Search request: F (((SU ANKYLOSING SPONDYLITIS OR KW ANKYLOSING SPONDYLITIS)
 OR KW REITERS SYNDROME) OR KW REACTIVE ARTHRITIS) AND ADDED
 FROM 05/22/2001 THRU 05/28/2001
 Search result: 2 citations in the Magazine & Journal Articles database

 Display: D CIT ABS TEXT
 Update id: ANS2939

 1. Laval, S. H.; Timms, A.; Edwards, S.; Bradbury, L.; and others.
 Whole-Genome Screening in Ankylosing Spondylitis: Evidence of Non-MHC
 Genetic-Susceptibility Loci.(Statistical Data Included)
 American Journal of Human Genetics v68, n4 (April, 2001):918.
 Pub Type: Statistical Data Included.

 Abstract:
 Author Abstract: Ankylosing spondylitis (AS) is a common inflammatory
 arthritis predominantly affecting the axial skeleton. Susceptibility to the
 disease is thought to be oligogenic. To identify the genes involved, we
 have performed a genomewide scan in 185 families containing 255 affected
 sibling pairs. Two-point and multipoint nonparametric linkage analysis was
 performed. Regions were identified showing "suggestive" or stronger linkage
 with the disease on chromosomes 1p, 2q, 6p, 9q, 10q, 16q, and 19q. The MHC
 locus was identified as encoding the greatest component of susceptibility,
 with an overall LOD score of 15.6. The strongest non-MHC linkage lies on
 chromosome 16q (overall LOD score 4.7). These results strongly support the
 presence of non-MHC genetic-susceptibility factors in AS and point to their
 likely locations. COPYRIGHT 2001 Published by University of Chicago Press.
 Text is not available for this record.

 2. Jawaheer, Damini; Seldin, Michael F.; Amos, Christopher I.; Chen, Wei V.;
 and others.
 A Genomewide Screen in Multiplex Rheumatoid Arthritis Families Suggests
 Genetic Overlap with Other Autoimmune Diseases.(Statistical Data Included)
 American Journal of Human Genetics v68, n4 (April, 2001):927.
 Pub Type: Statistical Data Included.

 Abstract:
 Author Abstract: Rheumatoid arthritis (RA) is an autoimmune/inflammatory
 disorder with a complex genetic component. We report the first major
 genomewide screen of multiplex families with RA gathered in the United
 States. The North American Rheumatoid Arthritis Consortium, using
 well-defined clinical criteria, has collected 257 families containing 301
 affected sibling pairs with RA. A genome screen for allele sharing was
 performed, using 379 microsatellite markers. A nonparametric analysis using
 SIBPAL confirmed linkage of the HLA locus to RA (P [is less than] .00005),
 with [[Lambda].sub.HLA] = 1.79. However, the analysis also revealed a
 number of non-HLA loci on chromosomes 1 (D1S235), 4 (D4S1647), 12
 (D12S373), 16 (D16S403), and 17 (D17S1301), with evidence for linkage at a
 significance level of P [is less than] .005. Analysis of X-linked markers
 using the MLOD method from ASPEX also suggests linkage to the telomeric
 marker DXS6807. Stratifying the families into white or seropositive
 subgroups revealed some additional markers that showed improvement in
 significance over the full data set. Several of the regions that showed
 evidence for nominal significance (P [is less than] .05) in our data set
 had previously been implicated in RA (D16S516 and D17S1301) or in other
 diseases of an autoimmune nature, including systemic lupus erythematosus
 (D1S235), inflammatory bowel disease (D4S1647, D5S1462, and D16S516),
 multiple sclerosis (D12S1052), and ankylosing spondylitis (D16S516).
 Therefore, genes in the HLA complex play a major role in RA susceptibility,
 but several other regions also contribute significantly to overall genetic
 risk. COPYRIGHT 2001 Published by University of Chicago Press.
 Text is not available for this record.

 Search request: F (XS SPONDYLITIS, ANKYLOSING OR XS REITERS DISEASE OR XS
 ARTHRITIS, REACTIVE ) AND ADDED FROM 05/17/2001 THRU
 05/23/2001
 Search result: 2 citations in the Medline database

 Display: D CIT AB
 Update id: PYF80867

 1. Legoupil N; Revelon G; Allain J; Voisin MC; Rahmouni A; Chevalier X;
 Claudepierr P.
 Iliac vein thrombosis complicating SAPHO syndrome: MRI and histologic
 features of soft tissue lesions.
 Joint Bone Spine, 2001 Feb, 68(1):79-83.
 (Unique ID/PMID: 0011235788)

 Abstract: Subclavian and superior vena cava obstruction complicating SAPHO
 (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis) syndrome has been
 described. We report the first case to our knowledge of iliac vein
 thrombosis complicating lumbar vertebral osteitis due to SAPHO syndrome.
 Lumbar MRI demonstrated a large tissue mass anterior to the involved
 vertebras and surrounding the right iliac vein. Histology of the mass
 showed aseptic inflammation.

