Clinical Pediatric Endocrinology
Online ISSN : 1347-7358
Print ISSN : 0918-5739
ISSN-L : 0918-5739
Volume 17, Issue 1
Displaying 1-4 of 4 articles from this issue
Original Article
  • Shinobu Ida, Norikazu Yoshimura, Mariko Nakacho, Makiko Ota, Hifumi Mi ...
    Article type: Original Article
    2008 Volume 17 Issue 1 Pages 1-7
    Published: 2008
    Released on J-STAGE: February 14, 2008
    JOURNAL FREE ACCESS
    Pain resulting from needle injection is a serious problem for patients that self-administer medication at home. We studied impressions of needle use by comparing PenNeedle® 32G Taper (NovoFine® 32G Tip), developed to reduce the sense of fear and pain of injection, with a conventional needle, in children self-injecting GH. A total of 34 patients self-injected themselves with needles coupled with Norditropin® NordiFlex® pre-filled recombinant human GH, and impressions of use were evaluated by a series of questionnaires. Compared to the conventional needle, PenNeedle 32G Taper was slightly less painful at time of insertion according to patient responses, though the difference was not statistically significant (P=0.06). PenNeedle 32G Taper has the same inner diameter as the conventional needle, thus there was no difference in the pain felt at time of injection between these two needles. Large differences in pain perception between the two needles were not seen probably due to their similar shape and appearance and as the subjects of this study were young. Nevertheless, based on the results of post-study questionnaires, significantly more patients (68%, P=0.02) expressed a desire to use PenNeedle 32G Taper for daily injections of GH. PenNeedle 32G Taper thus appears to be a superior needle which reduces insertion-associated pain in children receiving recombinant GH and improves patient QOL.
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  • Toshiaki Tanaka, Reiko Horikawa, Yasuhiro Naiki, Susumu Yokoya, Mari S ...
    Article type: Original Article
    2008 Volume 17 Issue 1 Pages 9-15
    Published: 2008
    Released on J-STAGE: February 14, 2008
    JOURNAL FREE ACCESS
    In estrogen replacement therapy in Turner syndrome, there is no report which recommends the timing of the start of estrogen therapy in relation to height or adult height prediction. We have established a prediction model for pubertal growth (height difference from the start of estrogen therapy until adult height) at the start of estrogen replacement therapy. Twenty-seven Turner girls without spontaneous puberty were divided into two groups according to birth years; Group I consisted of 16 patients born from 1980-1989 and Group II consisted of 11 patients born before 1980. Using clinical characteristics from Group I, stepwise multiple regression analysis taking pubertal growth as an independent factor, and chronological age, bone age (TW2 RUS method standardized for Japanese children), height and height SDS as dependent factors revealed following formula (p<0.001, R2=0.737): (pubertal growth) = - 1.01x (Chronological age at start of E) - 0.326x (height at start of E) - 1.779x (bone age at start of E) + 90.997. Predicted adult height was obtained by adding predicted pubertal growth to height at the start of estrogen therapy. The mean absolute difference between real adult height (tallest height after height velocity less than 1 cm/yr) and predicted adult height was 1.6 ± 0.9 cm (0.3-2.8 cm) in Group I. When this prediction model was applied to Group II, The mean absolute difference between real adult height and predicted adult height was 1.0 ± 0.7 cm (0.1-2.0 cm). A prediction model for pubertal growth at start of estrogen therapy in Turner syndrome was obtained. Using this prediction model, the timing of the start of estrogen therapy can be decided in consideration of the patient's desired adult height.
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  • Ichiro Miyata, Hideki Yoshikawa, Naokiyo Kurokawa, Kei-ichi Kanno, Yos ...
    Article type: Original Article
    2008 Volume 17 Issue 1 Pages 17-22
    Published: 2008
    Released on J-STAGE: February 14, 2008
    JOURNAL FREE ACCESS
    We experienced a case of familial hypoparathyroidism with an autosomal dominant pattern of transmission and performed molecular analysis of the calcium-sensing receptor (CASR) gene. The patient was a female neonate, born by cesarean section at term because of breech presentation. Her mother had been diagnosed with idiopathic hypoparathyroidism at the age of 9 yr and had been receiving vitamin D treatment since then. At birth, the patient's serum calcium concentration was 8.4 mg/dl, but it fell to 4.0 mg/dl on the fifth day after birth. Furthermore, her serum intact PTH level was inappropriately low, while hyperphosphatemia and hypomagnesemia were found. She was diagnosed with familial hypoparathyroidism, and was immediately started on oral administration of 1α(OH)D 3 (0.1 μg/kg/day) and continuous intravenous infusion of 8.5% calcium gluconate. Additionally, trichlormethiazide was administered because of elevated urinary calcium/creatinine (Ca/Cr) ratio. Her serum calcium concentration gradually improved thereafter. In this case, autosomal dominant hypocalcemia (ADH) due to abnormality in the CASR gene was clinically suspected, but DNA sequencing analysis revealed no mutation of the CASR gene in either the patient or her mother. This result suggests that the patient's hypoparathyroidism may have been caused by abnormality in a gene other than CASR.
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