Die verwendung der autologen vena femoralis bei vena-cava-superior-thrombose

We report on a 52-year old male patient who underwent implantation of an insulin pump because he had diabetes and in whom superior vena cava syndrome developed as a long-term complication. After unsuccessful lysis therapy superficial femoral vein was implanted to form a bypass from the internal jugular vein to the right atrium. The postoperative course was uneventful from the aspects of both the bypass and the leg after explantation of the superficial femoral vein. The bypass is still patent 7 months after the operation, and the patient has no symptoms. Autogenous superficial femoral vein can be used successfully in the reconstruction of large venous vessels. It should be the graft of choice for young patients with benign diseases. We compare our result and those obtained with different substitutes described in the literature that have been used for reconstruction in superior vena cava syndrome.

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Die verwendung der autologen vena femoralis bei vena-cava-superior-thromboseFallbericht mit literaturübersicht

Zusammenfassung Bei einem 52jährigen, männlichen Patienten trat nach Implantation einer Insulinpumpe als Spätkomplikation eine Thrombose der Vena cava superior auf. Nach erfolgloser Lysetherapie wurde ein Venajugularis-rechtsatrialer-Venenbypass mit autologer Vena femoralis durchgeführt. Der postoperative Heilungsverlauf war sowohl von Seiten des gefäßrekonstruktiven Eingriffs, als auch von Seiten der Venenentnahmestelle komplikationslos. Der Bypass ist 7 Monate postoperativ offen und der Patient beschwerdefrei. Die autologe Vena femoralis eignet sich zur Rekonstruktion großer venöser Gefäße ausgezeichnet. Sie sollte v. a. bei benignen Prozessen und jüngeren Patienten als autologes Bypassmaterial dem Kunststoff vorgezogen werden. Das Ergebnis wird mit verschiedenen Gefäßsubstituten, die bei Verschluß der oberen Hohlvene verwendet werden, verglichen.

     

Dorsal root ganglia cocultured with macrophages: an in vitro model to study experimental demyelination

The present investigation introduces an in vitro model to study macrophage properties during demyelination. Rat dorsal root ganglia (DRG) were cultured for obtaining myelinated peripheral nerve fibers. These cultures were exposed to non-resident macrophages. In untreated control cultures, there was no indication of myelin removal by the added macrophages. DRG were exposed to enzymatically generated oxygen radicals using the xanthin/xanthin oxidase or the glucose/glucose oxidase system. Assessment of Schwann cell viability and ultrastructural morphology revealed different patterns of cell cytotoxicity and morphological changes in different experiments. High concentrations caused complete tissue necrosis of the DRG, while low concentrations did not affect either cell viability or ultrastructural morphology. Under intermediate experimental conditions, oxygen radicals caused non-lethal Schwann cell damage leading to Schwann cell retraction and myelin sheath rejection. Myelin lamellae were disrupted and decompacted. These changes were followed by a selective macrophage attack on myelin sheats, resulting in demyelination. Axons, Schwann cells and sensory ganglion cells survived this attack. The specificity of the oxygen radical effects was tested in experiments using the oxygen radical scavengers catalase and superoxide dismutase. Catalase prevented the described effects on cell morphology and subsequently blocked demyelination by non-resident macrophages.Supported by a grant from the Deutsche Forschungsgemeinschaft (DFG) (Br 1274/1-1)     

Severe tubulopathy and kidney graft rupture after coadministration of mannitol and ciclosporin.

