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CMAJ. 2002 Jun 11;166(12):1517-24.
Vitamin D insufficiency in a population of healthy western Canadians.

Rucker D, Allan JA, Fick GH, Hanley DA.

Department of Medical Science, University of Calgary, Alta.

BACKGROUND: People with low levels of vitamin D and its metabolites are at increased risk for osteoporotic fractures. We wished to ascertain levels of vitamin D in a representative sample of adult western Canadians, to help assess the level of risk. We evaluated the prevalence of vitamin D insufficiency, defined as 25-hydroxyvitamin D [25(OH)D] less than 40 nmol/L, and seasonal variations in 25(OH)D, parathyroid hormone and related biochemical indices in a community-dwelling population of healthy Canadians living in Calgary (latitude 51 degrees 07'N). METHODS: During calendar year 1999, we collected fasting overnight blood samples every 3 months from 60 men and 128 women (age range 27 to 89 years) who had volunteered to participate in another study. We used commercial radioimmunoassay kits to measure calciotrophic hormones and other biochemical indices. Regression models for longitudinal data were used to assess the effect of season and other potential predictors on individual parameters. RESULTS: For a total of 64 participants (34%), vitamin D insufficiency, defined as 25(OH)D less than 40 nmol/L, was recorded at least once out of the 4 sampling times. After adjustment for age, body mass index and holiday travel, we observed the anticipated rise in serum 25(OH)D from a mean of 57.3 (standard deviation [SD] 21.3) nmol/L in the winter to 62.9 (SD 28.8) nmol/L in spring (p = 0.001) and 71.6 (SD 23.6) nmol/L in summer (p < 0.001), with a subsequent decline to 52.9 (SD 17.2) nmol/L in the fall (p = 0.008). The anticipated inverse relation between 25(OH)D and parathyroid hormone was not consistently observed: after adjustment for age, sex, body mass index and serum calcium, serum levels of parathyroid hormone did decrease significantly, from 39.5 (SD 18.8) ng/L in winter to 36.3 (SD 17.8) ng/L in summer (p = 0.001), but they continued to decline to 34.5 (SD 17.3) ng/L in the fall (p < 0.001). There was no association between 25(OH)D and parathyroid hormone (p = 0.21). INTERPRETATION: We documented a high prevalence of vitamin D insufficiency, which warrants consideration of dietary vitamin D supplementation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074117&dopt=Abstract

Int J Clin Pract. 2002 May;56(4):267-71.
14. Breast cancer prevention.

Salih AK, Fentiman IS.

Hedley Atkins Breast Unit, Guy's Hospital London, UK.

Increased risk of breast cancer may result from potentially modifiable causes such as endogenous hormone levels, obesity, HRT, and non-lactation, or non-modifiable factors including genetic susceptibility and increasing age. The Gail model, based on known factors, may be useful for estimating lifetime risk in some individuals, but those risk factors that are easier to modify may have a limited impact on the totality of breast cancer. Tamoxifen prevention still remains contentious, with a significant reduction in risk of breast cancer in women given tamoxifen in the NSABP P1 study but no effect in the Italian and Royal Marsden trials. Raloxifene, tested in the MORE trial, reduced the incidence of breast cancer by 65% but this was restricted to oestrogen receptor positive tumours. Lifestyle factors such as diet, obesity, exercise and age at first full term pregnancy and number of pregnancies have a mild to moderate impact on risk, so may have little effect on the incidence of breast cancer. Reduction of alcohol intake could lead to a modest reduction in the risk of breast cancer but possibly adversely affect other diseases. Fat reduction and GnRH analogue reduce mammographic density but have not yet been shown to affect risk. For women with BRCA1/2 mutation, options include unproven surveillance and prophylactic mastectomy with an unquantified risk reduction. Interesting new candidates for chemoprevention include aromatase inhibitors, new generation SERMs, demethylating agents, non-selective COX inhibitors, tyrosine kinase inhibitors and polyamine synthetic inhibitors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074209&dopt=Abstract

Eur Urol. 2002 Feb;41(2):144-53; discussion 153-4.
Age dependent secretion of LH and ACTH in healthy men and patients with erectile dysfunction.

Derouet H, Lehmann J, Stamm B, Luhl C, Romer D, Georg T, Isenberg E, Gebhardt T, Stoeckle M.

