Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parasitic rheumatism is a rare condition characterized by inflammatory joint manifestations due to a parasitic infestation without parasites into joint cavity, (but, with circulating immune complexes, in serum, and synovial fluid; and with immunoglobulins and complement deposits in synovium in some cases reported in the literature). The number of parasites (now 15) which can induce such an arthritis by immune mechanisms is steadily increasing. In all, but few cases of parasitic rheumatism, usual parasitic manifestations (diarrhea, abdominal pain, nausea...) are mild or absent; but, if present, they are a very good criteria to evoke the diagnosis. Clinical pictures of arthritis induced by parasitic infestation are very polymorphic, and non specific of the involved parasite; they seem to depend on genetic predisposition: the symptoms are monoarticular, pauciarticular, or polyarticular, involving small, medium, and or large joints. They can mimic the clinical picture of different inflammatory rheumatic diseases. The most striking feature of parasitic rheumatism is the failure of antirheumatic agents (especially non steroidal anti-inflammatory agents), contrasting with the dramatic efficacy of specific anti-parasitic treatment. The proof of the responsibility of parasitic infestation by indirect mechanism is given by an exceptional case report of a patient with arthritis, dramatically cured after removal of larvae from Anisakiasis gastric granuloma. To explain the uncommon occurrence of this variety of reactive arthritis, due to parasitic infestation, despite the high prevalence of parasitic infestation in the world, hypothesis of genetic predisposition seems valuable. Among 34 well documented reported cases of parasitic rheumatism in the literature, HLA B 27 antigen has been researched in 13; out of these 13, HLA B 27 is absent in 9; in 7 out of these 9, clinical picture is symmetrical polyarthritis. Out of the 13 cases, HLA B 27 is present in 4: In all these 4 cases, clinical picture is asymmetrical pauciarthritis, mimicking arthritis of Reiter's disease.
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PMID:[Is there a role for parasites in the etiology of inflammatory rheumatism?]. 227 83

Seven children with muscle paralysis due to hypokalaemia are reported. In four the weakness was of asymmetrical and patchy distribution invoking an initial diagnosis of poliomyelitis, while the other three children had symmetrical pareses, a more widely recognized presentation. Involvement of bulbar muscles occurred in three, one of whom also had intercostal weakness. Head lag was present in all. The cause of hypokalaemia was malnutrition and/or diarrhoea, but in only one case was the diarrhoea severe enough to prompt the mother to seek medical advice.
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PMID:Hypokalaemic muscle paresis in children. 618 50

Reactive spondylarthropathies include mono- or asymmetrical polyarthritis as well as axial skeletal involvement. Usually they occur after urogenital or gastrointestinal infections caused by Yersinia, Salmonella, Shigella or Campylobacter. Reactive arthritis can also result from infections with other agents. We report the case of a patient with clinical features of seronegative spondylarthropathy. The endoscopic examination revealed intestinal spirochetosis. Other possible arthritogenous agents were ruled out serologically. The pathogenicity of intestinal spirochetosis is controversial. It can be associated with diarrhea. In Western countries the prevalence of intestinal spirochetosis is below 2%, male homosexuals being especially prone to these infections. Spirochetosis is often associated with a mild inflammatory reaction only, while a local increase in IgE plasma cell count has been described.
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PMID:[Intestinal spirochetosis and seronegative spondylarthropathy: association or coincidence?]. 767 43

The patient was a 25-year-old male with acute multifocal motor neuropathy with conduction block (MMNCB) after Campylobacter jejuni enteritis. After having suffered from diarrhea for 3 days, he rapidly developed asymmetrical distal-dominant muscle weakness in all extremities. Sensory disturbance was unremarkable except for slight disturbance in deep sensation. Deep tendon reflexes were normal throughout the course of present illness. CSF analysis revealed increased protein up to 66 mg/dl without pleocytosis. In electrophysiological examinations, persistant multifocal conduction blocks in the motor nerves were predominantly noted in the distal part of the extremities. Serum titers of anti-Campylobacter jejuni antibody, anti-GM1 antibody and anti-GalNAc-GD1a antibody were elevated. Muscle weakness resolved completely within 7 weeks. The sural nerve biopsy did not reveal either axonal degeneration, nor demyelination. These clinical and laboratory findings suggested that this case was most likely an acute type of MMNCB after Campylobacter jejuni enteritis.
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PMID:[A case of acute multifocal motor neuropathy with conduction block after Campylobacter jejuni enteritis]. 959 9

