Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver transplantation (LT) represents the definitive treatment for end-stage liver disease. Cognitive impairment following LT is frequent, referred to as postliver transplant encephalopathy (PLTE). LT removes the underlying chronic liver disease, and until recently hepatic encephalopathy (HE) was assumed to be fully reversible after LT. However, increasing evidence indicates that some degree of cognitive impairment may be present after LT. To which extent PLTE reflects cognitive impairment caused by residual HE (RHE) or the combined effect of other factors affecting brain function before, during, and after LT is not clarified. None of the available psychometric and neurophysiological tests used for detecting HE is shown to be able to distinguish between etiologies. The available, mostly retrospective, clinical studies indicate a high prevalence of abnormal psychometric tests after LT, and not all seem to recover completely. The patients with earlier HE show the most marked improvements, suggesting that the clinical picture of the early PLTE, in fact, represents RHE. Other early post-LT etiologies for PLTE comprise cerebral ischemia, critical illness encephalopathy, and immunosuppressive therapy. Late-onset etiologies comprise diabetes and hypertension, among others. PLTE regardless of etiology is a worrying issue and needs more attention in the form of mechanistic research, development of diagnostic/discriminative tools, and standardized prospective clinical studies.
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PMID:Cognitive impairment after liver transplantation: residual hepatic encephalopathy or posttransplant encephalopathy? 3104 Jul 28

We report and discuss a case that illustrate the clinical utility of transcranial Doppler (TCD) ultrasound in a patient with cirrhosis. A 43-year-old female presented with acute decompensation of cirrhosis with hepatic encephalopathy, requiring mechanical ventilation. TCD showed low diastolic flow velocities and high pulsatility index (PI) consistent with increased cerebrovascular resistance (CVR). The flow velocities and PI normalized over a period of few days and correlated well with neurological improvement after treatment. Subsequently, the patient developed a large intracerebral hemorrhage with mass effect. The TCD measurements in intracranial hypertension were similar to those with cirrhosis and hepatic encephalopathy. However, the windkessel notch in the systolic phase of TCD waveform, related to the distensibility of arterial wall, was absent during raised intracranial pressure (ICP). The absence of a windkessel notch may help to differentiate a high downstream resistance due to raised ICP from increased CVR.
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PMID:Transcranial Doppler waveform changes due to increased cerebrovascular resistance and raised intracranial pressure in a patient with cirrhosis: A difference in shapes, not in numbers. 3177 80


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