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W. C. Tan, I. J. Goldsmith and Stretton Young

ABSTRACT

The conventional casein (phosphoprotein) assay by the rennin-Ca++ method precipitated for the most part non-phosphoproteins from the supernatant fluid of homogenised lactating mammary glands. The discrepancy was revealed by the determination of the phosphate content from the rennin-Ca++ precipitated proteins. Phosphate assay after the rennin-Ca++ precipitation should be used to give a more accurate estimation of the casein content.

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K. A. Ferguson, L. Lazarus, P. van Dooren and J. D. Young

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L. SCIBOR, A. K. MUKHOPADHYAY, A. H. ANDREWS, H. SHOWLER, H. G. BOHNET and J. L. YOUNG

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W. C. Tan, Stretton Young, I. J. Goldsmith and D. C. Livingston

ABSTRACT

Portions of rat mammary glands taken during lactation were subjected to homogenisation and to electron microscopy.

Biochemical evidence after homogenisation indicated that the phosphoprotein content was highest in the cellular supernatant fraction.

Electron microscopy revealed numerous spherical structures in the supernatant fraction and in milk.

These spherical structures were similar in size to the protein droplets that are found in the cytoplasm of mammary epithelium during lactation and which have been shown to contain abundant phosphoprotein.

This is further evidence for the hypothesis that the spherical protein particles contain casein.

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Arthur B Parkes, Christopher Darke, Sakinah Othman, Melanie Thomas, Neil Young, Colin J Richards, Reginald Hall and John H Lazarus

Parkes AB, Darke C, Othman S, Thomas M, Young N, Richards CJ, Hall R, Lazarus JH. Major histocompatibility complex class II and complement polymorphisms in postpartum thyroiditis. Eur J Endocrinol 1996;134:449–53. ISSN 0804–4643

The objective was to re-evaluate the association between class II HLA-DR and DQ MHC antigens and postpartum thyroiditis (PPT) and to determine the prevalence of the class III complement allotypes of Properdin factor B (Bf), C4A and C4B in this condition. Two hundred and sixty-five (of 2897) pregnant women screened positive for thyroid autoantibody activity took part. Further blood samples were obtained for HLA class II (185) and complement (193) typing. The severity of the ensuing PPT was assessed by measuring thyroid function during the postpartum year. The HLA-DR and DQ phenotypes were assigned from restriction fragment length polymorphism analysis, and Bf, C4A and C4B allotypes were determined by immunofixation with anti-Bf or anti-C4 antibodies after electrophoresis. A weak association between the HLA class II antigens and PPT, as indicated by a reduced frequency of DR15 and DQ6 together with an increased frequency of DR5 and DQ7. was confirmed. However, only the change in DR5 frequency remained significant after correction (corrected p < 0.05). Postpartum thyroiditis was also associated with frequency disturbances in Bf and C4A allotypes but not C4B allotypes. Whilst this study has not provided evidence of a strong marker gene for PPT, it does not preclude the involvement of the MHC in this condition. These data show disturbances in complement allotype frequencies, suggesting that the class III region may provide a useful focus for further study of this pathology.

AB Parkes, Autoimmunology Research Unit, Section of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK

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P Chanson, N De Roux, J Young, JM Bidart, P Jacquet, M Misrahi, E Milgrom and G Schaison

The monoclonal origin of gonadotropin-secreting pituitary adenomas has been well demonstrated but only few molecular abnormalities have so far been recognized in these tumors. For many years, several authors have suggested a role for GnRH and/or GnRH receptors (GnRH-R) in the development of these pituitary adenomas. To test the hypothesis that mutant genes encoding a constitutively activated GnRH-R might be involved in the pathogenesis of these tumors, the sequence of the GnRH-R gene was analyzed in tumoral pituitary tissue obtained from ten patients (six female, four male). The pituitary gonadotropin-secreting adenoma was associated with in vivo hypersecretion of FSH, LH and/or free alpha-subunit (n = 7) or was clinically silent (normal plasma levels of gonadotropins or free alpha-subunit, n = 3). In all cases, immunocytochemical studies of the removed adenoma confirmed their gonadotroph nature by revealing positivity for FSH, LH and/or alpha-subunit. Genomic DNA was extracted from the pathological tissue obtained at neurosurgery. Eight sequencing primers were used to amplify the three exons of the GnRH-R gene from tumoral DNA. The entire coding sequence of the GnRH-R gene was sequenced in the ten adenomas. No mutation was found in any of the tumor specimens examined. In conclusion, mutations in the GnRH receptor coding sequence occur infrequently if at all in gonadotropin-secreting pituitary adenomas.

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S Leboulleux, E Baudin, J Young, B Caillou, V Lazar, G Pellegriti, M Ducreux, G Schaison and M Schlumberger

Neuroendocrine tumors (NET) of the thyroid gland are rare. Apart from medullary thyroid carcinoma (MTC), metastases of gastroenteropancreatic (GEP) NET may also occur. Features of six patients (five men, one female: age range, 39-67 years) with thyroid metastases from a GEP-NET are described. Thyroid metastases were bilateral in all patients and were associated with enlarged neck lymph nodes in five. In four cases, the thyroid tumor was either the first sign of the disease (n = 2) or was an isolated site of recurrence (n = 2). The tumors were well (n = 3) or poorly differentiated (n = 3). Five tumors for which the primary site could be determined corresponded to foregut-derived tumors (3 lungs, 1 thymus and 1 pancreatic NET). One tumor demonstrated calcitonin (CT) production as shown by immunohistochemistry and elevated plasma CT levels. However, the disease history and the clinical features strongly favored a metastasizing GEP-NET. No tumoral RET proto-oncogene mutation was found in this patient. The differential diagnosis between metastatic GEP-NET and MTC is crucial because prognosis, work-up, and treatment differ greatly.

