Atlas of Bone Scintigraphy in the Developing Paediatric Skeleton

Hahn, Klaus; Fischer, Sibylle; Gordon, Isky

doi:10.1007/978-3-642-84945-9

Cited by 8 publications

(4 citation statements)

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“…Three of the four reported patients revealed partial conductorial unilateral hypakusis; in two of the male patients (the father and the cousin) this was due to otosclerosis. Sequential analysis of exons 2, 3,4,5,6,7,8,9 and 10 of the menin gene was negative in the reported patient. He felt stressed about the familial situation and refused further linkage analyses.…”

Section: Family Historymentioning

confidence: 49%

Cushing's Syndrome Caused by Primary Pigmented Adrenocortical Micronodular Dysplasia - A Familial Case

Alex¹,

Gallowitsch²,

Kresnik³

et al. 2001

International Journal on Disability and Human Development

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We present a 16 year-old male with Cushing's syndrome (CS). The leading symptoms were severe bilateral gynecomastia, weight gain and growth retardation, without hypertension, but with osteoporosis and delayed puberty. Laboratory findings and the results of endocrine tests were diagnostic for ACTH-independent CS. MRI of the abdomen revealed only a slight enlargement of the adrenals with left pronounced small nodularity. Iodo-cholesterol scan under dexamethasone suppression showed diffuse bilateral 131 I-cholesterol uptake, confirming the autonomous hyperfunction of both adrenal glands. Tc " m MDP bone scan localized the pathophysiological effects of osteoporosis. The rapid increase of free urinary Cortisol excretion/24 h within one year of observation led to a total bilateral adrenalectomy. Postoperative 5-year documentation of clinical recovery is presented. Family history revealed affected father (primary pigmented adrenocortical micronodular dysplasia [PPAMD]), aunt (adrenal incidentaloma) and a male cousin (PPAMD). Sequential analysis of the menin gene of the patient was negative. Molecular genetic studies for Carney complex were not yet available.

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Section: Family Historymentioning

confidence: 49%

Cushing's Syndrome Caused by Primary Pigmented Adrenocortical Micronodular Dysplasia - A Familial Case

Alex¹,

Gallowitsch²,

Kresnik³

et al. 2001

International Journal on Disability and Human Development

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“…Sie sind im Säuglingsalter ovalär geformt und zeigen später eine bandförmige und scharf begrenzte Konfiguration. Kenntnisse über die altersabhängigen Normalbefunde sind hier von wesentlicher Bedeutung, um falsche Befunde verhindern zu können [4]. Falsch positive Befunde können z.…”

Section: Normalbefunde Der Kindlichen Knochenszintigraphieunclassified

Zum Stellenwert der Knochenszintigraphie in der Pädiatrie

Hahn¹,

Fischer²

2002

Der Nuklearmediziner

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Erste Knochenszintigraphien bei Kindern wurden in den 60er-Jahren mit dem Radiopharmakon 85 Strontium durchgeführt. Aufgrund der langen physikalischen Halbwertszeit dieses Radionuklids von 64 Tagen und der damit verbundenen, nicht unerheblichen Strahlenexposition wurden damals von der Deutschen Gesellschaft für Kinderheilkunde als Indikation zur Durchführung von Knochenszintigraphien lediglich bösartige Knochenveränderungen bei Kindern zugelassen. Mit Einführung von mit 99m Technetium markierten Phosphatkomplexen Anfang der 70er-Jahre hat sich diese Situation grundlegend verändert; heute erfolgen Knochenszintigraphien in der Pädiatrie mit einem breiten Indikationsspektrum. Im Folgenden sollen die Vorbereitung der Kinder, die Durchführung der Untersuchung, die einzelnen Indikationsbereiche sowie die Interpretation der Ergebnisse besprochen werden. Dabei sei bereits jetzt auf die Richtlinie zur Durchführung von Skelettszintigraphien in der Pädiatrie verwiesen, die als deutsche Übersetzung der entsprechenden Guidelines des Paediatric Committee der EANM in ¹Der Nuklearmedizinerª im Jahre 2000 veröffentlicht wurde [1]. ZusammenfassungMit der Knochenszintigraphie steht eine sehr sensitive Methode zum Nachweis von verschiedenen benignen und malignen Erkrankungen im Kindesalter zur Verfügung. Obwohl die Spezifität der Methode prinzipiell gering ist ± jede einwirkende Noxe kann zu einem vermehrten Knochenstoffwechsel führen ± erlaubt dieses Verfahren in Verbindung mit klinischen und radiologischen Informationen in den meisten Fällen eine exakte klinische Aussage. Voraussetzung dafür sind jedoch fundierte Kenntnisse des Untersuchers auf dem Gebiet der altersabhängigen klinischen Normalbefunde, typischer Befundkonstellationen der einzelnen Krankheitsbilder sowie von technischen und methodischen Fehlermöglichkeiten. Schlüsselwörter Knochenszintigraphie´Pädiatrie´Entzündung´Trauma´OnkologieAbstract Bone scintigraphy is a very sensitive method for the detection of various skeletal nonneoplastic and neoplastic disorders in children. Specificity is low without additional information, but in combination with clinical information and other radiological examinations specificity can be improved significantly. To get good diagnostic results the knowledge of the normal appearances of the paediatric skeleton in bone scintigraphy, the typical appearances of this method in the different diseases and potential pitfalls must be known.