Spontaneous allograft rupture after kidney transplantation is a rare complication usually due to an acute rejection of the interstitial type. In a 32-year-old man kidney transplantation was performed under immunosuppression with prednisolone and ciclosporin (CS). The dose of CS was 5 mg/kg body weight intravenously for the first 24 h, on the 2nd day 10 mg/kg/day orally, with gradually decreasing doses thereafter. The patient remained oliguric in the postoperative period and received additionally 600 ml mannitol solution intravenously for osmodiuresis within a period of 6 days. On the 8th postoperative day, 48 h after the last intravenous infusion of mannitol, spontaneous renal rupture occurred. The CS concentrations in the blood during the days before the rupture were within the upper normal range for effective immunosuppression (300-600 ng/ml). Intraoperatively the kidney appeared enlarged due to edematous swelling of the graft, but it showed no signs of rejection. The histological finding was a toxic tubulopathy with extensive isometric vacuolization and peritubular congestion, a known side effect of both of CS and of mannitol. The rupture was successfully repaired. Thirty-four days after the transplantation diuresis increased and hemodialysis therapy could be discontinued. In a second biopsy of the kidney the signs of toxic tubulopathy with isometric vacuolization were reduced. On the following days the serum creatinine dropped below 160 mumol/l. It can be assumed that the combination of CS therapy and administration of massive and continued doses of mannitol in an oliguric patient with allograft kidney may potentiate severe tubulopathy with concomitant edematous swelling of the graft. This can result in an increasing danger of spontaneous renal rupture.     

An HLA-DRB α-helix motif shared by DR11 and DR8 alleles is implicated in the pluriallelic restriction of peptide-specific T-cell lines

The T-cell recognition of HLA-DR-peptide complexes is generally restricted by the polymorphism of the DRB molecules but pluriallelic restriction has been described. The molecular basis of restriction and promiscuity of such peptide-specific responses is poorly understood. We isolated a panel of T-cell lines specific for the tetanus toxin peptide p2 (TT830-843) exhibiting pluriallelic restriction by DR11 and DR8 alleles. Fine restriction specificity of the T-cell lines was examined in functional assays against DR oligotyped APCs expressing different variants of DR11 and DR8 alleles. Our results show that (a) polymorphisms between serologically related alleles are relevant in terms of restriction of the peptide-specific T-cell response; in some instances, a single amino acid substitution can determine the restriction of a T-cell line; (b) different patterns of restriction are not the result of specific differences in DR-p2 binding as p2 peptide binds to all DR11 and DR8 alleles tested (DRB1^* 1101, -1102, -1103, -1104, 110X, -0801, -0802, -0803, and -0806); and (c) pluriallelic restriction of the peptide-specific T-cell responses correlates with the presence of a DRB1 α-helix motif (67-71-86) shared by some DR11 and DR8 alleles. Possible implications of pluriallelic restriction of peptide-specific T-cell response in autoimmune disorders associated with DR11 and DR8 are discussed.     

Extraocular changes in congenital aniridia]

The authors draw attention to possible extraocular changes in children with congenital aniridia. Of 31 investigated patients they were found in 5 children. Among these changes, because of its serious character, Wilms tumour holds the first place; it was found by the authors in two children. To ensure its early detection, the authors emphasize the necessity to dispensarize all children with congenital aniridia. Collaboration with an experienced X-ray specialist and child oncologist is essential. In addition to Wilms' tumour congenital aniridia can be associated with serious somatic developmental changes. The authors observed in one child and AGR triad and in two patients deformities of the skeleton of the head and lower extremities.     

Human urotensin-II potentiates the mitogenic effect of mildly oxidized low-density lipoprotein on vascular smooth muscle cells: comparison with other vasoactive agents and hydrogen peroxide.

Human urotensin-II (U-II) is the most potent vasoactive peptide identified to date, and may be involved in hypertension and atherosclerosis. We investigated the effects of the interactions between U-II or other vasoactive agents and mildly oxidized low-density lipoprotein (mox-LDL) or hydrogen peroxide (H2O2) on the induction of vascular smooth muscle cell (VSMC) proliferation. Growth-arrested rabbit VSMCs were incubated with vasoactive agents (U-II, endothelin-1, angiotensin-II, serotonin, or thromboxane-A2) in the presence or absence of mox-LDL or H2O2. [3H]Thymidine incorporation into DNA was measured as an index of VSMC proliferation. On interaction with mox-LDL or H2O2, U-II induced the greatest increase in [3H]thymidine incorporation among these vasoactive agents. A low concentration of U-II (10 nmol/l) enhanced the potential mitogenic effect of low concentrations of mox-LDL (120 to 337%) and H2O2 (177 to 226%). U-II at 50 nmol/l showed the maximal mitogenic effect (161%), which was abolished by G protein inactivator (GDP-beta-S), c-Src tyrosine kinase inhibitor (radicicol), protein kinase C (PKC) inhibitor (Ro31-8220), extracellular signal-regulated kinase (ERK) kinase inhibitor (PD98059), or Rho kinase inhibitor (Y27632). Mox-LDL at 5 microg/ml showed the maximal mitogenic effect (211%), which was inhibited by free radical scavenger (catalase), intracellular and extracellular antioxidants (N-acetylcysteine and probucol), nicotinamide adenine dinucleotide phosphate oxidase inhibitor (diphenylene iodonium), or c-Jun N-terminal kinase (JNK) inhibitor (SP600125). These results suggested that U-II acts in synergy with mox-LDL in inducing VSMC DNA synthesis at the highest rate among these vasoactive agents. Activation of the G protein/c-Src/PKC/ERK and Rho kinase pathways by U-II together with the redox-sensitive JNK pathway by mox-LDL may explain the synergistic interaction between these agents.     

