Segmental dilatation of the ileum accompanying hypoproteinemia

Purpose

Segmental intestinal dilatation (SID) is a rare pathologic finding, which causes intestinal obstruction in newborn period and gastrointestinal bleeding, anemia, abdominal pain, malabsorption, and growth failure in older children. We present a case of SID causing hypoproteinemia.

Patient

A 10-year-old girl presented with recurrent abdominal distension since she was 8.5 months old. She was diagnosed to have protein-losing intestinal lymphangiectasia. Result of physical examination was normal except moderate growth retardation. Her blood workup showed depletion in total protein, albumin, and globulin levels. Gastrointestinal series revealed a dilated segment of small intestine, and Tc^99m-pertechnetate scintigraphy detected ectopic activity in abdomen. The patient was taken to operation with the presumptive diagnosis of intestinal duplication. A dilated segment of ileum was encountered, and segmental resection and anastomosis were performed.

Results

Patient was discharged on the postoperative fourth day and remains well. Histopathologic examination of the specimen revealed SID.

Discussion

Segmental intestinal dilatation is an uncommon congenital anomaly. Most of the cases were operated on in newborn period because of intestinal obstruction, and their diagnoses were made perioperatively; the others were diagnosed in older ages during the investigation of nonspecific symptoms. The index patient is the second case of SID having hypoproteinemia in the literature. Gastrointestinal series suggested the diagnosis, and segmental resection and anastomosis were the adequate treatments.     

A novel locus for restless legs syndrome on chromosome 13q

Background: Restless legs syndrome (RLS) is a sensorimotor disorder in which affected individuals suffer from uncomfortable sensations and an urge to move their lower limbs; it occurs mainly in resting situations during the evening or at night. Multiple chromosomal loci have been mapped for RLS through family-based linkage analysis, and genome-wide association studies but causative mutations have not been identified yet. Method: We identified an RLS family from the eastern part of central Turkey which has 10 patients suffering from this syndrome. Whole genome linkage analysis was performed in family members who consented for study (9 affected and 2 unaffected). Results: A theoretical maximum logarithm of the odds score of 3.29 was identified at chromosome 13q32.3-33.2. This result shows strong genetic linkage to this locus. Conclusions: We demonstrated a genetic linkage at chromosome 13 in a RLS family. Further investigation in this linkage area may reveal a causative gene leading to RLS phenotype and may illuminate the pathogenesis of this disease. This study supports the genetic heterogeneity in the pathogenesis of this syndrome.     

Ion release from metal-ceramic alloys in three different media

The aim of this in vitro study was to assess the effect of pH changes on ion release of metal-ceramic dental casting alloys. Samples from four commercially available alloys (Wirobond C, Wiron 99, Rematitan CP-Ti grade 1, and PontoStar) were prepared and polished. Ion release of alloys subjected to three different pH media (artificial saliva of pH 2.3, pH 6.5 and 0.9% saline solution of pH 7.3) for periods of 7, 15, 30, and 60 days were assessed by means of atomic absorption spectroscopy. Microscopic changes on surfaces of metallic samples before and after immersion were compared by scanning electron microscopy. ANOVA was used for statistical analysis of results. For all ions, pH and period interactions were statistically significant: highest amount of ion release occurred after 60 days of immersion regardless of pH value. For every alloy, ion release results were highest in artificial saliva of pH 2.3 and lowest in 0.9% saline solution. It was concluded that ion release from alloys was pH-dependent.     

Pyrrolidine dithiocarbamate prevents 60 minutes of warm mesenteric ischemia/reperfusion injury in rats

BACKGROUND: Pyrrolidine dithiocarbamate (PDTC) is a low-molecular-weight thiol antioxidant and potent inhibitor of nuclear factor-kappaB (NF-kappaB) activation. It has been shown to attenuate harmful effects of ischemia/reperfusion (I/R) injury in many organs. In recent animal studies, destructive effects of reperfusion injury has been demonstrated. In this study, we aimed to investigate whether PDTC prevents harmful effects of superior mesenteric I/R injury in rats. METHODS: Wistar-albino rats were randomly allocated into the following 4 groups: (1) sham-operated group--these animals underwent laparotomy without I/R injury (group I, n = 12); (2) sham+PDTC group--identical to sham-operated rats except for the administration of PDTC (100 mg/kg intravenous bolus) 30 minutes prior to the commencement of the experimental period (group II, n = 12); (3) I/R group--these animals underwent laparotomy and 60 minutes of ischemia followed by 120 minutes of reperfusion (group III, n = 12); (4) PDTC-treated group (100 mg/kg, intravenously, before the I/R, group IV, n = 12). All animals were killed, and intestinal tissue samples were obtained for investigation of intestinal mucosal injury, myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, glutathione (GSH) levels, and intestinal edema. RESULTS: There was a statistically significant decrease in GSH levels, along with an increase in intestinal mucosal injury scores, MPO activity, MDA levels, and intestinal tissue wet-to-dry weight ratios in group III when compared to groups I, II, and IV (P < .05). However, PDTC treatment led to a statistically significant increase in GSH levels, along with a decrease in intestinal mucosal injury scores, MPO activity, MDA levels, and intestinal tissue wet-to-dry weight ratios in group IV (P < .05). CONCLUSIONS: This study showed that PDTC treatment significantly prevented the reperfusion injury caused by superior mesenteric I/R. Further clinical studies are needed to clarify whether PDTC may be a useful therapeutic agent to use in particular operations where the reperfusion injury occurs.     

