Gómez AE, Estrada VE, Ortega GP, Lazos OM, Vicuña GRM, Martínez GJ, Arroyo VA, Chávez ML, Olvera RJE

Language: Spanish
References: 14
Page: 8-11
PDF size: 87.30 Kb.

ABSTRACT

Background: The metabolic encephalopathies are reversible disturbances which can give rise to structural changes in the central nervous system. The hepatic encephalopathy can occur clinically in chronic or acute diseases. Clinically the most characteristic neurologicmanifestation is asterixis, accompanied by hepatic fetidness and mental disturbances. Histologically Alzheimer’s type II astrocytes are found in the gray matter.
Objective: To determine the frequency of hepatic encephalopathy with microscopic changes in autopsies performed from 1969 to 1999.
Material and method: All autopsies for chronic hepatopaty were included; for each, age, gender and anatomical diagnosis of liver, clinical manifestation of hepatic encephalopaty and time of evolution were recorded, as well as presence of microscopic hepatic encephalopaty and death cause.
Results: The total number of autopsies was 22,559. Out of these 2,322 cases of chronic liver disease were included in the study. In 404 cases (17%) microscopic changes of hepatic encephalopathy were found; out of these 244 cases (58%) showed the clinical manifestations of hepatic encephalopathy. There were 375 cases in which no microscopic changes were found even though the encephalopathy was present clinically. In these the average time of evolution was three days, which contrasted with the 17 days of evolution in cases in which both clinical and microscopically presented positive findings
Conclusions: There are experimental studies in which astrocytes are cultured with ammonia; in these, changes such as basophilic staining of the cytoplasm and vacuolation are seen on the fourth day. However, only in cultures with longer exposure changes similar to Alzheimer’s II astrocytes are seen, with nuclei identical to those seen in histological sections. This fact coincides with the observation seen in this series of hepatic encephalopathy, that several days are required to produce the morphologic change of the astrocytes.

REFERENCES

1. Graham D, Lantos P. Nutritional and metabolic disorders. En:

2. Butterworth RF, Giguere JF, Michaud J, et al. Ammonia: key factor in the pathogenesis of hepatic encephalopathy. Neurochem Pathol 1987;6:1-12.

3. Lee L, Hard F, Moller L, et al. Alcohol-induced brain damage and liver damage in young males. Lancet 1979;ii:759-761.

4. Norenberg MD. Astrocyte response to CNS injury. J Neuropathol Exp Neurol 1994;53:213-220.

5. Klatzo J. Evolution of brain edema concepts. Acta Neurochir 1994;60(Suppl.):3-8.

6. Lo Pachin RMJ, Aschner M. Glial-neuronal interactions: Relevance to neurotoxic mechanisms. Toxicol Appl Pharmacol 1993;118:141-148.

7. Noremberg MD, Bender AS. Astrocyte swelling in liver failure. Role of glutamine and benzodiazepines. Acta Neurochir 1994;60(Suppl.):24-27 induced astrocyte swelling: Effect of temperature.

8. Acta Neurochir 1994;69(Suppl.):28-30. protein in hepatic encephalopathy: an immunohistochemical study.

9. J Neuropathol Exp Neurol 1981;40:625-632.

10. Norenberg MD, Neary JT, Norenberg LOB, et al. Ammonia astrocytes. J Neuropathol Exp Neurol 1990;49:399-405.

11. Gregorios JB, Mozes LW, Norenberg OB, et al. Morphologic effects of ammonia on primary astrocytes cultures. Light microscopic studies. J Neuropathol Exp Neurol 1985;44:397- 403.

12. Diemer NH, Glial and neuronal changes in experimental hepatic encephalopathy. Acta Neurol Scand 1978:58(Suppl 71):1-144.

13. Pilbeam CM, Anderson RM, Bhthal PS. The brain in experimental portal-systemic encephalopathy. Morphological changes in three animal models. J Pathol 1983;140:331-345.

14. Zamora AJ, Cavanagh JB, Kyn MH. Ultrastructural response of the astrocytes to portocaval anastomosis in the rat. J Neurol Sci 1973;18:15-4