ABSTRACT
Protease inhibitors such as Ritonavir have dramatically decreased HIV-related morbidity and mortality; however, they exhibit significant toxicities. Accordingly the present study was designed to evaluate the toxic effects of Ritonavir on rat as regard lipid profile, liver and kidneys biochemically and histologically, as well as ultrastructurally. Twenty adult Sprague-Dawley albino rats were used in the present study. They were divided into two equal groups; animals of group I served as control while the rats of group H were given Ritonavir in a dose of 10.8 mg per day for 12 weeks. The results of the present investigation revealed that Ritonavir group showed elevated serum cholesterol, triglycerides, low density lipoprotein and non significant change in serum high density lipoprotein. As regard hepatic effects there was elevation of liver transaminases, while renal effects were indicated by elevation of serum creatinine. Marked histological changes in the liver and kidney specimens were observed and confirmed ultra structurally. The liver showed periportal disturbed architecture and hepatocytes affection in the form of pleomorphic edematous mitochondria and increased glycogen granules. The kidney showed marked cortical affection especially in the podocytes of the glomeruli and focal tubular necrosis of the convoluted tubules. The present study concluded that Ritonavir has a significant hepatorenal toxicity as well as hyperlipidemia that need close monitoring of the dose with the hepatorenal parameters and lipid profile
ABSTRACT
A good deal of work was done on cadaveric feet to investigate the potential routes of spread of infection across the fascial planes. Accordingly, it has been assumed that pedal infection tends to spread proximally within compartmental borders along the path of least resistance, i.e. the fascial planes act as barriers to prevent the spread of infection between foot compartments. So, it was the objective of the present study to define the patterns of spread of soft-tissue infection across the fascial planes, in the living feet of both diabetics and non-diabetics. For this reason MR imaging was investigated in 19 feet having infection of primary compartment. The spread of inflammation was traced in the following foot compartments: toes, medial, central, lateral, interosseous, dorsal, hindfoot, malleoli, and lower leg. Radiological criteria for the presence of inflammation included; fat suppressed contrast enhancement, fat signal intensity loss on T1-weighted images, and high signal intensity on T2-weighted images. The nearest compartment to the ulcer that showed MR signs of infection was considered as the primarily infected compartment. In conclusion the present results showed that soft-tissue inflammation in forefoot infection is not confined by fascial planes but spreads into adjacent compartments, especially from the lateral and medial compartments to the adjacent central and interosseous compartments, whereas hindfoot infections tend to be confined with rare spread to other compartments. Inflammation in forefoot infections most frequently spreads distally into adjacent toes in the path of least resistance. Proximal spread to the midfoot and hindfoot occurs seldom and ascent to the calf is rare. These patterns of spread of inflammation occurred in both diabetics and non diabetics