 2. Block S.
 Index of suspicion. Case #1. Diagnosis: Nongroup A poststreptococcal
 reactive arthritis.
 Pediatrics in Review, 2000 Oct, 21(10):354-7.
 (Unique ID/PMID: 0011041668)

  Search request: F (((SU ANKYLOSING SPONDYLITIS OR KW ANKYLOSING
SPONDYLITIS)
  OR KW REITERS SYNDROME) OR KW REACTIVE ARTHRITIS) AND
ADDED
  FROM 05/08/2001 THRU 05/14/2001
  Search result: 2 citations in the Magazine & Journal Articles database
 
  Display: D CIT ABS TEXT
  Update id: ANS2939
 
  1. Fendler, C; Laitko, S; Sorensen, H; Gripenberg-Lerche, C; and others.
  Frequency of triggering bacteria in patients with reactive
arthritis and
  undifferentiated oligoarthritis and the relative importance of the
tests
  used for diagnosis.
  Annals of the Rheumatic Diseases v60, n4 (April, 2001):337.
  Text is not available for this record.
 
  2. Boonen, A; Chorus, A; Miedema, H; van der Heijde, D; and others.
  Employment, work disability, and work days lost in patients with
  ankylosing spondylitis: a cross sectional study of Dutch patients.
  Annals of the Rheumatic Diseases v60, n4 (April, 2001):353.
  Text is not available for this record.

  Search request: F (XS SPONDYLITIS, ANKYLOSING OR XS REITERS DISEASE OR
XS
  ARTHRITIS, REACTIVE ) AND ADDED FROM 05/10/2001 THRU
  05/16/2001
  Search result: 15 citations in the Medline database
 
  Display: D CIT AB
  Update id: PYF80867
 
  1. Laval SH; Timms A; Edwards S; Bradbury L; Brophy S; Milicic A; Rubin
L;
  Siminovitch KA; Weeks DE; Calin A; et al.
  Whole-genome screening in ankylosing spondylitis: evidence of
non-MHC
  genetic-susceptibility loci.
  American Journal of Human Genetics, 2001 Apr, 68(4):918-26.
  (Unique ID/PMID: 0011231900)
 
  Abstract: Ankylosing spondylitis (AS) is a common inflammatory arthritis
  predominantly affecting the axial skeleton. Susceptibility to the
disease
  is thought to be oligogenic. To identify the genes involved, we have
  performed a genomewide scan in 185 families containing 255 affected
sibling
  pairs. Two-point and multipoint nonparametric linkage analysis was
  performed. Regions were identified showing "suggestive" or stronger
linkage
  with the disease on chromosomes 1p, 2q, 6p, 9q, 10q, 16q, and 19q.
The MHC
  locus was identified as encoding the greatest component of
susceptibility,
  with an overall LOD score of 15.6. The strongest non-MHC linkage
lies on
  chromosome 16q (overall LOD score 4.7). These results strongly
support the
  presence of non-MHC genetic-susceptibility factors in AS and point
to their
  likely locations.
 
  2. Henry CH; Pitta MC; Wolford LM.
  Frequency of chlamydial antibodies in patients with internal
derangement
  of the temporomandibular joint.
  Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and
Endodontics,
  2001 Mar, 91(3):287-92.
  (Unique ID/PMID: 0011250625)
 
  Abstract: PURPOSE: This study investigates whether an increased
frequency of
  serum antibodies to Chlamydia trachomatis is found in patients with
  internal derangement of the temporomandibular joint (TMJ).Patients
And
  Methods: An indirect immunofluorescence antibody assay for the
detection of
  serum immunoglobulin G antibodies for C trachomatis was used for
most
  patients. Forty-one female patients were evaluated. RESULTS: Three
of 41
  patients (7%) had serum antibody titers that were considered
positive for
  active C trachomatis infection. Eleven patients (27%) were
considered to
  have had a past infection based on the immunoglobulin G or
immunoglobulin A
  titer results. Using the binomial test, we found that the
probability of
  observing 14 positive results (34%) was significant (P < .0001).
  CONCLUSIONS: An increase in the frequency of serum antibodies to C
  trachomatis was found in patients with internal derangement of the
TMJ.
  Serologic testing for antibodies to bacteria associated with
reactive
  arthritis might be useful in the evaluation of patients with
internal
  derangement of the TMJ.
 