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A Linglart, S Cabrol, P Berlier, C Stuckens, K Wagner, M de Kerdanet, C Limoni, J-C Carel, J-L Chaussain and French Collaborative Young Turner Study Group

Objective

Adult height deficit seen in Turner syndrome (TS) originates, in part, from growth retardation in utero and throughout the first 3 years of life. Earlier diagnosis enables earlier therapeutic intervention, such as with recombinant human GH (r-hGH), which may help to prevent growth retardation. In this open-label, multicentre phase III study, we investigated efficacy and safety in r-hGH treatment in young girls with TS.

Subjects and methods

Girls (n=61) aged <4 years with TS receiving 0.035–0.05 mg/kg per day r-hGH for 4 years were compared with an historical control group (n=51) comprising untreated, age- and height-matched girls with TS. The main outcome measure was change in height SDS (H-SDS). Other measures included changes in height velocity SDS, IGF1 levels and glucose metabolism.

Results

After 4 years, a gain in mean H-SDS of 1.0 SDS (from −2.33±0.73 to −1.35±0.86 SDS) was observed with r-hGH treatment, in contrast to the decrease in mean H-SDS of 0.3 SDS in the control group (from −2.09±0.81 to −2.44±0.73 SDS; P<0.0001). r-hGH treatment was the main predictor of H-SDS gain and accounted for 52% of variability (multivariate analysis). r-hGH was well tolerated. As expected, IGF1 levels rose with treatment. A case of transient glucose intolerance resolved after dietary adaptation.

Conclusion

Early treatment with r-hGH helps to prevent natural evolution towards short stature in most girls with TS. IGF1 levels and glucose metabolism should be monitored routinely during r-hGH therapy.

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S Leboulleux, D Deandreis, A Al Ghuzlan, A Aupérin, D Goéré, C Dromain, D Elias, B Caillou, J P Travagli, T De Baere, J Lumbroso, J Young, M Schlumberger and E Baudin

Context

Peritoneal carcinomatosis (PC) is a rare site of distant metastases in patients with adrenocortical cancer (ACC). One preliminary study suggests an increased risk of PC after laparoscopic adrenalectomy (LA) for ACC.

Objective

The objective of the study was to search for risk factors of PC including surgical approach.

Design

This was a retrospective cohort study conducted in an institutional practice.

Patients

Sixty-four consecutive patients with ACC seen at our institution between 2003 and 2009 were included. Mean tumor size was 132 mm. Patients had stage I disease in 2 cases, stage II disease in 32 cases, stage III disease in 7 cases, stage IV disease in 21 cases, and unknown stage disease in 2 cases. Surgery was open in 58 cases and laparoscopic in 6 cases.

Main outcome

The main outcome was the risk factors of PC.

Results

PC occurred in 18 (28%) patients. It was present at initial diagnosis in three cases and occurred during follow-up in 15 cases. The only risk factor of PC occurring during follow-up was the surgical approach with a 4-year rate of PC of 67% (95% confidence interval (CI), 30–90%) for LA and 27% (95% CI, 15–44%) for open adrenalectomy (P=0.016). Neither tumor size, stage, functional status, completeness of surgery, nor plasma level of op'DDD was associated with the occurrence of PC.

Conclusion

We found an increased risk of PC after LA for ACC. Whether this is related to an inappropriate surgical approach or to insufficient experience in ACC surgery should be clarified by a prospective program.

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F Castinetti, M Fassnacht, S Johanssen, M Terzolo, P Bouchard, P Chanson, C Do Cao, I Morange, A Picó, S Ouzounian, J Young, S Hahner, T Brue, B Allolio and B Conte-Devolx

Objective

Mifepristone is the only available glucocorticoid receptor antagonist. Only few adult patients with hypercortisolism were treated to date by this drug. Our objective was to determine effectiveness and tolerability of mifepristone in Cushing's syndrome (CS).

Design

Retrospective study of patients treated in seven European centers.

Methods

Twenty patients with malignant (n=15, 12 with adrenocortical carcinoma, three with ectopic ACTH secretion) or benign (n=5, four with Cushing's disease, one with bilateral adrenal hyperplasia) CS were treated with mifepristone. Mifepristone was initiated with a median starting dose of 400 mg/day (200–1000). Median treatment duration was 2 months (0.25–21) for malignant CS, and 6 months (0.5–24) for benign CS. Clinical (signs of hypercortisolism, blood pressure, signs of adrenal insufficiency), and biochemical parameters (serum potassium and glucose) were evaluated.

Results

Treatment was stopped in one patient after 1 week due to severe uncontrolled hypokalemia. Improvement of clinical signs was observed in 11/15 patients with malignant CS (73%), and 4/5 patients with benign CS (80%). Psychiatric symptoms improved in 4/5 patients within the first week. Blood glucose levels improved in 4/7 patients. Signs of adrenal insufficiency were observed in 3/20 patients. Moderate to severe hypokalemia was observed in 11/20 patients and increased blood pressure levels in 3/20 patients.

Conclusion

Mifepristone is a rapidly effective treatment of hypercortisolism, but requires close monitoring of potentially severe hypokalemia, hypertension, and clinical signs of adrenal insufficiency. Mifepristone provides a valuable treatment option in patients with severe CS when surgery is unsuccessful or impossible.