It is well known that during hepatic operative procedures, it is often critical that the irrigation is interrupted to avoid possible bleeding, blood transfusions, variable intensities, and their short and long-term consequences. It was believed in the past that the flow interruption should not exceed 20 minutes, which limited the use of this maneuver. However, it has been postulated that ischemia could be maintained for more than 60 minutes in healthy livers. The present paper review includes: 1) A brief introduction to justify the rationale of the review design; 2) Aspects of the pathophysiology of the three stages of the liver ischemia-reperfusion injury; 3) The innate and acquired immunity; 4) Oxidative stress; 5) Apoptosis and autophagy, Some essential biomarkers (Tumor Necrosis Factor-α, nitric oxide, metalloproteinases); and, finally; 6) Preventive ("cheating") strategies, non-pharmacological and pharmacological options to treat the liver IR injury.

Purpose: To evaluate whether pre-treatment with rivastigmine is able to attenuate the I/R induced lesions in rat liver. Methods: SHAM animals or those submitted to I/R, non-treated or pre-treated with rivastigminine (2mg/kg) either 50 or 15 minutes before ischemia, were used. After I/R protocol, these animals were killed and their livers were harvested to measurement of the mitochondrial swelling as well as the malondialdehyde (MDA), nitrite and nitrate tissue concentration. Blood was also harvested for serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) determinations. Results: I/R promoted a significant increase of mitochondrial swelling in the studied animals. This increase of mitochondrial swelling was partially prevented by rivastigmine, but only if administered 50 minutes before ischemia. No significant modification of MDA, nitrite or nitrate tissue concentrations was observed in consequence of I/R, followed or not by rivastigmine treatments. In addition, I/R elevated both AST and ALT. These elevations of serum enzymes were not reversed by the different rivastigmine treatments. Conclusions: Rivastigmine administered 50 minutes before ischemia attenuates I/R-induced mitochondrial swelling, that indicates liver injury. This protective effect may be related to a greater stimulation of α7nAChR present in the Kupffer cells by the non-methabolized ACh, leading to an attenuation of I/R-induced inflammation.

Context: Fahr’s syndrome is a rare disorder characterized by bilateral and symmetrical abnormal calcifications in basal ganglia and cerebral cortex. Those calcified deposits are due to changes in calcium and phosphorus metabolisms that can be caused by endocrine disorders, mitochondrial myopathies, dermatological and infectious diseases. Clinical manifestations may include a variety of extrapyramidal, cerebelar and neuropsychiatric syndromes. Case report: This study describes a 75-year-old female patient that underwent total thyroidectomy in 1985 due to a multinodular goiter and presented postsurgical hypoparathyroidism. The patient missed follow-up apppoointments with Endocrinology and stopped treating her parathyroid condition. Some time later, she presented with change in behavior, drowsiness, paraesthesias, limb spasms and seizures. A CT scan of the brain was performed, showing multiple and extensive calcifications reaching the cerebellar hemispheres, basal ganglia, thalamus and white subcortical substance symmetrically. Laboratory examinations revealed hypocalcemia, hyperphosphatemia, and low parathyroid hormone (PTH) levels. Intravenous calcium gluconate was used to corret the Ca/P dysfunction. Additionally, appropriate antiepileptic drugs for seizures were used. She presented with progressive improvement of symptoms after treatment. Conclusions: This case report demonstrates the importance of post- thyroidectomy follow-up and early recognition of Fahr syndrome’s symptoms, which prevents the progression of neurological conditions.

Context: Creutzfeld Jakob disease, a rare prion disease that leads to rapidly progressive dementia and movement disorders, through its pathophysiology will determine brain damage. Regardless of the cause, the course of the disease will be rapid and will invariably lead to death. Objective: The reason why the case is described is due to the low incidence of this disease and its unusual course in the case described. Case report: A 67-year-old male, had a personal history of smoking and obesity . Referred to our service due to sudden ataxia, in the presence of an unchanged MRI scan. The first sympton started when he woke up with a dizzying and inability to walk due to imbalance. In the initial assessment, the patient had appendicular ataxia in all 4 limbs, with an examination of his mental status without changes. New head MRI exam showing alterations compatible with CJD. Interned with hipotheses diagnoses of Wilson’s disease, encephalitis or CJD, he developed abdominal distension with surgical need and immediately after the procedure he already presented a comatose, spastic, and myoclonic condition compatible with the final phase of CJD, later protein 14-3-3 was found in the CSF. Conclusions: CJD, usually presents with rapidly progressive cognitive deficit associated with movement disorder. In the case presented, initially there was no change in cognition and after an urgent surgical procedure, there was an important advance in a shorter than expected period for the disease.