Bone turnover in postmenopausal women after withdrawal of estrogen/gestagen replacement therapy

Bone turnover before and after withdrawal of estrogen/gestagen treatment was studied in a randomized trial with 110 healthy female volunteers, who had passed a natural menopause 6 months to 3 years before the start of the study. Urinary excretion of intravenously injected 99m-technetium diphosphonate was measured as an index of bone turnover; plasma bone Gla protein and serum alkaline phosphatase were measured as indices of bone formation; and fasting urinary excretion of hydroxyproline and calcium were measured as estimates of bone resorption. During 2 years of hormone treatment, all variables decreased highly significantly (p less than 0.001) to a constant low level. Three months after withdrawal all variables increased highly significantly (p less than 0.001) towards, but not above, pretreatment and placebo levels. We conclude that withdrawal of estrogen/gestagen replacement therapy in postmenopausal women increases bone turnover, but not in excess of pretreatment values. This indicates that bone loss (after withdrawal) is similar to that seen in the placebo group and that a rebound phenomenon is unlikely.     

Conservative treatment for acute rupture of the Achilles tendon

Summary Sixty-six patients with acute ruptures of the Achilles tendon were treated by immobilisation in a plaster cast for 12 weeks. Fifty-seven were followed up for a mean time of 70 months. Four re-ruptures occurred shortly after the initial treatment. Most patients had no or only slight complaints, three had moderate and one severe, problems. The activity level dropped slightly from 5.3 to 5.03 (Tegner score). The results are satisfactory with a low complication rate. The method is an alternative to operative repair, especially in patients declining operation and in those in whom operation or anaesthesia is contraindicated.

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Résumé Soixante-six malades ont fait l'objet d'une étude à long terme concernant le traitement non-chirurgical des ruptures aiguës du tendon d'Achille. Le recul moyen était de 70 mois. Les patients avaient été immobilisés dans un plâtre pendant 12 semaines. 4 ruptures itératives survinrent précocément (6%). La plupart des malades n'avaient pas ou peu de séquelles, trois seulement se plaignaient d'une gêne modérée et 1 d'une gêne importante. Le niveau d'activité avait légérement diminué, de 5.3 à 5.03 (selon le score de Tegner). Les résultats paraissaient satisfaisants dans l'ensemble, avec une taux peu élevé de ruptures itératives ou d'autres complications. La méthode constitue une alternative valable au traitement chirurgical, notamment chez les sujets qui ne veulent pas être opérés ou chez ceux qui présentent des contrindications à l'anesthésie ou à la chirurgie.

     

Gastro-oesophageal reflux disease: Medical or surgical treatment? Report of an interactive workshop

Gastroesophageal reflux disease (GERD) is the most common disease of the upper gastrointestinal tract. With the introduction of proton pump inhibitors medical treatment of GERD has been significantly improved. However, the development of laparoscopic antireflux surgery resulted in an increasing interest of surgeons in this disease. An interactive meeting was organized in order to develop an agreement between gastoenterologists and surgeons regarding therapeutic decisions and this is the main topic of this paper.     

The Nordic concept of 'faellesskab'.

The complex of cultural, political and societal affiliations, both in a historic and a contemporary perspective, is expressed by a special term in the Nordic languages, 'faellesskab', often with the addition of 'folkelig', as 'folkeligt faellesskab', where 'folkelig' means of the people. No corresponding term exists in English. For medical ethics the concept 'faellesskab', or whatever wording is chosen to serve the semantics of this term, is vital. In research ethics and clinical decision-making complex ethical analyses and normative evaluations are necessary. They cannot be based solely on moral relativism, whether being based on results of opinion polls or on a widespread 'every man minds his own business' concept. 'Faellesskab' possesses the necessary base of common values.     

Beta-defensin genomic copy number is not a modifier locus for cystic fibrosis

Human beta-defensin 2 (DEFB4, also known as DEFB2 or hBD-2) is a salt-sensitive antimicrobial protein that is expressed in lung epithelia. Previous work has shown that it is encoded in a cluster of beta-defensin genes at 8p23.1, which varies in copy number between 2 and 12 in different individuals. We determined the copy number of this locus in 355 patients with cystic fibrosis (CF), and tested for correlation between beta-defensin cluster genomic copy number and lung disease associated with CF. No significant association was found.     

Missense FGFR3 mutations create cysteine residues in thanatophoric dwarfism type I (TD1)

Thanatophoric dwarfism (TD) is a sporadic lethal skeletal dysplasia with micromelic shortening of the limbs, macrocephaly, platyspondyly and reduced thoracic cavity. In the most common subtype (TD1), femurs are curved, while in TD2, straight femurs are associated with cloverleaf skull. Mutations in the fibroblast growth factor receptor 3 (FGFR3) gene were identified in both subtypes. While TD2 was accounted for by a single recurrent mutation in the tyrosine kinase 2 domain, TD1 resulted from either stop codon mutations or missense mutations in the extracellular domain of the gene. Here, we report the identification of FGFR3 mutations in 25/26 TD cases. Two novel missense mutations (Y373C and G370C) were detected in 8/26 and 1/26 TD1 cases respectively. Both mutations created cysteine residues in the juxta extramembrane domain of the receptor. Sixteen cases carried the previously reported R248C (9/26 cases), S249C (2/26 cases) or stop codon FGFR3 mutations (5/26 cases). Our results suggest that TD1 is a genetically homogeneous condition and give additional support to the view that newly created cysteine residues in the extracellular domain of the protein play a key role in the severity of the disease.