Bone mass and bone cellular variations after five months of physical training in rhesus monkeys: Histomorphometric study

Summary Five Rhesus Monkeys (Maccaca mulatta), a suitable nonhuman model, performed 5 months of ropeclimbing exercise. Duration of the training sessions was progressively increased to reach 1 hour/day after 1 month of training and was maintained until the end of the experiment. Bone mass parameters, bone resorption, and bone formation activity were measured by histomorphometric analysis on iliac crest bone biopsies before and after the experiment. Mineral apposition rate was measured in cortices and trabecular bone after double calcein labeling. Five months of rope-climbing exercise had determined a significant decrease of bone volume with a slight decrease of the number and thickness of trabeculae. This might induce an alteration of biomechanical properties of bone. These architectural modifications were associated with a nonsignificant decrease of bone resorption activity. But the main effect of training was an important decrease of bone formation activity without change of the mineral apposition rate. Endurance exercise at low intensity has determined a decreased bone turnover with osteoblastic depression. This animal experiment points out that exercise modalities might be important in the bone response to training and should be carefully defined for preventive use in humans.     

The effect of quinidine on the analgesic effect of codeine

Summary We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg). The study was performed in 16 extensive metabolizers of sparteine, using a double-blind, randomized, four-way, cross-over design. The treatments given at 3 h intervals during the four sessions were placebo/placebo, quinidine/placebo, placebo/codeine, and quinidine/codeine. We measured pin-prick pain and pain tolerance thresholds to high energy argon laser stimuli before and 1, 2, and 3 h after codeine or placebo.After codeine and placebo, the peak plasma concentration of morphine was 6–62 (median 18) nmol·.l^–1. When quinidine pre-treatment was given, no morphine could be detected (<4 nmol·l^–1) after codeine. The pin-prick pain thresholds were significantly increased after placebo/codeine, but not after quinidine/codeine compared with placebo/placebo. Both placebo/codeine and quinidine/codeine increased pain tolerance thresholds significantly. Quinidine/codeine and quinidine/placebo did not differ significantly for either pin-prick or tolerance pain thresholds.These results are compatible with local CYP2D6 mediated formation of morphine in the brain, not being blocked by quinidine. Alternatively, a hypoalgesic effect of quinidine might have confounded the results.     

Cerebral involvement in adult onset Still's disease

Still's disease was diagnosed in a 40-year-old patient as a cause of psycho-organic syndrome with complete disorientation and stupor, sensory and motor aphasia. There were no signs of a tumour, cerebrovascular accident, bacterial or viral infection. The patient recovered quickly from the cerebral disturbances under treatment with corticosteroids. Similar symptoms in adult patients with Still's disease are seldom found in the literature.     

Venous surgery in veno-occlusive dysfunction: long-time results after deep dorsal vein resection.

Follow-up of patients 1 year after deep dorsal vein resection gives evidence of an approximate 50-60% success rate. A careful selection of only this small percentage of patients, in whom abnormal drainage through the penile dorsum is obvious, is mandatory. Men with an arterial cofactor have to be excluded or to be subsequently treated by intracavernosal autoinjection of vasoactive substances. Late results from our study demonstrate a further loss of sufficient erection, also in men considered as persistent success by us, in the subjective view of the patient and/or his sexual partner.