  3. Kobayashi S; Hashimoto H.
  [Reactive arthritis(Reiter's syndrome)].
  Ryoikibetsu Shokogun Shirizu, 2000(32):518-20.
  Language: Japanese.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011212790)
 
  4. Mitsui H.
  [Ankylosing spondylitis].
  Ryoikibetsu Shokogun Shirizu, 2000(32):514-7.
  Language: Japanese.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011212789)
 
  5. Seta N; Granfors K; Sahly H; Kuipers JG; Song YW; Baeten D; Veys EM;
  Maksymowych W; Marker-Hermann E; Gu J; et al.
  Expression of host defense scavenger receptors in
spondylarthropathy.
  Arthritis and Rheumatism, 2001 Apr, 44(4):931-9.
  (Unique ID/PMID: 0011315932)
 
  Abstract: OBJECTIVE: Reactive arthritis (ReA) is postulated to be caused
by a
  defective host defense against gram-negative bacteria. HLA-B27 could
play a
  role in this process, but does not account for the many HLA-B27
negative
  patients. The objective of this study was to test the expression of
3
  macrophage scavenger receptors (SRs) that are responsible for innate
  immunity against gram-negative bacteria: SR class A type I (SR-AI),
SR-AII,
  and the macrophage receptor with collagenous structure (MARCO). We
  postulate that defects in such receptors might also contribute to
the host
  risk factors that increase the predisposition to ReA and perhaps
other
  subtypes of spondylarthropathy (SpA). METHODS: Peripheral blood,
synovial
  fluid, and synovial tissue samples were obtained from patients with
recent
  Salmonella infection, ReA, other SpA, and rheumatoid arthritis (RA).
The
  expression of SRs receptors was assessed by semiquantitative reverse
  transcriptase-polymerase chain reaction. RESULTS: Evaluation of the
  peripheral blood mononuclear cells (PBMC) from 4 patients who were
recently
  infected with Salmonella, showed that PBMC from 2 patients who
developed
  ReA expressed positive levels of MARCO, while PBMC from 2 patients
who
  recovered from infection without sequelae did not. The synovial
fluid
  mononuclear cells (SFMC) from some ReA patients expressed MARCO, but
the
  levels were only moderate. The level of MARCO in the SFMC from the
SpA
  patient group was low. In marked contrast, MARCO expression was high
in
  almost all samples of RA SFMC. These findings also extended to
synovial
  tissues. CONCLUSION: Expression of the host defense gene MARCO was
  susceptible to modulation, not only during infections, but also in
the
  inflammatory arthritis conditions RA and SpA. MARCO is a variable to
be
  considered as a candidate factor that might contribute to ReA.
 
  6. Jacobs A; Barnard K; Fishel R; Gradon JD.
  Extracolonic manifestations of Clostridium difficile infections.
  Presentation of 2 cases and review of the literature.
  Medicine, 2001 Mar, 80(2):88-101.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011307591)
 
  Abstract: Clostridium difficile is most commonly associated with colonic
  infection. It may, however, also cause disease in a variety of other
organ
  systems. Small bowel involvement is often associated with previous
surgical
  procedures on the small intestine and is associated with a
significant
  mortality rate (4 of 7 patients). When associated with bacteremia,
the
  infection is, as expected, frequently polymicrobial in association
with
  usual colonic flora. The mortality rate among patients with C.
difficile
  bacteremia is 2 of 10 reported patients. Visceral abscess formation
  involves mainly the spleen, with 1 reported case of pancreatic
abscess
  formation. Frequently these abscesses are only recognized weeks to
months
  after the onset of diarrhea or other colonic symptoms. C.
difficile-related
  reactive arthritis is frequently polyarticular in nature and is not
related
  to the patient's underlying HLA-B27 status. Fever is not universally
  present. The most commonly involved joints are the knee and wrist
(involved
  in 18 of 36 cases). Reactive arthritis begins an average of 11.3
days after
  the onset of diarrhea and is a prolonged illness, taking an average
of 68
  days to resolve. Other entities, such as cellulitis, necrotizing
fasciitis,
  osteomyelitis, and prosthetic device infections, can also occur.
Localized
  skin and bone infections frequently follow traumatic injury,
implying the
  implantation of either environmental or the patient's own C.
difficile
  spores with the subsequent development of clinical infection. It is
  noteworthy that except for cases involving the small intestine and
reactive
  arthritis, most of the cases of extracolonic C. difficile disease do
not
  appear to be strongly related to previous antibiotic exposure. The
reason
  for this is unclear. We hope that clinicians will become more aware
of
  these extracolonic manifestations of infection, so that they may be
  recognized and treated promptly and appropriately. Such early
diagnosis may
  also serve to prevent extensive and perhaps unnecessary patient
  evaluations, thus improving resource utilization and shortening
length of
  hospital stay.
 