With recent technical advances, increasing use of sonography in the initial evaluation of patients with abdominal disease may allow the detection of unexpected tumor within the abdominal cavity. Easiness of sonographic detection of bowel pathology, purposely or unexpectedly, warrants the inclusion of bowel loops during ultrasound examination when a patient complains of symptoms indicating diseases of the bowel. In patients complaining of acute abdominal symptoms or nonspecific gastrointestinal symptoms and showing signs such as abdominal pain, diarrhea, hematochezia, change of bowel habit, or bowel obstruction, sonography may reveal the primary causes and may play a definitive role in making a diagnosis. On ultrasonography, abnormal lesions may appear as fungating mass with eccentrically located bowel lumen (pseudokidney sign) or symmetrical or asymmetrical, encircling thickening of the colonic wall (target sign). In patients with mass or wall thickening detected on ultrasonography, additional work-up such as barium study, CT or endoscopy would be occasionally necessary for making a specific diagnosis.
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PMID:Ultrasound examination of gastrointestinal tract diseases. 1098 83

The aim of the systematic review was to determine the effect of cisapride compared with placebo or other non-surgical therapies for the treatment of symptoms of gastro-oesophageal reflux in children. We searched MEDLINE, EMBASE, the Cochrane Controlled Trials Register, Science Citation Index and reference lists for randomized controlled trials which compared cisapride with placebo or other non-surgical therapy in children. We included only trials which reported reflux-related symptoms as an outcome, provided that cisapride was administered orally for at least I week. Seven trials (286 children in total) compared cisapride with placebo. Two trials reported good concealment of treatment allocation. The pooled odds ratio for the 'same or worse' symptoms was 0.34 (95% CI 0.10, 1.19). There was substantial heterogeneity between studies (P < 0.00001) and the funnel plot was asymmetrical. Adverse effects (mainly diarrhoea) were not significantly increased with cisapride (pooled odds ratio (OR) 1.80: 0.87, 3.70). The reflux index was significantly reduced in children treated with cisapride (weighted mean difference -6.49: -10.13, -2.85). One study (50 children) compared cisapride with gaviscon plus carobel: the OR for the 'same or worse' symptoms was 3.26 (0.93, 11.38). There was no clear evidence that cisapride reduced symptoms of gastro-oesophageal reflux. As smaller, poorer quality studies were biased in favour of a positive treatment effect, the pooled OR overestimated the potential benefits of cisapride. There was some evidence to suggest that gaviscon plus carobel may be a more effective option than cisapride.
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PMID:Cisapride treatment for gastro-oesophageal reflux in children: a systematic review of randomized controlled trials. 1111 25

In adults, reactive arthritis (ReA) following Clostridium difficile-enterocolitis has been documented. In children, only one case of C. difficile-associated ReA has been reported. We now describe two other cases of ReA associated with C. difficile in children. The characteristics of ReA due to C. difficile appear to be similar in adults and children. Both children show polyarthritis after an episode of diarrhoea with positive stool cultures for C. difficile. Arthritis is asymmetrical with a self-limiting course. Nonsteroidal antiinflammatory drug (NSAID) therapy is sufficient. One case is remarkable because of its prolonged course of ReA despite NSAID therapy, and its association with the presence of HLA-B27 antigen.
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PMID:Clostridium difficile-associated reactive arthritis in two children. 1476 23

