Objective assessment of nerve injury after greater saphenous vein stripping.

AIM: The complication of nerve injury after greater saphenous vein stripping for varicosity is subjective, and a method for objective evaluation has never been established. The aim of this study was to evaluate postoperative sensory changes by quantitative assessment of current perception threshold (CPT), and to clarify the relation between CPT and symptoms. PATIENTS AND METHODS: Between January 2003 and August 2005, 27 limbs in 18 patients were enrolled. Quantitative sensory function was determined through CPT using a Neurometer (Neurotron, Inc., USA), with which saphenous nerve neural fiber selective minimum sensing values against three electrical stimuli (2000, 250, 5 Hz) were measured. CPT measurements were scheduled on the day before the operation, and 2-7 days, 1, 3, and 6 months after the operation. RESULTS: An increase in CPT value of more than 20% or decrease to below 50% compared to the preoperative value with at least two stimuli was defined as CPT abnormality. Subjective symptoms were observed in 13 limbs in the early postoperative period, and 10 limbs showed CPT abnormality. In 6 limbs with a CPT increase over 20% with all three stimuli, neurological symptoms continued for 6 months. CONCLUSIONS: CPT evaluation provides an objective indication of neurological symptoms in the lower limb following varicose vein surgery.     

Indirect carotid-cavernous sinus fistula: transvenous embolization from the external jugular vein using a superior ophthalmic vein approach. A case report

A case of indirect carotid-cavernous sinus fistula treated by combined transarterial and transvenous embolization is described. A 49-year-old woman with a right indirect carotid-cavernous sinus fistula draining solely to the right superior ophthalmic vein was treated first by transarterial embolization with polyvinyl alcohol particles. Then, by approaching through the superior ophthalmic vein from the right external jugular vein, the cavernous sinus was embolized with platinum wire using a tracker microcatheter, which resulted in marked clinical improvement. Transvenous embolization by approaching from the external jugular vein through the superior ophthalmic vein represents a promising alternative when shunted blood drains anteriorly to the superior ophthalmic vein.     

Retroperitoneal primary mucinous adenocarcinoma with a mural nodule of anaplastic tumor: a case report and literature review.

A 38-year-old female presented with a lower abdominal mass. During the operation the mass was found to be retroperitoneal and was excised. Gross examination revealed a mucin-containing cystic lesion with a mural nodule. On microscopic examination, the cystic areas were lined by an invasive mucinous adenocarcinoma and the nodule was composed of an anaplastic sarcomatoid tumor that was immunoreactive for cytokeratin. This present case is the 21st example of a retroperitoneal primary mucinous cystadenocarcinoma and the fourth with a mural nodule. Three of four cases with a mural nodule, including our case, had a rapidly fatal outcome.     

Suppression of in vitro hemopoiesis by the monocytes in a patient with aplastic anemia associated with hepatitis]

The cause of aplastic anemia associated with hepatitis (AAH) is as yet still unknown. There is a supposed relation to the immune mechanisms, however few reports have shown the effects of monocytes on the pathogenesis in the patients with AAH. We have reported a case of a 12-year-old boy with AAH related to cytomegaloviruses, and studied the hemopoietic progenitors. He showed pancytopenia and hypoplasia of the bone marrow on admission to our hospital. The culture studies showed that mononuclear cells (MNC) of the bone marrow produced few hemopoietic colonies in all cell lineages. However, the depletion of adherent cells from the MNC increased numbers of erythroid, neutrophil-macrophage and megakaryocyte colonies. Furthermore, the addition of adherent cells of the peripheral blood suppressed the colony formation in the aforementioned cell lineages by marrow MNC from which adherent cells, phagocytic cells and T-cells were abrogated. The results way suggest that monocytes play some soles in the pathogenesis of aplasia through inhibitor of hemopoiesis.     

Mitochondrial trifunctional protein deficiency. Catalytic heterogeneity of the mutant enzyme in two patients.

We examined the enzyme protein and biosynthesis of human trifunctional protein harboring enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase activity in cultured skin fibroblasts from two patients with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency. The following results were obtained. (a) In cells from patient 1, immunoblot analysis and pulse-chase experiments indicated that the content of trifunctional protein was < 10% of that in control cells, due to a very rapid degradation of protein newly synthesized in the mitochondria. The diminution of trifunctional protein was associated with a decreased activity of enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase, when measured using medium-chain to long-chain substrates. (b) In cells from patient 2, the rate of degradation of newly synthesized trifunctional protein was faster than that in control cells, giving rise to a trifunctional protein amounting to 60% of the control levels. The 3-hydroxy-acyl-CoA dehydrogenase activity with medium-chain to long-chain substrates was decreased drastically, with minor changes in activities of the two other enzymes. These data suggest a subtle abnormality of trifunctional protein in cells from patient 2. Taken together, the results obtained show that in both patients, long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency is caused by an abnormality in the trifunctional protein, even though there is a heterogeneity in both patients.     

