Functional reconstruction of Achilles tendon defects combined with overlaying skin defects using a free tensor fasciae latae flap.

We present our experience in functional reconstruction of the Achilles tendon with large tissue defects following after trauma and infection. To cover the skin defect and to reconstruct the Achilles tendon we used the free tensor fasciae latae (TFL) flap. From 1997 to 2003 six males, ranging from 22 to 71 (average 38.6) years, underwent this reconstructive procedure. All of them had sustained a trauma with following loss of the tendon and of the overlying tissue. After initial debridements the reconstruction with a tensor fascia latae free flap was performed. To achieve a strong distal fascia lata attachment to the calcaneal bone, we developed a special method of fixation. After vertical osteotomy in the calcaneus the distal part of the fascia flap was introduced between the bone segments, which were fixed together with a spongiosa screw. For functional outcome, it was important to fix the foot in a 90 degrees position with tension on the vascularised fascia lata. The range of motion of the ankle of the reconstructed foot showed 93.7% in comparison to the normal foot. No flap failure occurred in any of the six patients. Simultaneous soft-tissue and function restoration of the foot with TFL free flap is in our opinion an optimal one-stage reconstructive procedure.     

DSA—Control of implanted devices for arterial hepatic perfusion

In contrast to conventional film angiography, the perfusion pattern of hepatic arterial chemotherapy was consistently visualized by DSA in 40 patients with implanted Infusaid pump or Port-A devices. Incomplete perfusion of a liver region by the cytotoxic agent was recognized by DSA as accurately as by nuclide scintigraphy. Furthermore, DSA appeared to be more sensitive in determining aberrantly perfused extrahepatic regions; this was especially true when there was a nonligated right hepatic artery. Specific details of vascular lesions and associated complicating events also could be satisfactorily analyzed by DSA only.     

A method for repair of aortic dissection originating in the transverse arch using two sutureless intraluminal prostheses

We present a method for repair of ascending aortic dissections that originate in the transverse aortic arch. The technique utilizes two sutureless intraluminal prostheses, which are joined together and inserted during hypothermic circulatory arrest. A diamond-shaped opening between the two grafts is anastomosed about the orifices of the brachiocephalic arteries. This method affords the advantage of excluding the intimal tear, thereby preventing further propagation of the dissection. Additionally, the method offers the time-saving advantage of the sutureless prosthetic rings for the proximal and distal anastomoses.     

Early and late results of coronary artery bypass after failed angioplasty. Actuarial analysis of late cardiac events and comparison with initially successful angioplasty

We reviewed the results of early (less than 24 hours) coronary artery bypass after unsuccessful percutaneous coronary artery angioplasty in 146 patients treated between October 1979 and July 1986. Overall operative mortality was 2.7%, and risk was significantly increased among patients with hemodynamic instability and new occlusion or further narrowing of the dilated vessel (3.8 versus 0%, p less than 0.05). Actuarial analysis was used to compute the rates of cardiac events during the follow-up interval, and event rates were also estimated in a comparison group of 776 patients who had successful first-time PTCA during the same time period. At a follow-up interval of 5 years, the cumulative risks of recurrence of angina and need for an additional procedure (bypass or angioplasty) were significantly (p less than 0.05) lower for patients who had undergone bypass than for those who had successful angioplasty (angina 21% versus 56%, PTCA 2% versus 21%, CAB 6% versus 16%). Cumulative risks of myocardial infarction and death were 4% versus 9% and 6% versus 9% in the two groups. The differences between late outcomes in the bypass and angioplasty groups persisted when patients were stratified into cohorts with single-vessel and multivessel disease, and the highest late event rate occurred in patients in the angioplasty group who had incomplete revascularization. The difference in late events after bypass or angioplasty was greatest during the first year. These late data should be considered when the mode of revascularization (bypass or angioplasty) is selected for symptomatic patients, especially those with multivessel disease.     

Immunohistochemical detection of transforming growth factor-beta 1 in fibrotic liver diseases.

Transforming growth factor-beta 1 was localized by means of immunohistochemical reaction in liver biopsy specimens taken from patients having different chronic liver diseases with extending fibrosis. Two polyclonal antibodies that were produced in rabbits were directed against the amino terminal of transforming growth factor-beta 1. Staining by anti-CC(1-30) was primarily extracellular and located in the portal and periportal fibrotic areas of all seven cases with chronic active hepatitis. No staining was noted in the four chronic persistent cases studied. A strong reaction was seen with the antibody in nine of the ten cirrhotic samples, whereas it was negative in one inactive cirrhosis case and in all five cases with normal liver histological findings. No positive staining could be detected by the anti-LC(1-30) in any of the liver tissues. Detection of transforming growth factor-beta 1 in active liver diseases at the site of fibrosis suggests that transforming growth factor-beta 1 might have a role in the process and progression of fibrosis during the development of the disease.     

