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W Kuis

Publications and source records attributed to W Kuis.

At least 91 records · Page 5Linked to original sources
PubMed1994

Destructive synovitis in contralateral Perthes' disease. A report of 2 cases.

2 boys had unilateral Perthes' disease at the age of 5 years. After 6 and 7 years, respectively, both patients developed contralateral femoral head necrosis with rapid destruction leading to ankylosis of the hip. Histology of the synovium showed nonspecific synovitis. Both patients fulfilled criteria for oligo-articular juvenile chronic arthritis (JCA). The association with Perthes' disease suggests a common etiology.

Ankylosis↗
PubMed1993

[3 adolescents with hip pain caused by idiopathic chondrolysis].

The cases are described of three adolescents in whom hip pain was found to be due to chondrolysis. Arthroscopy revealed chronic synovitis in all three cases. It is stated that the synovitis is probably the cause of the articular damage and that the disorder should be regarded as juvenile chronic arthritis of the oligoarticular type. Treatment with intra-articular triamcinolone acetonide and in two patients with an anti-inflammatory agent as well resulted in almost complete recovery of hip function.

Adolescent↗
PubMed1993

T cell development in a major histocompatibility complex class II-deficient patient.

In this report we show that the major histocompatibility complex (MHC) class II-negative thymus of a bare lymphocyte syndrome (BLS) patient contains a reduced CD4+ CD8- T cell population when compared to thymocytes derived from a MHC class II-expressing thymus. Of these CD4+ CD8- BLS thymocytes, approximately only one third co-expressed the CD3 antigen, moreover at a lower expression level when compared to control thymocytes. This suggests a partial maturation of the CD4+ CD8- T cells in the absence of MHC class II expression. Among the BLS thymocytes, CD4+ CD8+ thymocytes could easily be detected. Noteworthy, the number of CD4- CD8+ thymocytes was significantly increased. CD4+ CD8- T cells could also be found among the BLS peripheral blood mononuclear cells, albeit at reduced numbers. Despite the absence of peripheral MHC class II expression, the majority of these CD4+ CD8- T cells co-expressed the CD45RO marker. In the BLS patient, thymocytes as well as peripheral CD4+ CD8- T cells were not restricted in the use of the available T cell receptor (TcR) V gene family pool. However, the lack of detectable levels of thymic and peripheral MHC class II antigen expression in the BLS patient had altered the CD4-skewing patterns of TcR V gene families which were present in normal individuals. In conclusion, the lack of MHC class II expression in the BLS patient does not completely inhibit the CD4+ CD8- T cell development.

CD4 Antigens↗
PubMed1993

Reversed gamma-nail: preliminary results of a new intramedullary implant.

Preliminary results of treatment with the reversed gamma-nail, an experimental intramedullary device for fixation of supracondylar fractures, are presented. The reversed gamma-nail was used 11 times; six in primary supracondylar fracture treatment, five in revision surgery of a supracondylar non-union or pseudarthrosis. Three consolidated fractures and six complications were noticed at a mean follow-up of 9 months. General results were moderate but slightly better in primary fracture treatment. The reversed gamma-nail has a limited indication; primary treatment of a supracondylar extra-articular fracture in elderly patients is probably the best one. The osteosynthesis method and implant deserve further development.

Aged↗
PubMed1993

Defective antipneumococcal polysaccharide antibody response in children with recurrent respiratory tract infections.

BACKGROUND: Recurrent pyogenic infections are known to occur in patients with an impaired response to polysaccharide antigens. We investigated the occurrence of deficient responses to pneumococcal capsular polysaccharides in patients with recurrent respiratory tract and recurrent systemic infections. METHODS: Forty-five patients, 1.7 to 17.1 years of age, were immunized with 23-valent pneumococcal polysaccharide vaccine. Antibody levels to seven pneumococcal serotypes (3, 4, 6A, 9N, 14, 19F, 23F) were determined by ELISA before and after immunization. In addition, patients received a booster immunization with diphtheria toxoid, tetanus toxoid, and poliomyelitis virus vaccine. RESULTS: Thirty-five patients had normal serum immunoglobulin levels. Five of these patients (14%) had low antipneumococcal preimmunization antibody levels and failed to respond to pneumococcal vaccination, whereas the response to booster immunization with protein antigens was appropriate. Three patients were younger than 3 years old, and one had a family history of IgG2 deficiency. Low IgG developed in a fifth patient during follow-up. Ten patients had a humoral immunodeficiency. Seven of these patients failed to respond to pneumococcal vaccination. CONCLUSIONS: We conclude that a defective immune response to polysaccharide antigens in patients requires long-term follow-up to distinguish transient maturational delay from a persistent selective impaired response to polysaccharide antigens, which on occasion may precede the development of humoral immunodeficiency disease.

