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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 2002;8(2):63-71.
[Growth velocity in children after chemo- and radiotherapy]

[Article in Polish]

Birkholz D, Balcrerska A, Kaminska H, Korpal-Szczyrska M, Dorant B.

Klinika Pediatrii, Hematologii, Onkologii i Endokrynologii AM w Gdansku.

The increasing number of childhood cancer survivors has resulted in growing interest in the late effects of chemo- and radiotherapy including growth also. The aim of study: The aim of study was to evaluate growth in children treated for acute lymphoblasic leukaemia (ALL) and Wilms' tumour who achieved complete continuous first remission following treatment. Patients and methods: 52 children included in this study: 30 treated for ALL - group I and 22 with Wilms' tumour - group II since 1986 to 1996. Group I- all children received prophylactic cranial irradiation at the total dose 12 and 18 Gy and chemotherapy according to therapeutic course BFM 83 and BFM 90. Group II - all children received abdomen irradiation with total dose 15-35 Gy, chemotherapy according to therapeutic course SIOP 9 and SIOP 92. We analysed growth velocity from the time of diagnosis to the time of examination. Results were reported as standard deviation score (SDS) to allow for comparison of patients of different age and sex. Results: We observed significant growth deceleration in the first year of treatment and catch-up after 12 months from completion of therapy in both groups. The greatest reduction in yearly decrements in height SDS occurred in the first year after diagnosis. Patients of group I treated with prophylactic cranial irradiation with total dose 12 Gy presented significantly higher catch-up growth than treated with dose 18 Gy one year from completion of cancer therapy (p=0.001). Growth hormone deficiency in children of both groups was not observed. Bone age deceleration was retarded one year or more in both groups (group I p=0.025, group II p=0.001). Conclusions: 1) The chemotherapy and radiotherapy contribute to growth retardation in the first year of treatment in both groups 2) It seems that prophylactic cranial irradiation in children with ALL with total doses 12 and 18 Gy does not contribute to retardation of growth velocity after cancer treatment 3) Endocrine follow-up should be introduced in order to detect and treat complications as early as possible

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818116&dopt=Abstract [PubMed]

Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 2002;8(2):97-103.
[Calcium and phosphorus homeostasis in the developmental population. Part I: Homeostatic mechanisms in health]

[Article in Polish]

Otto Buczkowska E.

Gornoslaskie Centrum Zdrowia Dziecka i Matki, Poradnia Diabetologiczna w Katowicach.

Calcium and phosphorus form the major inorganic constituents of bone and play a vital role in cell function and cell metabolism. About 80% of total body P and 98% of total body Ca are in bone. Bone minerals exist in two physical forms: amorphous and cristalline. Serum Ca is found in three forms: approximately 40% is bound predominantly to albumin, approximately 10% is complexed with serum anions, and approximately 50% is ionized. The total P in serum can be divided into organic ester phosphate and inorganic phosphate. In the cell, phosphate is mostly in the form of organic phosphate. Parathyroid hormone is synthesized in the parathyroid gland. In physiological terms, PTH is the most important regulator of extracellular Ca concentration. Parathyroid hormone increases bone mobilization of Ca, increases renal Ca reabsorption, and possibly increases Ca absorption in the intestine. Increased serum Ca suppresses PTH production. Calcitonin is secreted from thyroid C cells. Calcitonin decreases Ca mobilization from bone and increases Ca excretion in the kidney. Ca stimulates the production of calcitonin. Vitamin D3 is synthesized in the skin from precursors. Vitamin D is catalyzed to 25(OH)D and it is metabolized to most active metabolite 1.25(OH)2D. Vitamin D through 1.25(OH)2D acts on the intestine to increase Ca absorption, mobilizes Ca from bone, and reabsorbs Ca in the kidney. The feedback loop might be completed by inhibition of PTH production by Ca, which in turn results in decreased production of 1.25(OH)2D.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818122&dopt=Abstract [PubMed]

Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 2002;8(1):17-21.
[Assessment of thyrotropin concentrations in children with somatotropin deficiency treated with growth hormone]

[Article in Polish]

Kalina-Faska B, Kalina M, Koehler B.

Katedra i Klinika Endokrynologii i Diabetologii Dzieciecej Slaskiej AM w Katowicach.