Activated caspase expression and apoptosis increase in keloids: cytochrome c release and caspase-9 activation during the apoptosis of keloid fibroblast lines

To characterize apoptosis in keloids and the mechanisms responsible for this process, the expression of activated caspase-9 and -3 in fibroblasts obtained from keloids was analyzed. Immunohistochemistry revealed that the number of fibroblasts positive for terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) or activated caspase-9 or -3 was low but was significantly higher in keloid tissues than in normal scar tissues. Significant relationships between the number of caspase-positive fibroblasts and TUNEL-positive fibroblasts suggested that the activation of caspase-9 and -3 induces apoptosis in a subpopulation of keloid fibroblasts. All keloid fibroblast cell lines established in this study showed activation of caspase-9 and -3 after serum deprivation for 3 or 4 hours, as shown using Western blotting. Furthermore, serum deprivation-induced apoptosis in a keloid fibroblast line was blocked by a caspase-9 inhibitor (acetyl-Leu-Glu-His-Asp-al), indicating that activation of caspase-9 was necessary for the process of apoptosis in keloid fibroblasts. Although serum deprivation did not significantly change the level of apoptosis protease activating factor-1 in any of the lines, cytochrome c release was detected in cytosolic fractions of the lines after serum deprivation for 3 or 4 hours. These results strongly suggest that keloid fibroblasts are predisposed to apoptosis and cytochrome c release and that caspase-9 activation may underlie regulation of apoptosis in keloid fibroblasts in vivo.     

Laser Doppler skin perfusion pressure in the assessment of Raynaud's phenomenon.

OBJECTIVES: In the assessment of Raynaud's phenomenon, objective evaluation of digital microcirculatory flow is important, and so we investigated whether the measurement of laser Doppler skin perfusion pressure could be of use. MATERIALS AND METHODS: Ten fingers of five patients with secondary Raynaud's phenomenon due to systemic sclerosis, 22 fingers of 11 patients with primary Raynaud's phenomenon and 10 fingers of five control patients were examined. Skin perfusion pressure was measured on the third finger of both hands at rest, and then again 3 min after local cold exposure. RESULTS: Laser Doppler skin perfusion pressure at rest in patients with secondary Raynaud's phenomenon was significantly lower than that in patients with primary Raynaud's phenomenon and the control patients (p<0.05). Skin perfusion pressure decreased significantly in both patient groups upon local cold exposure (p=0.005). There were significant differences in perfusion pressure after cold exposure among both groups (p<0.05). CONCLUSIONS: The low skin perfusion pressure at rest in patients with secondary Raynaud's phenomenon suggested the presence of obstructive arterial lesions. The marked pressure decrease in all Raynaud's patients after local cold exposure might be due to vasospasm of the microvasculature in the digits. These results indicate that the measurement of laser Doppler skin perfusion pressure is valuable in the diagnosis of Raynaud's phenomenon.     

Antibodies against saline-soluble components of skeletal muscle in myasthenia gravis

Summary Antibodies against phosphate-buffered-saline extracts (SE) of non-acetylcholine receptor (AChR) skeletal muscle antigens were found in patients with myasthenia gravis (MG). The antigenicity of SE was distributed in three fractions with molecular masses of over 200 kDa, 90–150 kDa and 7–14 kDa on gel filtration. These fractions shared common antigenicities. Further analysis of 90–150 kDa fractions on sodium dodecyl sulphate polyacrylamide gel electrophoresis showed five major bands, ranging from 105 kDa to 275 kDa. The antibodies against SE were detected in 52% (58/112) of the MG patients; incidence and titres were higher in the thymoma group (n=21; 90% and 0.872 respectively) than in the non-thymoma group (n=91; 43% and 0.200, P<0.001). In patients without a thymoma, these antibodies were frequently observed in late-onset disease and the severe generalized form (P<0.01). In 4 of 7 ocular MG patients without anti-AChR antibodies, low but appreciable levels of anti-SE antibodies were found. In 73% (11/15) of generalized MG patients treated with prednisolone and thymectomy, anti-SE antibody titres changed in association with those of anti-AChR antibodies and with the clinical course. Both antibody titres increased synchronously in patients who developed crises.