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“…1), although male epiphyseal growth plates of most bones normally close by the age of 18-20 years [2,3]. These uptake patterns are normally seen during late adolescence [4]. At the time of bone scintigraphy, his hormone assays revealed a luteinizing hormone level of 0.4 mIU/m (reference, 0.8-10.0 mIU/m), a follicle-stimulating hormone level of 0.0 mIU/m (reference, 0.9-8.9 mIU/m), and a testosterone level of 2.72 ng/ml (reference, 2.45-18.36 ng/ml).…”

mentioning

confidence: 99%

Incidentally Detected Juvenile-Pattern Bone Scintigraphy in a Young Man with Kallmann’s Syndrome

Kwon

Chung

Lee

et al. 2014

Nucl Med Mol Imaging

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We report a case of incidentally detected juvenile-pattern bone scintigraphy in a 30-year-old male with Kallmann's syndrome. He had osteoporosis, and complained back and chest wall pain. Bone scintigraphy showed mild growth plate uptake in long bones, and multiple focal uptakes in bilateral costochondral junctions. Although he had been receiving hormone replacement therapy since his early teens, the treatment was insufficient because he failed to visit the clinic regularly. We assume that his insufficient hormone replacement resulted in the juvenile-pattern bone scintigraphy.A 30-year-old man underwent Tc-99m dicarboxypropane diphosphonate bone scintigraphy to evaluate the cause of back and chest wall pain. He had been receiving testosterone replacement therapy since being diagnosed with Kallmann's syndrome in his teens. Kallmann's syndrome is a genetic condition presenting several symptoms of hypogonadotrophic hypogonadism [1]. He had typical Kallmann's symptom with anosmia. Mild growth plate uptake was detected in both humeral heads, the distal femur, and the proximal tibia, and focal uptakes were noted in the bilateral costochondral junctions on bone scintigraphy (Fig. 1), although male epiphyseal growth plates of most bones normally close by the age of 18-20 years [2,3]. These uptake patterns are normally seen during late adolescence [4]. At the time of bone scintigraphy, his hormone assays revealed a luteinizing hormone level of 0.4 mIU/m (reference, 0.8-10.0 mIU/m), a follicle-stimulating hormone level of 0.0 mIU/m (reference, 0.9-8.9 mIU/m), and a testosterone level of 2.72 ng/ml (reference, 2.45-18.36 ng/ml). Although his testosterone level was within normal limit at that time, he has not had treatment regularly. Thus, his testosterone level was very unsteady with wide variation (range, <0.2-8.85). Sex steroids, both estrogen and testosterone, are essential controllers of bone growth and maturation. In both men and women, estrogen is needed for the acquiring of maximal peak bone mass [5], and testosterone plays an important role not only in stimulating bone growth and maturation but also in increasing bone density and strength [6]. Delay of skeletal maturation due to lack of testosterone results from the hypogonadotropic hypogonadism related with Kallmann's syndrome [7]. Also, the hypogonadotropic hypogonadism can be a cause for unsuccessful closure of epiphyseal growth zones at the proper time; thus, the lengths of the long bones are increased. Generalized osteoporosis is also present in Kallmann's syndrome [8]. His bone mineral densitometry was below the expected range for age in both femur wards (Z-score, -2.9) and lumbar spine (Z-score, -2.7). Although there was no demonstrable focal

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Atlas of Bone Scintigraphy in the Developing Paediatric Skeleton

Cited by 8 publications

References 0 publications

Cushing's Syndrome Caused by Primary Pigmented Adrenocortical Micronodular Dysplasia - A Familial Case

Cushing's Syndrome Caused by Primary Pigmented Adrenocortical Micronodular Dysplasia - A Familial Case

Zum Stellenwert der Knochenszintigraphie in der Pädiatrie

Incidentally Detected Juvenile-Pattern Bone Scintigraphy in a Young Man with Kallmann’s Syndrome

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