Background: There are contradictory literature opinions on the influence of GH therapy on the hypothalamus-hypophysis-thyroid gland axis concerning TSH secretion. Some researchers describe the possibility of complete inhibition of TSH secretion followed by overt hypothyroidism, the others do not confirm it. Objective: The aim of the study was to assess influence of the rGH therapy on TSH concentrations in GH-deficient children, who were euthyroid prior to the treatment. Material and methods: The study was carried out in a group of 32 children with isolated GH-deficiency in the 1st stage of sexual development according to the Tanner scale, in whom disorders of thyroid gland were excluded (T4, T3, fT4, fT3, TRH test). Recombinant GH (Genotropin a 16U-Pharmacia) was used for the treatment in the dose of 0.7 U/kg/week. Before the treatment, as well as in the 6th and 12th month of GH administration, the TRH test was performed and TSH levels were assessed in 0', 20', 30', 60' and 120 minute. The results were statistically analysed [p(a)<0.05]. Results: Basal TSH levels prior to rGH administration were within normal range and the TSH response on TRH was normal with the maximal increase in the 20th minute. A statistically significant decrease of TSH concentrations was noted after 6 and 12 months of treatment in respective minutes of the test in all children. However, decreased TSH concentrations during the therapy were within normal range. Conclusions: During rGH therapy there is a decrease of basal and simulated TSH concentrations, however within the normal range. This phenomenon is probably connected with a direct effect of administered rGH on the release of somatostatin, a natural TSH inhibitor.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818126&dopt=Abstract [PubMed]

Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 2001;7(2):85-8.
[Growth assessment in children with intrauterine growth retardation (IUGR) - preliminary results]

[Article in Polish]

Janus D, Starzyk J, Dziatkowiak H.

Klinika Endokrynologii Dzieci i Mlodziezy Collegium Medicum UJ w Krakowie.

In 28 children aged 2.3-12 years born with birth weight less than -2 SD for gestational age we assessed growth according to birth weight and height, duration of gestation, mid- parental height, and somatotropic axis. All children were subjected to auxological evaluation every 3 months. The assessment included changes of height for chronological age standard deviation score (DH SDS CA), height for bone age (DH SDS BA), growth velocity (GV SDS) and height - mid-parental height (H SDS-MPH SDS). We observed a significant growth improvement in children with lower birth weight (r=-0.5, p<0.0059), a positive correlation between IGF-1 level and catch -up growth (DH SDS CA) (r=0.5, p<0.048) and maximum GH level (stimulation test) and growth velocity (GV SDS) (r=0.8, p<0.01). These data suggest that children with lower IGF-1 and GH levels, as well as birth weight within -2 SDS could be treated with growth hormone. However, this theory requires further evaluation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818136&dopt=Abstract [PubMed]

Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 2001;7(1):57-62.
[Primary or tertiary hypothyroidism as a cause of growth disturbances in 13-month old boy?]

[Article in Polish]

Wikiera B, Barg E, Bieniasz J, Wasikowa R.

Katedra i Klinika Endokrynologii Wieku Rozwojowego AM we Wroclawiu.

Due to the screening examination it is possible to diagnose primary hypothyreosis at the very beginning. On the other hand, hypothyreosis may be also caused by insufficient secretion of TSH or TRH. We present a 13-month old boy (A.I.) admitted to our Department because of short stature. The child was from normal pregnancy, birth spontaneus at full term with weight 4400 g, length 56 cm, 10 points in Apgar scale, TSH - 1,87 micro IU/ml in the screening examination. The psychomotor development was normal. At the admission the height was 72 cm (below 3 c), weight - 10,1 kg, body proportions normal, atresic fontanels, 7 teeth. Additional examinations revealed: skeletal age - 3 months, blood cell count normal, biochemical examinations normal except for level of cholesterol (209 mg/dl). We found lack of the GH secretion after clonidine. TSH value was slightly above normal range. The levels of free thyroid hormones, anti-TPO antibodies and thyroid ultrasonography were normal. The TSH level was increased in the stimulation test with TRH. Result of the MR examination of the brain was normal. On the basis of the whole picture tertiary hypothyreosis can not be excluded. The normalisation of thyroid hormone levels and GH in stimulation test with glucagone was obtained after therapy with L-thyroxine. Conclusion: In cases of unclear growing disorders the full diagnostics of the hypothalamic-hypophyseal-thyroid axis should be done because of the possibility of regulatory centres insufficiency.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818150&dopt=Abstract [PubMed]

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.

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