  7. Glant TT; Bardos T; Vermes C; Chandrasekaran R; Valdez JC; Otto JM;
Gerard
  D; Velins S; Lovasz G; Zhang J; et al.
  Variations in susceptibility to proteoglycan-induced arthritis and
  spondylitis among C3H substrains of mice: evidence of genetically
acquired
  resistance to autoimmune disease.
  Arthritis and Rheumatism, 2001 Mar, 44(3):682-92.
  (Unique ID/PMID: 0011263784)
 
  Abstract: OBJECTIVE: To identify and screen the level of arthritis
  susceptibility in C3H murine strains known to be resistant to
proteoglycan
  (aggrecan)-induced arthritis, and to measure and correlate various
  immunologic and inflammatory parameters with susceptibility to
either
  arthritis or spondylitis in various C3H substrains. METHODS: Mice of
10 C3H
  substrains (subcolonies) were immunized with cartilage proteoglycan
  (aggrecan) for induction of arthritis. Animals were assessed for
clinical
  symptoms, and the peripheral joints and spine were studied by
histologic
  methods. Proteoglycan-specific T cell responses (T cell
proliferation and
  production of interleukin-2 [IL-2], interferon-y, and IL-4) and the
B cell
  response to lipopolysaccharide (LPS) were measured in spleen cell
cultures.
  Serum levels of heteroantibodies and autoantibodies as well as
various
  cytokines (IL-6, IL-10, IL-12, and tumor necrosis factor alpha) and
soluble
  CD44 were determined by enzyme-linked immunosorbent assay. RESULTS:
  Immunization with cartilage proteoglycan induced severe arthritis in
the
  C3H/HeJCr substrain (95-100% incidence), whereas the original parent
mice
  of the C3H/HeJ colony were resistant to proteoglycan
(aggrecan)-induced
  arthritis. Furthermore, the progressive polyarthritis that is
  characteristic in susceptible C3H/HeJCr mice was accompanied by
progressive
  inflammation around the spine. In subsequent experiments, 10
different C3H
  colonies with largely identical genetic backgrounds (all originating
from
  the National Institutes of Health or Jackson Laboratory) exhibited
extreme
  differences in susceptibility. Although none of the laboratory
findings,
  including LPS hyporesponsiveness, immunologic parameters, and
inflammatory
  markers, showed a correlation with susceptibility or resistance in
the
  C3H/HeJCr and C3H/HeJ substrains, respectively, significant
differences
  were found when all arthritic C3H mice were compared with all
nonarthritic
  animals, regardless of their substrain origin. CONCLUSION: Because
many of
  the C3H substrains lost arthritis susceptibility or acquired
resistance,
  our results suggest that a preferred site for a mutation(s) in a
gene(s) in
  a relatively upstream position of the inflammatory cascade is
present. This
  is the first autoimmune model that exhibits extreme differences in
  arthritis susceptibility in the same murine strain, and is therefore
a
  valuable tool for identification of arthritis-susceptible (or
  arthritis-suppressive) genes.
 
  8. Vaverka M; Hrabalek L.
  [Injuries of the cervical spine in patients with ankylosing
spondylitis].
  Rozhledy V Chirurgii, 2001 Jan, 80(1):5-8.
  Language: Czech.
  (Unique ID/PMID: 0011265347)
 
  Abstract: A brittle and rigid, osteoporotic and injury prone "bamboo"
spine
  which develops as a result of transformation of the normal spine in
the
  final stage of Bekhterev's disease contains normal neural elements.
  Unstable fractures occur frequently even after a minimal injury and
the
  morbidity and mortality is significantly higher than in the group of
  routine injuries of the cervical, spine, in particular as a result
of
  pulmonary complications. Diagnosis of the fracture based on simple
X-ray
  pictures is difficult, CT examination is essential. The authors
present an
  account on their experience with three patients. They draw attention
to
  problems of skeletal traction when the spinal axis is altered by
disease
  and to risks associated with semiconservative treatment. The authors
  therefore recommend traction with a minimal load and with subsequent
early
  decompression and stabilization by a combined anterior and posterior
  approach in a single session. By this approach secondary affection
of
  neural structures in unstable fractures can be prevented, and early
  rehabilitation with verticalization without restriction of
respiratory
  excursions by an orthesis then significantly reduces the risk of
pulmonary
  complications.
 
