Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Image localized 31P magnetic resonance spectroscopy of the spleen was performed in six normal volunteers, 13 patients with splenomegaly due to haematological malignancies, and two patients with benign causes of splenomegaly. The malignant disorders had elevated phosphomonoesters (PME) compared to controls, probably due to increased turnover of membrane phospholipids, with variable alterations in high energy phosphates. There appeared to be no relationship between grade of malignancy and relative PME peak area. An overlap in spectral characteristics between the benign and malignant cases of splenomegaly existed. Serial studies in a patient with high grade lymphoma receiving combination chemotherapy showed changes in phosphorus spectra, with an increase in the phosphodiester/beta adenosine triphosphate ratio.
NMR Biomed 1989 Nov
PMID:Characterization of the spleen by in vivo image guided 31P magnetic resonance spectroscopy. 264 99

In-vivo 31P-NMR spectroscopy of the spleen was carried out in 15 patients with splenomegaly from various causes (Hodgkin's disease, non-Hodgkin lymphoma, polycythaemia vera, chronic lymphatic leukaemia, chronic myeloid leukaemia). Volume selection was with the ISIS technique, voxel size was between 3 x 5 x 5 and 8 x 6 x 7 cm3. There was a markedly elevated (PM+Pi)/beta-NTP quotient (mean 3.41 with a standard deviation of 0.37) (p < 0.001) and raised PDE/beta/NTP quotient as compared with 8 normals, who showed an (PME+Pi)/beta-NTP quotient of 2.32 and a PDE/beta/NTP quotient of 1.11. These raised quotients were interpreted as indicating increased membrane phospholipid metabolism due to increased cell turnover. The data suggest there may be some clinical value in performing 31P-NMR spectroscopy for defining splenic involvement in myeloproliferative diseases but further confirmatory studies will be necessary.
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PMID:[Initial results of in vivo 31P-NMR spectroscopy of the spleen in patients with splenomegaly]. 835 66

Mucopolysaccharidosis IVA (Morquio-Brailsford syndrome) results from an inborn deficiency of n-acetyl-galactosamine-6-sulphate sulphatase. Clinical features include skeletal deformities with hypoplasia or absence of the odontoid process of the axis. The resulting atlanto-axial subluxation compresses the spinal cord, resulting in cervical myelopathy. Without treatment, quadriplegia ensues sooner or later; consequently, surgical decompression and dorsal fusion of the cervical vertebrae is recommended, either prophylactically or therapeutically. Anaesthesiological management must focus on protection of the airway without compromising integrity of the cervical spinal cord; quadriplegia subsequent to positioning of the head under anaesthesia has been reported. We have performed fiberendoscopic nasotracheal intubation in a 23-month-old child presenting for neurosurgical treatment of cervical myelopathy resulting from Morquio-Brailsford syndrome. CASE REPORT. A 23-month-old girl (84 cm, 11 kg) with Morquio-Brailsford syndrome presented for surgical decompression and dorsal fusion of the cervical spine. Pre-anaesthetic examination revealed enamel defects, chronic bronchitis, and splenomegaly; the neck was immobilised with a collar. Radiological examinations (X-ray and NMR) revealed narrowing of the atlanto-occipital and atlanto-axial spaces (Fig. 1) and compression of the cervical spinal cord (Figs. 2 and 3). Pre-anaesthetic medication consisted of midazolam juice (4 mg). After establishing intravenous access, atropine (0.5 mg), midazolam (1 mg), and ketamine (10 mg) were administered. A 22 Fr nasopharyngeal airway (Wendl) was lubricated with local anaesthetic gel and introduced into the right nostril; oxygen was administered through a probe to the left nostril. The Wendl-airway was then removed, another 5 mg ketamine was administered, and a 3.5-mm flexible fiberendoscope--over which a 20 Fr armored tube was slipped--was introduced through the right nostril. With the child spontaneously breathing, the glottis was visualised and the fiberscope introduced into the trachea (Fig. 4); 1 mg midazolam and 35 mg ketamine was administered and the endotracheal tube was advanced through the nose into the trachea, utilizing the fiberscope as a guide. The distance between endotracheal tube and carina was assessed endoscopically, the fiberscope withdrawn, and the tube connected to the breathing system. Pulse oxymetric readings were 98% during induction of anaesthesia including endotracheal intubation. Anaesthesia was continued with enflurane, alfentanil, midazolam, and atracurium; 315 min after induction the trachea was extubated and the child discharged to the paediatric intensive care unit. The postsurgical course was uneventful, and the child resumed co-ordinated gait. DISCUSSION. Airway management in patients with mucopolysaccharidoses may be extremely difficult. Recommended methods such as blind nasal intubation are not feasible in small children. Anaesthetic management in children younger than 2 years with Morquio-Brailsford syndrome presenting for cervical spine surgery has not yet been described. Fiberoptically guided nasotracheal intubation is a means of airway management that does not require repositioning of the head and may be performed with the stabilising collar left in place (Fig. 4); preservation of cervical spinal cord integrity may hence be assumed. Analgosedation with ketamine and midazolam allows sufficient spontaneous breathing and--to some extent--maintenance of protective laryngeal reflexes. In conclusion, anaesthetic management of patients with Morquio-Brailsford syndrome is a challenge that is further increased by extending indications for surgical intervention to include infants. With respect to protecting the airway, fiberoptic nasotracheal intubation of the spontaneously breathing child is our method of choice.
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PMID:[Securing the airway in children with the Morquio-Brailsford syndrome]. 836 34

