We describe the fatal outcome of an elective TIPS procedure performed in a 43-year-old man with alcoholic cirrhosis. Wedged hepatic venography with CO(2) was the reason for infarction and laceration of liver parenchyma resulting in a subcapsular hematoma and subsequent intra-abdominal bleeding. This is the first report of this complication after the use of CO(2) in a cirrhotic patient.

Adult↗

PubMedDate not supplied

Influence of NH(4)CI on polarized release of endogenous protein degradation products and on morphology in LLC-PK(1) cells.

Increased renal ammoniagenesis is thought to be a causative factor for renal hypertrophy which occurs in several disorders accompanied by metabolic acidosis. We studied the influence of ammonia on the polarized release of degradation products of endogenous proteins in LLC-PK(1) cells. Release of acid-soluble radioactivity to the extracellular space decreased under the influence of NH(4)Cl with a remarkable transient reduction of basolateral release. Electron microscopically NH(4)Cl-treated cells showed numerous enlarged lysosomes suggesting an accumulation of incompletely degraded cytoplasmatic material in the lysosomal compartment. We conclude that split products of lysosomal degradation of endogenous proteins are preferentially transported to the extracellular space via the basolateral plasma membrane.

Ammonium Chloride↗

PubMedDate not supplied

Multiple macroregenerative nodules in liver cirrhosis due to Budd-Chiari syndrome. Case reports and review of the literature.

Clinical, radiological, histological and immunohistochemical methods were used to define the nature of multiple rapidly growing hepatic nodules in 2 young patients with Budd-Chiari syndrome due to myeloproliferative diseases. In one patient, the arterial hyperperfusion of large nodules was demonstrated by dynamic computed tomography and angiography. The explanted livers of these patients showed multiple well-demarcated nodules up to 3 cm in diameter on the background of liver cirrhosis resulting from chronic hepatic congestion. Histologically, these nodules covered a spectrum ranging from adenoma-like lesions to nodules resembling focal nodular hyperplasia. They consisted of essentially normal hepatocytes, and variably contained fibrous septa including neoductules and large, mostly dysmorphic arteries. Sometimes, they were located close to still patent or recanalized veins. These rapidly growing hepatic nodules are best defined as macroregenerative nodules. The knowledge of this entity may help the physician to avoid misinterpretation of such nodules as carcinomas.

Adolescent↗

PubMedDate not supplied

Involvement of autophagic degradation in ACTH-induced skeletal muscle atrophy.

Intracellular autophagic breakdown was investigated in skeletal myocytes undergoing atrophy under the influence of ACTH. Adult male Sprague-Dawley rats received s.c. injections of ACTH (12.5 U/kg body wt) or physiological saline as control twice daily. 5 experimental and 5 control animals were sacrificed by perfusion fixation after 6, 9, and 12 days of treatment. While the weight of the left pectoralis minor muscle decreased significantly in the ACTH-treated animals compared with controls, the volume fraction of autophagic vacuoles, as determined by quantitative electron microscopy, increased significantly after 9 days (2.6-fold) and 12 days (2.9-fold) in the atrophying skeletal myocytes of experimental animals compared with controls. Only non-myofibrillar components were detected as contents of autophagic vacuoles. Since, however, the ratio of myofibrils to other cytoplasmic components remained constant, the degradation of myofibrils seems to occur via a non-lysosomal pathway. The data suggest that the breakdown of cytoplasmic components by cellular autophagy is important for the development of skeletal muscle atrophy as observed following long-term ACTH treatment or in Cushing's syndrome.

Adrenocorticotropic Hormone↗