Gluteal muscle fibrosis with abduction contracture of the hip.

PURPOSE: Gluteal muscle fibrosis with hip contracture is a rare condition and causes major disability; literature reports are sparse. The aim of this study is to present, for the first time in Iraq and the region, a case series of gluteal fibrosis and the results of surgical treatment. METHODS: Seven children--six boys and one girl--diagnosed as having gluteal muscle fibrosis with hip contracture, were investigated and treated by open surgical release of fibrotic bands and physiotherapy. RESULTS: All patients improved dramatically over the subsequent weeks, and were able to sit and squat in the normal position. CONCLUSIONS: Gluteal muscle fibrosis with hip contracture is present in Iraq and more awareness is needed for early diagnosis. Surgical treatment provided excellent results. More studies are needed to delineate the aetiology of the condition.

Amelioration of doxorubicin-induced cardiac and renal toxicity by pirfenidone in rats.

PURPOSE: Doxorubicin (DXR) is an anthracycline glycoside with a broad spectrum of therapeutic activity against various tumors. However, the clinical use of DXR has been limited by its undesirable systemic toxicity, especially in the heart and kidney. This study was designed to test the effectiveness of dietary intake of pirfenidone (PD) against DXR-induced cardiac and renal toxicity. METHODS: Male Sprague Dawley rats were placed into four treatment groups: saline injected intraperitoneally (i.p.) plus regular diet (SA+RD); DXR i.p. plus regular diet (DXR+RD); saline i.p. plus the same diet mixed with 0.6% PD (SA+PD); and DXR i.p. plus the same diet mixed with 0.6% PD (DXR+PD). The animals were fed regular or regular plus PD diets 3 days prior to i.p. injections of either saline or DXR and continuing throughout the study. A total dose of DXR (16.25 mg/kg) or an equivalent volume of saline was administered in seven injections (2.32 mg/kg per injection) three times per week with an additional dose on the 12th day. At 25 days following the last DXR or saline injection, some animals were anesthetized for the measurement of cardiac and pulmonary function, and others were killed by an overdose of pentobarbital. At the time the animals were killed, abdominal fluid was collected. Kidney and heart were removed, weighed, fixed with 10% formalin or frozen in liquid nitrogen. The fixed tissues were used for histological examination and the frozen tissues were used for biochemical studies. RESULTS: The average volumes of abdominal fluid in the DXR+RD and DXR+PD groups were 9.42 ml and 3.42 ml and the protein contents of abdominal fluid in the DXR+RD and DXR+PD groups were 218 mg and 70 mg, respectively. A 12.5% mortality occurred in the DXR+RD group as compared to 0% in DXR+PD group. There were no changes in any of the cardiac or pulmonary physiological parameters in any of the four groups. The changes in the heart and kidney of the DXR+RD group included reduction in organ weight, increase in hydroxyproline content of heart, increase in hydroxyproline, and lipid peroxidation in the kidney and plasma, and increase in protein concentration in urine as compared to rats in the control, SA+RD and SA+PD groups. Treatment with PD abrogated the DXR-induced increases in hydroxyproline content in the heart and kidney, lipid peroxidation of the kidney and plasma, and protein content of the urine in the DXR+PD group. DXR treatment alone caused disorganization of cardiac myofibrils, vacuolization of the myofibers, and renal tubular dilation with protein casts in both the cortical and medullary regions. Treatment with PD minimized the DXR-induced histopathological changes of heart and kidney in the DXR+PD group. CONCLUSIONS: Treatment with PD reduced the severity of DXR-induced toxicity as assessed by reduced mortality, diminished volume of recovered fluid in the abdominal cavity, and severity of cardiac and renal lesions at both the biochemical and morphological levels. These results indicate that PD has the potential to prevent DXR-induced cardiac and renal damage in humans on DXR therapy.

Effect of pirfenidone against vanadate-induced kidney fibrosis in rats.

Renal fibrosis is a complication of kidney injury and can contribute to organ failure. Currently, there are no drugs for the treatment of renal fibrosis. Pirfenidone (PD) has been proven to have antifibrotic effects in animal models of fibrosis. We tested the ability of PD against vanadate-induced kidney fibrosis in rats. The rats were injected subcutaneously with vehicle or vanadate solution (1mg vanadate/kg/day) for 12 or 16 days to produce varying degrees of kidney fibrosis. The vanadate- and vehicle-treated rats were fed a laboratory diet or the same diet mixed with 0.6% PD ad lib. One vanadate-injected group was initially fed the same diet without PD and later switched to the diet containing PD 2 days after the last injection. The rats were killed at 12 and 25 days following the last dose. The changes found in the kidney of vanadate-treated rats included increases in RNA and DNA content and increases in kidney weight. Treatment with PD diminished the vanadate-induced increases in kidney weight and RNA content. The hydroxyproline content of the kidney in vanadate-treated animals was increased significantly (P< or =0.05) from the control level of 1452 microg/kidney to 1765 microg/kidney. Treatment with PD for 37 days caused significant reductions in the vanadate-induced increases in the hydroxyproline level. Similarly, treatment for 41 days also caused significant reductions (1744 microg/kidney) in vanadate-induced increases in the hydroxyproline level (1996 microg/kidney). The histological evaluation revealed that the severity of the lesions in the vanadate-treated group was moderate to severe, and treatment with PD for 41 days decreased the severity to a mild level. In addition, the delayed treatment with PD also minimized the vanadate-induced increases in the collagen content of the kidney. Although it is speculative, PD may potentially be therapeutic in the management of renal fibrosis.