Depletion of glutathione by buthionine sulfoximine decreases random-pattern skin flap viability in rats

BACKGROUND: Glutathione (GSH) is one of the most highly concentrated intracellular antioxidants. Exogenous GSH has been shown to increase random-pattern skin flap survival. However, the effects of endogenous GSH depletion on random-pattern skin flap viability have never been studied. MATERIALS AND METHODS: To evaluate the effects of systemic glutathione depletion on random-pattern skin flap survival in rats, 28 Wistar albino rats were divided into control, sham, and BSO (buthionine sulfoximide, a selective inhibitor for gamma-glutamylcysteine synthetase) groups. Dorsal, cranial-based random-pattern skin-flaps were elevated and the percentage of flap necrosis was measured in all rats at the postoperative day 7. RESULTS: BSO-treated rats showed increased skin flap necrosis when compared with untreated animals (P < 0.001). High-dose BSO treatment group had more clinically evident necrosis than low dose group (P < 0.05). CONCLUSIONS: This study reveals the importance of endogenous GSH for random skin-flap viability.     

Ischemia-reperfusion injury in rat skeletal muscle is attenuated by zinc aspartate

BACKGROUND: Oxygen-derived free radical-induced cell injury has been suggested to have a pivotal role in the etiology of ischemia-reperfusion injury. Thus, several lines of evidence indicate that antioxidant agents may be useful therapeutics in this condition. In this regard, the effect of zinc aspartate on ischemia-reperfusion injury was investigated in skeletal muscle. MATERIALS AND METHODS: Tourniquet ischemia-reperfusion injury method was applied to Sprague-Dawley rats. Experimental groups were as follows: 1) sham control, 2) rats received zinc aspartate, 3) rats received hind limb tourniquet operation (left side), and 4) rats received hind limb tourniquet operation and zinc aspartate. Viability of muscle was evaluated by triphenyltetrazolium chloride dye method by using a spectrophotometer. Malondialdehyde, superoxide dismutase, catalase, glutathione, and glutathione peroxidase were measured in muscle, heart, lung, and blood via a spectrophotometer. RESULTS: The viabilities of ischemic limbs, percentage of the contralateral control muscle, in group 1, 2, 3, and 4 were 114 +/- 12%, 87% +/- 5%, 20% +/- 2%, and 95 +/- 10%, respectively. In muscle, increased malondialdehyde and decreased superoxide dismutase, catalase, and glutathione levels in group 3 were normalized by zinc aspartate in both left and right limbs. While malondialdehyde levels in heart and blood increased in group 3, the levels of superoxide dismutase, catalase, glutathione, and glutathione peroxidase were lower in group 3 than those in group 1. All these alterations were prevented by zinc aspartate. Malondialdehyde level of lung in group 3 was significantly higher than group 1 and 2. However, this augmentation was halted by zinc aspartate. The decrease in superoxide dismutase levels in group 3 was statistically reversed by the administration of zinc aspartate. CONCLUSION: Zinc aspartate seems to be an effective treatment option against ischemia-reperfusion injury.     

Should we operate all extradural spinal arachnoid cysts? Report of a case

Spinal canal extradural arachnoid cyst is an uncommon, expanding lesion which may communicate with the subarachnoid space. They may be either intra or extradural with intradural cysts being less common. Spinal arachnoid cysts are usually in the thoracic spine, and they may cause symptoms due to spinal cord compression. Although surgery is the preferred way of management, there are reported cases with long term follow-up in the literature. Here we present a 14-year-old female who presented with intermittent low back pain for 1 year and a spinal arachnoid cyst that was followed for two years without any neurological deterioration.     

Adult polysplenic syndrome accompanied by aberrant right subclavian artery and hemangioma in a cleft spleen: a case report

We present a case of adult polispleny syndrome accompanied by cleft spleen containing a cavernous hemangioma and an aberrant right subclavian artery. Patients with polysplenic syndrome are usually lost in childhood and rarely reach adulthood. The most frequently accompanying vascular abnormality is an interrupted inferior vena cava with azygous-hemiazygous continuation. Arterial vascular anomalies are rather rare, and there are several reports in the medical literature where cases of childhood polyspleny syndrome are accompanied by pulmonary arteriovenous fistulas or a main hepatic artery originating from the superior mesenteric artery. The case presented here seems to be the first report of adult polysplenic syndrome with an aberrant subclavian artery and a splenic cavernous hemangioma. The possible congenital vascular anomalies which eventually could accompany adult polysplenic syndrome cases are clinically important for the approach to the patient and planning of eventual vascular interventions.