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Eur J Endocrinol. 1999 Jan;140(1):48-50.
Why is the retention of gonadotrophin secretion common in children with panhypopituitarism due to septo-optic dysplasia?

Nanduri VR, Stanhope R.

Great Ormond Street Hospital for Children NHS Trust, London, UK.

Septo-optic dysplasia (De Morsier syndrome) is a developmental anomaly of mid-line brain structures and includes optic nerve hypoplasia, absence of the septum pellucidum and hypothalamo-pituitary abnormalities. We describe seven patients (four female, three male) who had at least two out of the three features necessary for the diagnosis of septo-optic dysplasia. Four patients had hypopituitarism and yet normal gonadotrophin secretion: one of these also had anti-diuretic hormone insufficiency; three had isolated GH deficiency and yet had premature puberty, with the onset of puberty at least a year earlier than would have been expected for their bone age. In any progressive and evolving anterior pituitary lesion it is extremely unusual to lose corticotrophin-releasing hormone/ACTH and TRH/TSH secretion and yet to retain gonadotrophin secretion. GnRH neurons develop in the nasal mucosa and migrate to the hypothalamus in early fetal life. We hypothesise that the arrival of GnRH neurons in the hypothalamus after the development of a midline hypothalamic defect may explain these phenomena. Progress in spontaneous/premature puberty in children with De Morsier syndrome may have important implications for management. The combination of GH deficiency and premature puberty may allow an apparently normal growth rate but with an inappropriately advanced bone age resulting in impaired final stature. GnRH analogues may be a therapeutic option. In conclusion, some patients with De Morsier syndrome appear to retain the ability to secrete gonadotrophins in the face of loss of other hypothalamic releasing factors. The migration of GnRH neurons after the development of the midline defect may be an explanation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10037251&dopt=Abstract

Eur J Endocrinol. 1999 Jan;140(1):43-7.
Trans-sphenoidal surgery for microprolactinoma: an acceptable alternative to dopamine agonists?

Turner HE, Adams CB, Wass JA.

Department of Endocrinology, Radcliffe Infirmary, Oxford, UK.

AIMS: Reported cure rates following trans-sphenoidal surgery for microprolactinoma are variable and recurrence rates in some series are high. We wished to examine the cure rate of trans-sphenoidal surgery for microprolactinoma, and to assess the long-term complications and recurrence rate. DESIGN: A retrospective review of the outcome of trans-sphenoidal surgery for microprolactinoma, performed by a single neurosurgeon at a tertiary referral centre between 1976 and 1997. PATIENTS: All thirty-two patients operated on for microprolactinoma were female, with a mean age of 31 years (range 16-49). Indications for surgery were intolerance of dopamine agonists in ten (31%), resistance in six (19%) and resistance and intolerance in four (12.5%). Two patients were from countries where dopamine agonists were unavailable. RESULTS: The mean pre-operative prolactin level was 2933 mU/l (range 1125-6000). All but 1 had amenorrhoea or oligomenorrhoea, with galactorrhoea in 15 (46.9%). Twenty-five (78%) were cured by trans-sphenoidal surgery, as judged by a post-operative serum prolactin in the normal range. During a mean follow-up of 70 months (range 2 months to 16 years) there was one recurrence at 12 years. Post-operatively, one patient became LH deficient, two patients became cortisol deficient and two became TSH deficient. Out of 21 patients tested for post-operative growth hormone deficiency, 6 (28.6%) were deficient. Five patients developed post-operative diabetes insipidus which persisted for greater than 6 months. There were no other complications of surgery. The estimated cost of uncomplicated trans-sphenoidal surgery, and follow-up over 10 years, was similar to that of dopamine agonist therapy. CONCLUSION: In patients with hyperprolactinaemia due to a pituitary microprolactinoma, transsphenoidal surgery by an experienced pituitary surgeon should be considered as a potentially curative procedure. The cost of treatment over a 10 year period is similar in uncomplicated cases to long-term dopamine agonist therapy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10037250&dopt=Abstract

Obes Res. 1999 Jan;7(1):76-82.
Endocrine regulation of fetal adipose tissue metabolism in the pig: interaction of porcine growth hormone and thyroxine.

Hausman DB, Hausman GJ, Martin RJ.