  9. Coventry TL; Jessop DS; Finn DP; Crabb MD; Kinoshita H; Harbuz MS.
  Endomorphins and activation of the hypothalamo-pituitary-adrenal
axis.
  Journal of Endocrinology, 2001 Apr, 169(1):185-93.
  (Unique ID/PMID: 0011250660)
 
  Abstract: Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides recently
located
  in the central nervous system and immune tissues with high
selectivity and
  affinity for the mu-opioid receptor. Intracerebroventricular
(i.c.v.)
  administration of morphine stimulates the
hypothalamo-pituitary-adrenal
  (HPA) axis. The present study investigated the effect of centrally
  administered EM-1 and EM-2 on HPA axis activation. Rats received a
single
  i.c.v. injection of either EM-1 (0.1, 1.0, 10 microg), EM-2 (10
microg),
  morphine (10 microg), or vehicle (0.9% saline). Blood samples for
plasma
  corticosterone determinations were taken immediately prior to i.c.v.
  administration and at various time points up to 4 h post-injection.
Trunk
  blood, brains and pituitaries were collected at 4 h.
  Intracerebroventricular morphine increased plasma corticosterone
levels
  within 30 min, whereas EM-1 and EM-2 were without effect. In
addition,
  pre-treatment of i.c.v. EM-1 did not block the rise in
corticosterone after
  morphine. Corticotrophin-releasing factor (CRF) mRNA and arginine
  vasopressin (AVP) mRNA in the paraventricular nucleus (PVN) and POMC
mRNA
  in the anterior pituitary were found to be unaffected by either
morphine or
  endomorphins. Since release of other opioids are elevated in
response to
  acute stress, we exposed rats to a range of stressors to determine
whether
  plasma EM-1 and EM-2 can be stimulated by HPA axis activation.
Plasma
  corticosterone, ACTH and beta-endorphin were elevated following
acute
  restraint stress, but concentrations of plasma EM-1-immunoreactivity
(ir)
  and EM-2-ir did not change significantly. Corticosterone, ACTH and
  beta-endorphin were further elevated in adjuvant-induced arthritis
(AA)
  rats by a single injection of lipopolysaccharide (LPS), but not by
  restraint stress. In conclusion, neither EM-1 or EM-2 appear to
influence
  the regulation of the HPA axis. These data suggest that endomorphins
may be
  acting on a different subset of the mu-opioid receptor than
morphine. The
  failure to induce changes in plasma EM-ir in response to the chronic
  inflammatory stress of AA, the acute immunological stress of LPS, or
the
  psychological stress of restraint, argues against an important role
for
  endomorphins in mediating HPA axis activity.
 
  10. Gause A; Manger B; Kalden JR; Burmester GR.
  [Therapy of inflammatory rheumatic diseases: from current practice
  standards to future].
  Internist, 2001 Feb, 42(2):223-32, 234-6.
  Language: German.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011244877)
 
  11. Zink A; Mau W; Schneider M.
  [Epidemiological and public health aspects of inflammatory
rheumatic
  systemic diseases].
  Internist, 2001 Feb, 42(2):211-6, 219-22.
  Language: German.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011244876)
 
  12. Sieper J; Burkhardt H; Gross WL.
  [Immunopathogenetic hypotheses in inflammatory rheumatic
diseases].
  Internist, 2001 Feb, 42(2):198-210.
  Language: German.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011244875)
 
  13. EppLen JT; Marker-Herrmann E; Melchers I.
  [Immunogenetics of inflammatory rheumatic diseases].
  Internist, 2001 Feb, 42(2):188-91, 194-7.
  Language: German.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011244874)
 
  14. Fuessl HS.
  [Diagnostic quiz. A sclerosed vertebral body. Paget disease].
  Mmw Fortschritte der Medizin, 2001 Jan 11, 143(1-2):43-4.
  Language: German.
  (Unique ID/PMID: 0011216015)
 
  15. Kobayashi S; Tamura N; Inoue H.
  [Physiopathological interpretation and progress in diagnosis and
  treatment. 4. Psoriatic arthritis and ankylosing spondylitis].
  Nippon Naika Gakkai Zasshi. Journal of Japanese Society of Internal
  Medicine, 2000 Oct 10, 89(10):2099-104.
  Language: Japanese.
  Pub type: Journal Article; Review; Review, Tutorial.
  (Unique ID/PMID: 0011215123)