate.

Leri-Weill syndrome (LWS) is a dominant (pseudoautosomal) skeletal dysplasia with mesomelic short stature and bilateral Madelung deformity, due to dyschondrosteosis of the distal radius. It results from the loss of one copy of the Short Stature Homeobox Gene (SHOX) from the tip of the short arm of the X or Y chromosome. SHOX molecular testing enabled us to evaluate the histopathology of the radial physis in LWS patients with a documented SHOX abnormality. A widespread disorganisation of physeal anatomy was revealed with disruption of the normal parallel columnar arrangement of chondrocytes. Tandem stacking of maturing chondrocytes within columns was replaced by a side-by-side arrangement. The presence of hypertrophic osteoid with micro-enchondromata in the radial metaphysis suggests abnormal endochondral ossification. The Vickers' ligament was confirmed to blend with the triangular fibrocartilage complex (TFCC). This histopathological study demonstrates that the zone of dyschondrosteosis in LWS is characterised by marked disruption of normal physeal chondrocyte processes and that a generalised physeal abnormality is present.

Adolescent↗

Short-term fasting suppresses leptin and (conversely) activates disorderly growth hormone secretion in midluteal phase women--a clinical research center study.

Short term fasting activates the corticotropic and somatotropic, and suppresses the reproductive, axis in men. Analogous neuroendocrine responses are less well characterized in women. Recently, we identified a negative association between the adipocyte-derived nutritional signaling peptide, leptin, and pulsatile GH secretion in older fed women. In the present study, we investigated the impact of acute nutrient deprivation on pulsatile GH and LH secretion and mean leptin concentrations in eight healthy young women in the sex-steroid replete milieu of the midluteal phase of the normal menstrual cycle. Volunteers underwent 24-h blood sampling during randomly ordered, short term (2.5-day), fasting vs. fed sessions in separate menstrual cycles. Pulsatile GH and LH secretion over 24 h was quantified by deconvolution analysis, nyctohemeral rhythmicity was quantified by cosinor analysis, and the orderliness of the GH or LH release process was quantified by the approximate entropy statistic. By paired statistical analysis, a 2.5-day fast failed to alter mean (pooled) 24-h serum concentrations of LH, progesterone, estradiol, or PRL, but increased cortisol levels more than 1.5-fold (P = 0.0003). Concurrently, mean (pooled) serum leptin concentrations fell by 75% (P = 0.0003), and insulin-like growth factor I (IGF-I; P < 0.05) and insulin decreased significantly (P = 0.0018). In contrast, the daily pulsatile GH secretion rate rose 3-fold (P < 0.001). Amplified daily GH secretion was attributable mechanistically to a 2.3-fold rise in GH secretory burst mass, reflecting an increased GH secretory burst amplitude (P < 0.01). The GH half-life, duration of GH secretory bursts, and GH pulse frequency did not vary during short term fasting. The disorderliness of GH release increased significantly with nutrient restriction (P = 0.005). The mesor and amplitude of the nyctohemeral serum GH concentration rhythm also rose with fasting (P < 0.01), but the timing of maximal serum GH concentrations did not change. Thus, short-term (2.5-day) fasting during the sex steroid-replete midluteal phase of the menstrual cycle in healthy young women profoundly suppresses 24-h serum leptin and insulin (and to a lesser degree, IGF-I) concentrations, augments cortisol release, but fails to alter daily LH, estradiol, or progesterone concentrations. In contrast, the GH axis exhibits strikingly amplified pulsatile secretion, increased nyctohemeral rhythmicity, and marked disorderliness of the release process. We conclude that the somatotropic axis is more evidently vulnerable to short-term nutrient restriction than the reproductive axis in steroidogenically sufficient midluteal phase women. This study invites the question of whether normal (nutritionally replete) GH secretory dynamics can be restored in fasting women by human leptin, insulin, or IGF-I infusions.

Adult↗

[Growth disorders following fractures of the midface in children].

12 patients who had suffered mid face fractures during their childhood were examined for skeletal deformities of the facial skull. The cephalometric data showed that neither the position nor the inclination of the maxilla were significantly different from normal anatomy. No correlation was found between the age, the severity of injuries and surgical treatment and resulting deformities.

Adolescent↗