Department of Food and Nutrition, University of Georgia, Athens 30602-3622, USA. dhausmarches.fcs.uga.edu

OBJECTIVE: This study tested the hypothesis that combined treatment of thyroxine (T4) and growth hormone (GH) could normalize cellular and metabolic aspects of adipose tissue development of hypophysectomized fetal pigs. RESEARCH METHODS AND PROCEDURES: On day 70 of gestation, pig fetuses were hypophysectomized by microcauterization or remained intact. Hypophysectomized fetuses remained untreated or were treated from day 90 to day 105 of gestation with T4, GH, or a combination of both hormones. RESULTS: Body weights were unaffected by hypophysectomy or hormone treatment. De novo lipogenesis in subcutaneous adipose tissue was increased 10-fold by hypophysectomy, consistent with our previous results. This increase was abolished by GH treatment in the hypophysectomized fetuses. In contrast, T4 treatment of the hypophysectomized fetuses resulted in a 12-fold further increase in adipose tissue lipogenesis, an effect that was negated by concomitant administration of GH. Lipolytic response to isoproterenol was decreased by hypophysectomy, unaffected by GH treatment, and restored to intact values by T4 or by T4+GH treatment in the hypophysectomized fetuses. DISCUSSION: In contrast to T4, GH does not influence serum insulin-like growth factor-I or adipose tissue lipolysis, but decreases lipogenesis in the fetal pig. However, replacing both T4 and GH normalized hypophysectomized fetuses to a greater extent than either GH or T4 alone. Thus, any influence of thyroid hormones on stimulating adipose tissue lipogenesis in the developing fetal pig may be normally counterregulated by pituitary-derived growth hormone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10023733&dopt=Abstract

J Clin Endocrinol Metab. 1999 Feb;84(2):795-8.
Reduced retinal vascularization in children with growth hormone deficiency.

Hellstrom A, Svensson E, Carlsson B, Niklasson A, Albertsson-Wikland K.

Department of Clinical Neuroscience's, International Pediatric Growth Research Center, University of Goteborg, Sweden. ann.hellstroedfak.gu.se

The neovascularization in diabetic retinopathy is believed to involve locally produced angiogenic factors. In addition, there are indications that GH may influence retinal vascularization. To investigate the role of GH in retinal vascularization, we examined the retinal vascular pattern in children with congenital GH deficiency. Retinal vessel morphology was evaluated by digital image analysis of ocular fundus photographs in 39 children (5 girls and 34 boys, aged 3.6-18.7 yr) with congenital GH deficiency, and it was compared to that of 100 healthy controls. Twenty children had received GH treatment (0.1 IU/kg daily). All children were born at term, and none of the children had any clinical signs of ocular disease or reduced vision. Children with GH insufficiencies, regardless of whether they were treated with GH, had a significantly lower number of vascular branching points than the reference group (P < 0.0001). Thirty-three percent of the GH-insufficient individuals had a number of vascular branching points less than or equal to the fifth percentile of the reference group. The reduced retinal vascularization observed in children with congenital GH deficiency suggests that GH may be of importance for angiogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10022455&dopt=Abstract

J Biol Chem. 1999 Feb 26;274(9):5851-60.
Characterization of a novel calcium response element in the glucagon gene.

Furstenau U, Schwaninger M, Blume R, Jendrusch EM, Knepel W.

Department of Molecular Pharmacology, University of Gottingen, D-37070 Gottingen, Germany.

To maintain blood glucose levels within narrow limits, the synthesis and secretion of pancreatic islet hormones is controlled by a variety of extracellular signals. Depolarization-induced calcium influx into islet cells has been shown to stimulate glucagon gene transcription through the transcription factor cAMP response element-binding protein that binds to the glucagon cAMP response element. By transient transfection of glucagon-reporter fusion genes into islet cell lines, this study identified a second calcium response element in the glucagon gene (G2 element, from -165 to -200). Membrane depolarization was found to induce the binding of a nuclear complex with NFATp-like immunoreactivity to the G2 element. Consistent with nuclear translocation, a comigrating complex was found in cytosolic extracts of unstimulated cells, and the induction of nuclear protein binding was blocked by inhibition of calcineurin phosphatase activity by FK506. A mutational analysis of G2 function and nuclear protein binding as well as the effect of FK506 indicate that calcium responsiveness is conferred to the G2 element by NFATp functionally interacting with HNF-3beta binding to a closely associated site. Transcription factors of the NFAT family are known to cooperate with AP-1 proteins in T cells for calcium-dependent activation of cytokine genes. This study shows a novel pairing of NFATp with the cell lineage-specific transcription factor HNF-3beta in islet cells to form a novel calcium response element in the glucagon gene.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10026208&dopt=Abstract

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