Adult↗
PubMed1993

Antibodies to human HSP60 in patients with juvenile chronic arthritis, diabetes mellitus, and cystic fibrosis.

The 60-kD heat shock protein (hsp60) has been implicated in the etiology and pathogenesis of both experimental and naturally occurring autoimmune diseases such as juvenile chronic arthritis (JCA). Human hsp60 is expressed in inflamed synovial tissue, and T lymphocytes both from peripheral blood and synovial fluid show reactivity to human hsp60. Because the anti-hsp60 B lymphocyte response has been less well studied, we have determined the occurrence of IgG anti-human hsp60 antibodies in patients with JCA and various other autoimmune diseases of childhood. Serum IgG anti-human hsp60 antibodies in JCA patients were significantly higher compared with control children (358 and 163 U/mL, respectively). Within the group of JCA patients, the highest antibody titers were found in the subgroup with a polyarticular onset of JCA. IgG anti-human hsp60 antibody levels in synovial fluid were 3- to 4-fold higher compared with paired serum samples. Because this difference was not found for total IgG or for irrelevant antibodies (anti-polyribosylribitol phosphate), this suggests local anti-hsp60 antibody production in the synovial compartment. The occurrence of anti-hsp60 antibodies is not specific for JCA but also is found in children with systemic lupus erythematosus and in cystic fibrosis, whereas mixed connective tissue disease and insulin-dependent diabetes are negative in this respect. Whether the anti-human hsp60 antibodies are directed toward species-specific sequences or to conserved sequences of the hsp60 molecule remains to be determined.

Adolescent↗
PubMed1992

Castleman's disease in POEMS syndrome with elevated interleukin-6.

POEMS syndrome is a rare multisystem affliction known for its signs, from which it also takes its acronym name "peripheral neuropathy, organomegaly, endocrinopathy, monoclonal (M) protein, and skin lesions." Our study chronicles the course of this syndrome in a young woman with Castleman's disease (angiofollicular lymph node hyperplasia). Cerebrospinal fluid (CSF) and serum interleukin-6 (IL-6) levels were abnormally elevated at various times during a 9-month period. The authors conclude that the plasma cell dyscrasia associated with the POEMS syndrome of this patient was Castleman's disease. Elevation of serum IL-6 levels might contribute to the pathogenesis of the POEMS syndrome.

Adult↗
PubMed1992

Atypical Kawasaki disease: an often missed diagnosis.

We describe four patients with vasculitis of the coronary and other medium sized arteries. Three of them died as a consequence of cardiac failure and the fourth had a ruptured aneurysm of the left common iliac artery. Coronary vasculitis is pathognomonic for Kawasaki disease (KD), but our patients had few other signs of this disorder, suggesting so called atypical KD. Because the described patients lacked most of the clinical criteria, the diagnosis was delayed. We focus on other clinical features in these patients and stress the importance of early recognition and treatment.

Child, Preschool↗
PubMed1991

Recognition of human 60 kD heat shock protein by mononuclear cells from patients with juvenile chronic arthritis.

A postulated mechanism for autoimmune disorders is that the immunoreactivity develops against bacterial antigens which show a high degree of sequence homology with mammalian proteins. The mycobacterial 65 kD heat shock protein (hsp) has been implicated in several forms of arthritis. Substantial amounts of the human 60 kD homologue (hsp60) were produced by insertion of the gene into Escherichia coli. To investigate the hypothesis that T-cell reactivity is directed against the endogenous hsp, T-cell proliferation of synovial-fluid and peripheral-blood mononuclear cells in response to hsp60 was studied in samples from six patients with juvenile chronic arthritis (JCA) and nine adult patients with rheumatoid arthritis (RA). There was no T-lymphocyte proliferative response to purified fractions of hsp60 in mononuclear cells from RA patients or healthy children and young adults. However, both synovial-fluid and peripheral-blood mononuclear cells from JCA patients showed substantial proliferative responses. There was a significant correlation between the stimulation indices for human hsp60 and for mycobacterial hsp65 (r = 0.948, p less than 0.02). A similar correlation for hsp60 and mycobacterial hsp70 did not achieve significance. Immunohistochemistry showed that hsp65 and hsp70 homologues were expressed in the synovial membrane in these patients but not in controls. These findings suggest a sequence of events in which hsps become expressed during synovial inflammation and function as autoantigens. In JCA this may be manifested by specific T-cell reactivity which apparently is lost in the more bone-eroding and non-remitting adult disease.

Adolescent↗
PubMed1991

Differential processing of proenkephalin-A by human peripheral blood monocytes and T lymphocytes.