Aortic reconstruction in kidney transplant recipients

Renal transplantation has increased the longevity of patients with uremia. An increasing number undergo aortic reconstruction, which exposes the transplanted kidney to ischemic injury. To evaluate the risk for renal failure, loss of the transplant, and methods of renal protection, we reviewed our experience. Clinical data were reviewed for 10 consecutive patients (7 men, 3 women; mean age 52.7 years [range 32 to 75 years]) with a transplanted kidney who underwent aortic reconstruction between 1977 and 1994 at our institution. Mean interval between renal transplantation and aortic reconstruction was 5.9 years (range 1 month to 12.7 years). Seven patients required emergency repair because of dissection (2 patients), aneurysm rupture (4 patients), or symptomatic aneurysm (1 patient); three underwent elective repair. Reasons for reconstruction included aortic dissection (2 patients), aneurysm of the descending thoracic (2 patients), thoracoabdominal (1 patient), or abdominal aorta (3 patients), and aortoiliac occlusive disease (2 patients). Patients with thoracic or thoracoabdominal reconstructions underwent repair with atriofemoral, aortofemoral, or femorofemoral shunt placement or bypass. Of the five abdominal aortic reconstructions, the kidney was protected with aortofemoral shunt placement in one patient and cold renal perfusion in three. In two of them, topical cooling of the kidney also was used. One patient with acute aortic dissection died at 39 days as a result of respiratory failure. Loss of the recently transplanted kidney was caused by acute rejection. One patient had a transient increase in serum creatinine concentration. Eight had no worsening of renal function, and none of the nine survivors lost the transplanted kidney. We conclude that aortic reconstruction can be safely performed in kidney transplant recipients. Patients in whom thoracic or thoracoabdominal aortic reconstruction was required were protected with an atriofemoral or aortofemoral bypass or shunt. Patients undergoing abdominal aortic reconstruction did well when cold renal perfusion with or without local cooling of the transplant was used for renal protection. Transplanted kidneys appeared to tolerate ischemic injury similarly to native kidneys.Presented at the Twentieth Annual Meeting of the Peripheral Vascular Surgery Society, New Orleans, La., June 10, 1995.     

Connective tissue metabolism in children with chronic renal failure

To assess the characteristics of connective tissue metabolism in chronic renal failure (CRF), urinary excretion of glycosaminoglycan (GAG) fractions and hydroxyproline (HYP) was determined in ten patients with CRF and in ten age-matched healthy children. CRF was found to be associated with elevated free HYP (19.9±6.1 vs 9.8±3.6 mol/day,P<0.05) and depressed peptide HYP excretion (33.1±13.5 vs 225.2±17.7 mol/day,P<0.01), a low rate of total GAG excretion (7.0±2.4 vs 16.1±1.9 mol uronic acid/day,P<0.05) with low chondroitin 4 — sulphate + chondroitin 6 — sulphate (Ch-Ss) (14.0±9.9 vs 65.0±22.1%) and a high proportion of non-sulphated or under-sulphated fractions, i.e. hyaluronic acid + chondroitin + heparan sulphate (HA+Ch+HS) (75.3±11.4 vs 31.5±5.7%). Urinary 3-methyl-histidine (3-met-HIS) excretion and plasma essential free amino acids did not differ in the two groups. In response to haemodialysis no consistent change occurred in urinary excretion of 3-met-HIS, peptide-bound HYP, total GAG or percentage distribution of individual GAG fractions. After haemodialysis all plasma amino acids decreased significantly, and there was a significant increase in urinary excretion of free HYP (P<0.05). We conclude that the alterations in urinary excretion of total and individual GAGs observed in CRF may reflect disturbed connective tissue metabolism which does not appear to be accounted for by protein malnutrition or enhanced protein breakdown and remains uninfluenced by haemodialysis therapy.     

Analysis of the genetic variability of the 1st (CCC/ACC,P52T) and the 10th exons (bp 1012–1704) of the TSH receptor gene in Graves’ disease

We determined the genetic variability of the 1st (CCC/ACC, P52T polymorphic variant) and 10th exons (bp 1012–1704) of the TSH receptor (TSHR) gene in Graves’ disease. A total of 101 Graves’ patients and 163 control subjects were screened. The A253 mutant allele was carried by nine patients with Graves’ disease (8.91%) and 13 control subjects (7.98%) in heterozygous genotype. No significant difference in the frequency of the mutant allele was found between Graves’ patients and control subjects. These results provide evidence that the A253 polymorphism has no genetic relevance in Graves’ disease. Moreover, the DNA nucleotide sequence of 693 bp of the 10th exon (bp 1012–1704) of the TSHR gene was determined in 15 Graves’ patients. Six patients were homozygous for the wild‐type allele and nine were heterozygous for the mutant allele at the 253rd nucleotide of the first exon. No polymorphism was found in the DNA sequences obtained from leukocytes of Graves’ patients, similarly to the sequences obtained from the nine control subjects. None of the nine patients carrying the A253 polymorphism in the 1st exon of the TSHR had polymorphism in the examined part of the 10th exon, including two additional patients whose thyroid tissue was directly analysed. In all likelihood, the polymorphisms of the examined regions of either the 1st or the 10th exon of the THSR gene do not contribute to the genetic susceptibility to Graves’ disease.     

Retinoids induce Fas(CD95) ligand cell surface expression via RARgamma and nur77 in T cells

Cells from the CD4+ murine T hybridoma line IP-12-7 enter the apoptotic suicide program via the Fas ligand (FasL)/Fas-mediated pathway upon TCR stimulation. This stimulus regulates the sensitization of the Fas death pathway and the cell surface appearance of preformed FasL. The apoptosis is dependent on new mRNA and protein synthesis and involves up-regulation of nur77.Two groups of nuclear receptors for retinoic acids (RA) have been identified: retinoic acid receptors (RAR) and retinoid X receptors. IP-12-7 cells express RARalpha and RARgamma. Here we show that,in the IP-12-7 T cells, RA also induced the expression and DNA binding of nur77, and the cell surface appearance of FasL. The induction was mediated via RARgamma. Despite the induced expression of cell surface FasL, only two structurally related RARgamma-selective compounds, CD437 and CD2325, initiated apoptosis in these cells. The lack of apoptosis induction by natural RA was related to the inability of RARgamma to sensitize the Fas death-pathway. Cell surface FasL, however, was able to induce cell death in Fas-bearing target cells. Natural RA also induced the expression of FasL in phytohemagglutinin-activated peripheral murine T cells. It is proposed that therapeutically administered RA might induce apoptosis in Fas-sensitive cells via induction of FasL expression in activated Tcells.