Novel mutations in PIEZO1 cause an autosomal recessive generalized lymphatic dysplasia with non-immune hydrops fetalis

نویسندگان

  • Elisavet Fotiou
  • Silvia Martin-Almedina
  • Michael A Simpson
  • Shin Lin
  • Kristiana Gordon
  • Glen Brice
  • Giles Atton
  • Iona Jeffery
  • David C Rees
  • Cyril Mignot
  • Julie Vogt
  • Tessa Homfray
  • Michael P Snyder
  • Stanley G Rockson
  • Steve Jeffery
  • Peter S Mortimer
  • Sahar Mansour
  • Pia Ostergaard
چکیده

Generalized lymphatic dysplasia (GLD) is a rare form of primary lymphoedema characterized by a uniform, widespread lymphoedema affecting all segments of the body, with systemic involvement such as intestinal and/or pulmonary lymphangiectasia, pleural effusions, chylothoraces and/or pericardial effusions. This may present prenatally as non-immune hydrops. Here we report homozygous and compound heterozygous mutations in PIEZO1, resulting in an autosomal recessive form of GLD with a high incidence of non-immune hydrops fetalis and childhood onset of facial and four limb lymphoedema. Mutations in PIEZO1, which encodes a mechanically activated ion channel, have been reported with autosomal dominant dehydrated hereditary stomatocytosis and non-immune hydrops of unknown aetiology. Besides its role in red blood cells, our findings indicate that PIEZO1 is also involved in the development of lymphatic structures.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

CCBE1 mutations can cause a mild, atypical form of generalized lymphatic dysplasia but are not a common cause of non-immune hydrops fetalis.

To the Editor : Generalized lymphatic dysplasia (GLD) results from an inherent developmental abnormality of the lymphatic system involving the viscera. The onset of failure of lymphatic drainage can be preor postnatal and can result in any combination of peripheral lymphoedema, pleural and pericardial effusions, ascites, chylous effusions and pulmonary or intestinal lymphangiectasia (1). GLD, i...

متن کامل

Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia

Piezo1 ion channels are mediators of mechanotransduction in several cell types including the vascular endothelium, renal tubular cells and erythrocytes. Gain-of-function mutations in PIEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditary stomatocytosis. However, the phenotypic consequence of PIEZO1 loss of function in humans has not previously been document...

متن کامل

EPHB4 kinase–inactivating mutations cause autosomal dominant lymphatic-related hydrops fetalis

Hydrops fetalis describes fluid accumulation in at least 2 fetal compartments, including abdominal cavities, pleura, and pericardium, or in body tissue. The majority of hydrops fetalis cases are nonimmune conditions that present with generalized edema of the fetus, and approximately 15% of these nonimmune cases result from a lymphatic abnormality. Here, we have identified an autosomal dominant,...

متن کامل

Spontaneous repigmentation of silvery hair in an infant with congenital hydrops fetalis and hypoproteinemia.

Silvery hair is a characteristic finding of 3 rare autosomal recessive disorders: Chédiak-Higashi syndrome (CHS), Elejalde syndrome (ES), and Griscelli syndrome (GS). We report the case of a 2-month-old male infant with transient silvery hair and generalized hypopigmentation of the skin and eyes who did not have one of these classic causative disorders. The patient was delivered at 35 weeks' ge...

متن کامل

A rare cause of non-immune hydrops fetalis: congenital sialidosis

Sum mary Sialidosis is a rare congenital lysosomal storage disease with autosomal recessive transmission caused by a deficiency of alpha-N-acetylneuraminidase (sialidase). The findings begin in the intrauterine period in congenital type of sialidosis and the cases die in the postnatal period due to hydrops fetalis with multiorgan failure. Here, a case of premature baby born to a consanguineous ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015