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  • familial polyposis
    °¡Á·¼º Æú¸³Áõ
  • familial progressive hyperpigmentatio
    °¡Á·¼º ÁøÇ༺ °ú»ö¼ÒÁõ.
  • familial progressive hyperpigmentation
    °¡Á·¼º ÁøÇ༺ °ú»ö¼ÒÄ§Âø
  • familial progressive sensorineural
    °¡Á·¼º ÁøÇà(¼º)
  • familial recurrent polyserositis
    °¡Á·¼º Àç¹ß¼º ´Ù¹ßÀ帷¿°.
  • familial scleroderma
    °¡Á·¼º ÇǺΠ°æÈ­Áõ
  • familial spastic paralysis
    °¡Á·¼º °­Á÷¼º ô¼ö¸¶ºñ.
  • familial spastic paraplegia
    °¡Á·¼º ¿¬Ã༺ ´ë¸¶ºñ.
  • familial spastic paraplegia
    °¡Á·¼º ¿¬Ã༺ ´ë¸¶ºñ.
  • familial spinal muscular atrophy
    °¡Á·¼º ô¼ö¼º ±ÙÀ§Ãà(Áõ).
  • familial splenic anemia
    °¡Á·¼º ºñ¼ººóÇ÷ (¡­Þ¡àõÞ¸úì).
  • familial telangiectasia
    °¡Á·¼º ¸ð¼¼Ç÷°ü È®Àå
  • familial teleangiectasis
    °¡Á·¼º ¸»ÃÊÇ÷°üÈ®Àå(Áõ)(¡­ØÇõªúì
  • familial woolly hair
    °¡Á·¼º ¾ç¸ð
  • fatal familial insomnia(FFI)
    Ä¡¸í¼º °¡°è ºÒ¸éÁõ
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FHM familial hemiplegic migraine; fathead minnow [cells]
FHR familial hypophosphatemic rickets; fetal heart rate
FHTG familial hypertriglyceridemia
FIGD familial idiopathic gonadotropin deficiency
FIH familial isolated hypoparathyroidism; fat-induced hyperglycemia
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FD familial dysbetalipoproteinaemia
FSS familial short stature
-FS familial sinistrality
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familial splenic anaemia <disease> A chronic congenital disease of lipid metabolism caused by a deficiency of the beta-glucocerebrosidase enzyme. The defect is most common in Ashkenazi Jews. Clinical features are hepatosplenomegaly (enlargement of liver and spleen) and in severe early onset forms of the disease, with neurological dysfunction.
Inheritance: autosomal recessive.
(27 Sep 1997)
familial white folded dysplasia An autosomal dominant condition of the oral cavity characterised by soft, white or opalescent, thickened and corrugated folds of mucous membrane; other mucosal sites are occasionally involved simultaneously.
Synonym: familial white folded dysplasia, oral epithelial nevus.
(05 Mar 2000)
lipoprotein lipase deficiency, familial A rare familial condition characterised by massive chylomicronaemia and decreased levels of other lipoproteins. It is due to deficiency of lipoprotein lipase, an alkaline triglyceride hydrolase which catalyses an important step in the extrahepatic removal of triglyceride-rich lipoproteins from the blood.
(12 Dec 1998)
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