The protozoan Giardia lamblia is the most frequent intestinal parasite of first-world countries and a major cause of waterborne disorder often referred to as traveler's diarrhea. We have previously noticed that the putrescine analog 1,4-diamino-2-butanone (DAB) remarkably inhibits the growth of anaerobic trichomonad and Trypanosoma cruzi parasites. Here, we examined the role of polyamines in Giardia cells using this putrescine analog. DAB impaired parasite proliferation dose-dependently. The analog induced increased flagella numbers and sometimes four ventral disks as well as asymmetrical division, indicating truncated or deregulated cytokinesis. Electron microscopy analysis revealed that DAB also triggered the encystment process. Oxidative stress was evaluated by measuring lipid peroxidation by thiobarbituric acid reactive substances (TBARS) detection. Trophozoites incubated either with 1 mM of DAB or putrescine for 18 h displayed increased lipoperoxide levels. Addition of 200 microM aminoguanidine, a polyamine/diamine oxidase inhibitor, partially reverted the DAB, but not the putrescine effects, indicating that the DAB effects are due, at least in part, to DAB oxidation end products. These data indicate that polyamines play a role in Giardia cell division, differentiation, and antioxidant defenses.
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PMID:Effects of a putrescine analog on Giardia lamblia. 1843 21

Direct hyperbilirubinemia, may result from a variety of pathologies, including structural obstructions with biliary tract occlusions (as in cholelithiasis), infections (e.g. hepatitis) and genetic disorders (Rotor's and Dubin-Johnson's syndrome). One of the less common and probably more frequently underdiagnosed causes is benign recurrent intrahepatic cholestasis (BRIC). First described in 1959, BRIC was further classified into two subgroups which differ in their pathogenesis and clinical manifestation. Both BRIC types originate from impaired function bile salt excretion from hepatocytes to the canaliculi which is mediated by the bile salt export pump (BSEP) which is located on the hepatyocyte membrane, unevenly distributed within the membrane lipid bilayer. In BRIC type-I, a mutation impairs the asymmetrical distribution of BSEP. In BRIC type-II, a mutation occurs directly damaging the BSEP. Apart from cholestasis, clinical manifestations of BRIC type-I include extra-hepatic symptoms such as watery diarrhea, pancreatitis and hearing impairment. Patients with BRIC type-II present mainly with hepatobiliary disease such as colelithiasis. In the past, BRIC was conventionally considered to result in no more than canalicular cholestasis, however several reports have associated BRIC with fibrosis and porto-portal septa formation. Disease course may last between weeks and months, more common in females, at any age, and usually resolves spontaneously, although chronic liver disease has also been described. Treatment modalities range from expectant management, medication (cholestyramine, ursolit) or even surgery (biliary bypass/liver transplantation). This report describes a patient with BRIC type-II and reviews the relevant literature.
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PMID:[Benign recurrent intrahepatic cholestasis type-II--a rare cause of direct hyperbilirubinemia exacerbations with hepatic fibrosis]. 1877 Sep 56

A 46-year-old woman with a medical history of chronic juvenile arthritis with bilateral prosthetic hips presented with vulvoperineal ulcerations of 3 years' duration. There was no diarrhea or recent weight loss. Cutaneous examination showed asymmetrical vulvar edema of the labia minora and labia majora with deep and linear ulcerations having verrucous borders located on the inguinocrural regions and the buttocks fold (Figure 1). On physical examination there was bilateral limited mobilization of the hips. A biopsy specimen was taken from the border of the vulvar ulceration and histologic examination showed under a hyperplasic epidermis an epithelioid granuloma with multinucleated giant cells of the dermis without caseification. Laboratory analyses and results from chest x-ray were normal. Results for Koch bacilla in the spittle, microbiologic studies (staining for microorganisms and cultures), and tuberculin intradermoreaction were negative. There was no Crohn's disease aspect on colonoscopy, and there was normal small bowel enterography. Systematic intestinal biopsies were also with normal aspect. Based on the clinical data and granulomatous histologic characteristics, the diagnosis of metastatic Crohn's disease without digestive involvement was obtained. The patient was started on metronidazole 1 g/d. After 6 months of treatment, there was an almost-complete healing of ulcerations (Figure 2). Treatment was well-tolerated.
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PMID:Vulvoperineal Crohn's disease: response to metronidazole. 2113 14


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