Pituitary stalk interruption syndrome: an uncommon presentation

2019 ◽  
Author(s):  
Lopez Valverde Maria Eugenia ◽  
Ojeda Luna Florencio ◽  
Lopez Manuel Martin ◽  
Rebollo Perez Maria Isabel
Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.


2016 ◽  
Vol 22 ◽  
pp. 116
Author(s):  
Maha Sulieman ◽  
Delamo Isaac Bekele ◽  
Jennifer Marquita Carter ◽  
Rabia Cherqaoui ◽  
Vijaya Ganta ◽  
...  

2016 ◽  
Vol 22 ◽  
pp. 196
Author(s):  
Viviana Ortiz-Santiago ◽  
Oscar Ruiz ◽  
Milliette Alvarado Santiago ◽  
Loida Gonzalez-Rodriguez ◽  
Margarita Ramirez-Vick

Author(s):  
Vitória Duarte ◽  
Catarina Ivo ◽  
David Veríssimo ◽  
Sara Franco ◽  
Filipa Bastos ◽  
...  

2012 ◽  
Vol 3 (5) ◽  
pp. 455-457
Author(s):  
Dr .KOUSHIK GUDAVALLI ◽  
◽  
Dr .SHILPA CHIKATI ◽  
Dr .MOHAN RAO JAKKAMPUTI ◽  
Dr .KAMAL LOCHAN BEHERA ◽  
...  

2016 ◽  
Vol 25 (1) ◽  
pp. 99-103 ◽  
Author(s):  
Benoit Brilland ◽  
Johnny Sayegh ◽  
Anne Croue ◽  
Frank Bridoux ◽  
Jean-François Subra ◽  
...  

Light chain deposition disease (LCDD) is a rare multisystemic disorder associated with plasma cell proliferation. It mainly affects the kidney, but liver and heart involvement may occur, sometimes mimicking the picture of systemic amyloidosis. Liver disease in LCDD is usually asymptomatic and exceptionally manifests with severe cholestatic hepatitis. We report the case of a 66-year-old female with κ-LCDD and cast nephropathy in the setting of symptomatic multiple myeloma who, after a first cycle of bortezomib-dexamethasone chemotherapy, developed severe and rapidly worsening intrahepatic cholestasis secondary to liver κ-light chain deposition. Intrahepatic cholestasis was attributed to LCDD on the basis of the liver histology and exclusion of possible diagnoses. Chemotherapy was maintained and resulted in progressive resolution of cholestasis. We report here an uncommon presentation of LCDD, with prominent liver involvement that fully recovered with bortezomib-based chemotherapy, and briefly review the relevant literature. Abbreviations: AKI: Acute kidney injury; ALP: alkaline phosphatase; ALT: alanine aminotransferase; AST: aspartate aminotransferase; CMV: Cytomegalovirus; EBV: Epstein–Barr virus; GGT: gamma-glutamyl transferase; HSV: Herpes simplex virus; LC: light chain; LCDD: Light chain deposition disease; MIDD: Monoclonal immunoglobulin deposition disease; MM: Multiple myeloma.


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