A significant fraction of global population is under the threat of malaria. Majority of annual death is due to the more complicated form of the infection i.e. the cerebral form, also known as Cerebral Malaria (CM). Host parasite interaction is known to cause a cascade of events in various tissues like brain, liver, kidney, and spleen. We have employed (1)H NMR based metabolomics to understand the specific perturbations of various tissues in CM. In our previous paper we have delineated the differences between CM vis-a-vis non-cerebral malaria (NCM) mice in serum, liver and brain. In this paper we focus on their differences of metabolic profile in kidney and spleen as kidney dysfunction and splenomegaly are known to be associated to neurological outcome of the disease. Moreover we have also looked into how the biological compartments (kidney, spleen and serum) interact with each other. The various metabolites involved in such interactions and their correlational aspects across the compartments have been studied in CM, NCM and control mice. The idea was to find out the specific pathways that are altered in CM mice. Our results demonstrate that both the kidney as well as spleen metabolism are differentially perturbed in CM with respect to NCM. The results point out that glutamate levels are decreased in CM mice with respect to NCM mice both in case of spleen and kidney while creatine, myo-inositol and betaine levels are increased in kidney of CM mice with respect to NCM mice. From the analysis of Multiway Principal Component Analysis (MPCA) we see that lipid metabolism and TCA cycle is altered in kidney and spleen.
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PMID:Metabolic perturbations of kidney and spleen in murine cerebral malaria: (1)H NMR-based metabolomic study. 2403 68

Salmonella typhimurium is a bacterial pathogen that poses a great threat to humans and animals. In order to discover hosts' responses to S. typhimurium infection, we collected and analyzed biofluids and organ tissues from mice which had ingested S. typhimurium. We employed (1)H NMR spectroscopy coupled with multivariate data analysis and immunological techniques. The results indicate that infection leads to a severe impact on mice spleen and ileum, which are characterized by splenomegaly and edematous villi, respectively. We found that increased levels of itaconic acid were correlated with the presence of splenomegaly during infection and may play an important role in Salmonella-containing vacuole acidification. In addition, metabonomic analyses of urine displayed the development of salmonellosis in mice, which is characterized by dynamic changes in energy metabolism. Furthermore, we found that the presence of S. typhimurium activated an anti-oxidative response in infected mice. We also observed changes in the gut microbial co-metabolites (hippurate, TMAO, TMA, methylamine). This investigation sheds much needed light on the host-pathogen interactions of S. typhimurium, providing further information to deepen our understanding of the long co-evolution process between hosts and infective bacteria.
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PMID:Systemic responses of BALB/c mice to Salmonella typhimurium infection. 2520 11

Tsutsugamushi disease is an infectious disease transmitted to humans through the bite of the Orientia tsutsugamushi-infected chigger mite; however, host-pathogen interactions and the precise mechanisms of damage in O. tsutsugamushi infections have not been fully elucidated. Here, we analyzed the global metabolic effects of O. tsutsugamushi infection on the host using 1H-NMR and UPLC-Q-TOF mass spectroscopy coupled with multivariate statistical analysis. In addition, the effect of O. tsutsugamushi infection on metabolite concentrations over time was analyzed by two-way ANOVAs. Orthogonal partial least squares-discriminant analysis (OPLS-DA) showed distinct metabolic patterns between control and O. tsutsugamushi-infected mice in liver, spleen, and serum samples. O. tsutsugamushi infection caused decreased energy production and deficiencies in both remethylation sources and glutathione. In addition, O. tsutsugamushi infection accelerated uncommon energy production pathways (i.e., excess fatty acid and protein oxidation) in host body. Infection resulted in an enlarged spleen with distinct phospholipid and amino acid characteristics. This study suggests that metabolite profiling of multiple organ tissues and serum could provide insight into global metabolic changes and mechanisms of pathology in O. tsutsugamushi-infected hosts.
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PMID:Metabolic responses to Orientia tsutsugamushi infection in a mouse model. 2556 62