Human peripheral blood mononuclear cells are analyzed for preproenkephalin gene expression and peptide processing. Met-enkephalin immunoreactivity as detected with a specific antiserum is found in the cytoplasm of monocytes but not in T lymphocytes. Secretion of met-enkephalin was analyzed with an RIA that is specific for the met-enkephalin pentapeptide. Unfractionated PBMC spontaneously released 40 pg/ml met-enkephalin and this increased two- to fourfold after stimulation with PHA. Lower levels (less than 100 pg/ml) of met-enkephalin were detected in supernatants from purified T cells that were activated with PHA and IL-2. In contrast, stimulation of purified monocytes with LPS or PMA resulted in the release of up to 600 pg/ml of the processed peptide. To examine whether T cells can produce met-enkephalin precursor peptides, T cell conditioned media were treated with trypsin and carboxypeptidase-B, which is known to release met-enkephalin from the propeptide. This increased levels of met-enkephalin to 400 pg/ml, indicating that lymphocytes secrete the propeptide but do not process it to met-enkephalin. The 1.4-kb preproenkephalin mRNA is detected in activated blood mononuclear cells and in purified monocytes and T cells. To determine whether monocytes or lymphocytes express met-enkephalin in vivo, lymphoid tissues were analyzed by immunohistochemistry. In human spleen tissue, positive cells were found in the red pulp but not in the follicles, which is also consistent with met-enkephalin expression in monocytes. In summary, these results show that human peripheral blood mononuclear cells express preproenkephalin mRNA and that monocytes, but not T cells, process the propeptide to metenkephalin.

Adult↗
PubMed1991

[Systemic juvenile chronic arthritis].

Juvenile chronic arthritis, systemic onset, is a form of juvenile chronic arthritis with severe systemic and constitutional involvement. We discuss the clinical findings, therapy and outcome of a series of forty patients we have seen in our hospital from 1979-1991.

Adolescent↗
PubMed1991

[The relationship between the neuroendocrine system and juvenile chronic arthritis: a hypothesis].

During the last decennium it has become clear that the course of an inflammatory reaction is not only governed by the immune system. In this paper we describe which other organ systems than the immune system may influence chronic inflammatory responses such as observed in Juvenile Chronic Arthritis (JCA). Attention will be focussed on the role of glucocorticoids, catecholamines and of the neurotransmitter substance P.

Arthritis, Juvenile↗
PubMed1991

[Recognition of joint symptoms in childhood].

Joint complaints do occur frequently in childhood. Mostly the underlying cause is innocent and the complaints are mostly self-limiting. It is of the utmost importance to recognize diseases with joint involvement. The symptoms and differential diagnosis of arthritis in childhood are briefly discussed.

Arthritis↗
PubMed1990

[Wrist disorders in juvenile chronic arthritis].

In Juvenile Chronic Arthritis the wrist often is involved. Synovitis of this joint gives rise to several types of disintegration, which can lead to serious deformities and loss of function. Therapeutical considerations should be based upon knowledge of these types of disintegration and the natural history.

Adolescent↗
PubMed1990

Antibodies to the mycobacterial 65-kd heat-shock protein are reactive with synovial tissue of adjuvant arthritic rats and patients with rheumatoid arthritis and osteoarthritis.

The expression of 65-kd mycobacterial heat-shock protein (HSP)-related antigens in synovial membrane from rats and humans with arthritis was studied using three monoclonal antibodies and one polyclonal antiserum directed to antigens of mycobacteria. The antibodies labeled synovial tissue sections from both adjuvant arthritis (AA) rats and from patients with either rheumatoid arthritis (RA) or osteoarthritis (OA); especially the synovial lining cells appeared to be positive. The cytoplasmic staining patterns in rats and humans were essentially the same and were not related to the extent of inflammation ie, the size of lymphoid infiltration. In control tissues no cytoplasmic staining was observed. The results suggest a role for a 65-kd HSP or a cross-reactive molecule in the immunopathologic process of arthritic disease.

Animals↗
PubMed1990

The periarteriolar lymphocyte sheath in immunodeficiency T- or B-lymphocyte area?

T- and B-lymphocyte populations in peripheral lymphoid tissues occur in distinct compartments (e.g., the periarteriolar lymphocyte sheath of the splenic white pulp is a T-cell area). The authors report on two patients with severe combined immunodeficiency (SCID) and one patient with immunodeficiency after anti-T-cell treatment for rejection of a heart transplant, in which the area surrounding the central arteriole in spleen white pulp was well-populated despite T-cell deficiency (documented by, for example, severe depletion of lymph node paracortex). Immunologic phenotyping showed the B-lymphoid lineage of lymphocytes at this location. The framework in the periarteriolar area consisted of follicular dendritic cells, which are typical framework components of B-cell areas. We conclude that assessment of only conventional histopathology of the spleen in these patients leads to erroneous conclusions about the type of immunodeficiency and that immunologic phenotyping is required to document the exact nature of the deficiency.

Adult↗