Abnormal liver function tests associated with severe rhabdomyolysis

Rhabdomyolysis is a syndrome of skeletal muscle injury with release of cellular constituents such as potassium,phosphate,urate and intracellular proteins such as myoglobin into the circulation,which may cause complications including acute kidney injury,electrolyte disturbance and cardiac instability.Abnormal liver function tests are frequently observed in cases of severe rhabdomyolysis.Typically,there is an increase in serum aminotransferases,namely aspartate aminotransferase and alanine aminotransferase.This raises the question of liver injury and often triggers a pathway of investigation which may lead to a liver biopsy.However,muscle can also be a source of the increased aminotransferase activity.This review discusses the dilemma of finding abnormal liver function tests in the setting of muscle injury and the potential implications of such an association.It delves into some of the clinical and experimental evidence for correlating muscle injury to raised aminotransferases,and discusses pathophysiological mechanisms such as oxidative stress which may cause actual liver injury.Serum aminotransferases lack tissue specificity to allow clinicians to distinguish primary liver injury from muscle injury.This review also explores potential approaches to improve the accuracy of our diagnostic tools,so that excessive or unnecessary liver investigations can be avoided.     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

Bone Mineral Density in the Proximal Femur and Contralateral Knee After Total Knee Arthroplasty

Osteoarthrosis (OA) is often associated with pain and disability, which are relieved after total knee arthroplasty (TKA), but the nature of bone changes associated with OA is controversial. We examined preoperative hip and contralateral knee bone mineral density (BMD) in patients requiring TKA and monitored the BMD changes postoperatively. Sixty-nine patients, scheduled to have TKA for osteoarthrotic knees, had both hips and contralateral knee BMD measured by dual-energy X-ray absorptiometry (DXA) at the time of operation (baseline) and at 1 yr after operation. X-rays of the knee joints were also taken to evaluate the severity of OA. Preoperatively, 27% and 38% of the patients had total hip BMD Z-score more than 1 SD in the operated side and contralateral hips, respectively. In all regions of interest (ROI), the mean baseline BMD of the affected side proximal femur was significantly lower than that of the contralateral side (p < 0.0005-0.019). The severity of OA was not associated with BMD. During 1-yr follow-up, the postoperative knee status and the physical activity of the patients (AKS score) improved. However, neither the hip nor the nonoperated knee BMDs increased. Knee OA is associated with significantly lower BMD values in the affected side compared with the contralateral hip, and these levels remained similar or decreased during a 1-yr follow-up. We conclude that improved mobility after TKA does not improve the effects of preoperative disuse-associated bone loss in the short term.     

MRI of pancreatic gastrinomas.

Pancreatic islet cell tumors are often small and multiple, and preoperative diagnosis can be difficult. In a woman with hypergastrinemia, angiography and CT each depicted a solitary lesion. Magnetic resonance images, acquired using fat suppression, fast spin echo, and contrast material injection, depicted seven separate lesions, which were surgically confirmed.     

The effects of THA on scopolamine and nucleus basalis lesion-induced EEG slowing

The effectiveness of THA (an anticholinesterae) on scopolamine (0.4 mg/kg) and nucleus basalis (NB) lesion-induced change in neocortical spectral electroencephalography (EEG) were investigated. Scopolamine increased the amplitudes of all the spectral components in waking-immobility. In the movement-related EEG spectral values, only the alpha power was increased. THA 7.5 mg/kg, but not THA 3 mg/kg, could reverse scopolamine-induced amplitude change. NB lesioning increased delta and theta amplitudes, but decreased beta amplitude. Delta amplitude was increased during movement recordings in NB-lesioned rats. THA 7.5 mg/kg and pilocarpine 10 mg/kg, but not THA 3 mg/kg, could partially reverse the increase of delta and theta amplitudes induced by NB lesions. However, the beta power decrease could not be restored with cholinomimetics. This study demonstrates that quantitative EEG activity analysis may reflect the THA-induced restoration of the function of the cholinergic nucleus basalis.     

Faecal lipids in familial adenomatosis coli

Faecal sterols and bile acids from six patients with familial adenomatosis coli (FPC) and 61 healthy men were analysed preoperatively. Faecal concentrations and secretion of neutral sterols, plant sterols, and degradation products of cholesterol were identical in the two groups. No increase was found in the faecal bile acid excretion, and the distribution of individual bile acids was normal in FPC. The results suggest that the development of adenomas in FPC is not associated with abnormal cholesterol and bile acid excretion.     

Patterns of keratin subsets in normal and abnormal uterine cervical tissues. An immunohistochemical study.

We investigated the use of three monoclonal antikeratin antibodies on routinely formalin-fixed and paraffin-embedded punch and cone biopsies of the normal human uterine cervix and its metaplastic and premalignant lesions. Monoclonal antibodies used were AE8, which is specific for keratin 13; 34BE12, which reacts with keratins of the stratified squamous epithelium; and CAM5.2, which is specific for keratin 8. All these antibodies performed well in routinely processed surgical pathology material. AE8 antibody stained the suprabasal layer of the normal squamous epithelium. Squamous metaplasia and dysplasia were stained in 50% of the cases. Normal suprabasal distribution of the keratin 13, however, was lost in all positive dysplasia cases. CAM5.2 reacted with normal columnar cells in all cases, and squamous metaplasia was focally positive in 20% of the cases. Dysplasia showed a positive reaction in 30% to 40% of the cases. The 34BE12 antibody was reacting with the full thickness of the squamous epithelium. Squamous metaplasia and dysplasia were positive in 80% of the cases. In addition, 34BE12 stained reserve cell hyperplasia, making it a useful marker for this condition. Our results demonstrate that keratin immunohistochemistry with the above-listed antibodies gives pathogenetically interesting information on cervical lesions.