Department of Urology and Pediatric Urology, University of Saarland, Homburg/Saar, Germany. drderoueol.com

OBJECTIVES: Age dependent secretion of testicular and adrenal androgens was examined in healthy men and patients with erectile dysfunction (ED). METHODS: In 95 healthy men (age 20-74 years) and 739 patients with ED, luteineizing hormone (LH, n = 739), adrenocorticotropic hormone (ACTH, n = 480) and the secretion products of testis and adrenal gland testosterone (T, n = 750), free testosterone (fT, n = 718), dehydroepiandrosteronesulfate (DHEAS, n = 598) and cortisol (n = 538) were measured. RESULTS: In healthy men, LH was measured from 0.75-8.58 mIU/ml and ACTH from 10.59-121.7 pg/ml. Statistically, age was not correlated to LH (P = 0.573) and ACTH (P = 0.833) in healthy men. The secretion products T (P < 0.05), fT (P < 0.001), DHEAS (P < 0.001) and cortisol (P < 0.05) declined significantly with age in healthy persons. In patients with ED, a significant age dependent increase of LH (P < 0.05, n = 739), but not ACTH (P = 0.469, n = 480) was found. T (P < 0.001, n = 736), fT (P < 0.001, n = 718) and DHEAS (P < 0.001, n = 598), but not cortisol (P = 0.307, n = 538) declined in age dependent patients with ED. Age matching revealed a statistical significant elevation (P < 0.05) only for LH (n = 659) in comparison to healthy men (n = 94), all other hormones were not different in both groups. CONCLUSION: An LH-increase in patients with erectile dysfunction underlines the importance of Leydig cell degeneration in this disease, but age dependent decline of T secretion was comparable to healthy men, demonstrating a working hypophyseal-testicular-axis. Indication of androgen replacement is therefore limited to selected cases.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074401&dopt=Abstract

Endocrinology. 2003 Jan;144(1):29-39.
Follicle-stimulating hormone-responsive cytoskeletal genes in rat granulosa cells: class I beta-tubulin, tropomyosin-4, and kinesin heavy chain.

Grieshaber NA, Ko C, Grieshaber SS, Ji I, Ji TH.

Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA.

FSH regulates gene expression for granulosa cell differentiation and follicular development. Therefore, FSH-responsive genes are crucial, but only a few genes have been identified for the early stage of follicular development. In particular, little is known about cytoskeletal genes, which likely play essential roles in the morphological changes such as the antrum formation, a major landmark. FSH is also known to induce the differentiation of an immature, undifferentiated rat ovary granulosa (ROG) cell line. Our data show that FSH induced massive yet distinct reorganization of microtubules and the actin cytoskeletons as well as morphological changes. To identify those genes responding to FSH during the differentiation, differential display was performed on ROG cells. Of the 80 FSH-responsive genes identified, there were three cytoskeleton-related genes (class I beta-tubulin, tropomyosin 4, and kinesin heavy chain), which are crucial for intracellular morphogenesis, transport, and differentiation. Northern blots show that the level of these gene transcripts reached a peak at 6 h after FSH treatment and subsided at 24 h. FSH induced the similar temporal expression not only in granulosa cells isolated from immature rats, but also in vivo. For instance, in situ hybridization showed that beta-tubulin mRNA was transiently expressed in the granulosa cells of large preantral and early antral follicles. Despite the same temporal expression, the regulatory mechanisms of the three genes were strikingly different. As an example, cycloheximide blocked the beta-tubulin mRNA expression, whereas it increased tropomyosin-4 (TM4) mRNA. Yet, it did not impact kinesin heavy chain (Khc) mRNA. In conclusion, FSH induces the massive reorganization of the cytoskeletons and morphological changes by the selective regulation of the gene expression, protein synthesis, and rearrangement of the cytoskeletal proteins in the ROG cells and probably, specific follicles and granulosa cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12488327&dopt=Abstract

Eur Urol. 2002 Feb;41(2):167-71.
Gain in chromosome 8q correlates with early progression in hormonal treated prostate cancer.

Steiner T, Junker K, Burkhardt F, Braunsdorf A, Janitzky V, Schubert J.

Department of Urology, Friedrich-Schiller-University, Jena, Germany. thomas.steineed.uni-jena.de

OBJECTIVE: Development and especially hormone refractant progression of prostate cancer are incompletely understood. Clinical studies evaluating genetic aberrations of prior therapy biopsies in correlation with progression data in patients receiving hormone therapy for prostate cancer have not been performed until now. METHODS: After DNA isolation from histological sections of primary prostate cancer biopsies, comparative genomic hybridization (CGH) was performed according to standard protocols. Primary staging, clinical course and PSA levels of the patients were assessed. RESULTS: CGH was performed on 28 primary prostate cancer samples. After a mean follow-up of 36 months 11 (39%) of the patients showed progression of disease under hormonal treatment. In patients without and with progression we found the following results, respectively: losses of 6q (41/36%), 8p (41/45%), 16q (23/18%), 18q (30/9%), and gains of 8q (12/64%; P < 0.0001) and 17 (47/26%). CONCLUSIONS: Gain of 8q is found predominantly in primary core biopsies of local advanced or metastasized prostate cancers. It shows in univariate analysis significant correlation with progression in hormone treated prostate cancer. This fact suggests that gain in 8q represents a marker of aggressiveness in prostate cancer.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074404&dopt=Abstract

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