[Rheumatic disorders of the back].
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Biomedical subjects
Publications and source records attributed to A Cats.
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Dietary factors are major determinants of colorectal cancer risk. Especially a diet high in fat and low in fiber is recognized to be a risk factor. Dietary calcium has been suggested to be protective against colorectal cancer through the binding of intraluminal fatty acids and bile acids. Because of their cell-damaging properties these substances may stimulate colorectal epithelial cell proliferation and so promote colorectal cancer development. In this article data from in vitro, animal and human studies on the intraluminal effects of calcium, on its effects on colorectal epithelium and on the association between calcium intake and colorectal cancer are reviewed. It is concluded that at present it should be advised to bring dietary calcium intake into agreement with general dietary guidelines, but that high expectations of extra calcium as an effective mode of colon cancer prevention should not be encouraged.
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The use of sulfasalazine as a long acting anti-rheumatic drug in patients with systemic JCA was studied in an open trial. Severe toxic side-effects in three of the four patients entered required discontinuation of the trial. These adverse effects included high fevers and a generalised exanthem. The symptoms were considered to represent an allergic reaction, most likely to the sulfa component of sulfasalazine. After resolution of these episodes the joint disease was suppressed for several weeks in these three children.
In 153 patients with mainly inflammatory joint disorders alizarin red S staining was used to detect calcium-containing crystals in synovial fluid (SF). The reproducibility of the results of this staining technique in 207 SF samples proved to be fairly good (65% concordant results after two observations). Electron-microscope studies confirmed the presence of apatite or calcium pyrophosphate dihydrate (CPPD) crystals in 92% of the alizarin red S positive samples, and in 27% of the weakly positive samples. Based on these figures it can be estimated that approximately 16% of SF samples obtained from patients with inflammatory joint disorders contain apatite and/or CPPD crystals. In contrast with other studies, mainly involving patients with degenerative joint disorders, no correlation was found between alizarin red S staining results and either radiological joint destruction (n = 130) or age.
IgE-containing circulating immune complexes (IgE-CIC) were determined with a 2.5% PEG-precipitation assay in 98 patients with classical or definite rheumatoid arthritis (RA). Of the 45 IgE-CIC positive sera, only 4 had elevated total serum IgE. IgE-CIC positive patients had more active disease than patients without IgE-CIC, as determined by their more swollen joints and higher Ritchie indices (p less than 0.04 and 0.02, respectively). Apart from IgE, other immunoglobulin isotypes, rheumatoid factor (RF) of the IgG-, IgA- and IgM-classes, C3 and antinuclear antibodies could be demonstrated in the IgE-containing PEG-precipitates. IgE-RF could not be demonstrated in serum or in IgE-CIC. Anti-IgE of the IgM-class (IgMaIgE) were frequently found (28/45 patients) in the IgE-positive PEG-precipitates. All 14 patients positive for IgGaIgE in the IgE-CIC were also positive for IgMaIgE in the CIC. As in the serum, there was a good correlation in the CIC between the level of IgGaIgE and the level of IgMaIgE (r = 0.64). The correlation between the respective levels of IgGaIgE and IgMaIgE in serum and in CIC was high (r = 0.93 and 0.79, respectively). On the other hand, only 1 patient was positive for IgAaIgE in the IgE-CIC. We conclude that IgE and aIgE of the IgM- and IgG-classes are frequently present in the immune complex form in RA and that they are correlated with the clinical activity of arthritis.
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The occurrence of renal scleroderma (RSc) was sought retrospectively in 36 consecutive patients with scleroderma, seen in a single rheumatology unit, over a 12-year period. The diagnosis RSc was considered when at least one of the following findings was present: systolic blood pressure greater than or equal to 95 mmH, proteinuria greater than or equal to 0.5 gr/24 hr., and creatinine clearance less than or equal to 50 ml/min.: at least one of these features was found in 16 patients. Hypertension was the most frequent feature of RSc (15 out of 16 patients). Two forms of hypertension were observed. Firstly: malignant hypertension occurring early in the course of RSc, seen in 5 patients, 4 of whom rapidly developed terminal renal insufficiency. Secondly: a moderate hypertension, seen in 10 patients with a more favourable outcome, occurring on average 53 months after the diagnosis of scleroderma was made. Proteinuria was only seen in association with malignant hypertension. Renal impairment occurred in 7 patients. Of the 36 patients with scleroderma, 14 died; 10 of these 14 patients had RSc. Thus the death rate in patients with RSc was very high, whereas only 4 out of 20 died in the group without RSc.
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The case described concerns a patient initially presenting the clinical symptoms of rheumatoid arthritis, including the presence of nodules, and slowly developing into systemic lupus erythematosus (SLE). Besides the signs of chronic inflammation in the synovial tissue, many granulocytes and PAS-positive macrophages were present. At electronmicroscopy the basal membranes of the vessels were multilaminated and the endothelial cells enlarged while many macrophages contained large clumps of electrondense material which could easily be interpreted as rough endoplasmatic reticulum (RER) of plasma cells. Immunoflourescence studies showed deposition of immunoglobulins and complement in the vessel walls of the synovium, thus suggesting an immune-complex pathogenesis.
Results obtained in 43 Rheumatoid arthritis (RA) patients with cervical myelopathy are described; all patients showed several alarm signs together with neurological disturbances. Thirty-four cases were operable; nine patients were not operated upon for various reasons (refusal, and general condition). In the surgically treated patients, the changes were localized in the C1-C2 area (n = 20), in the area below C2 (n = 5), or in both (n = 9). The patients were put on skull traction pre- and post-operatively and nursed on a circo-electric bed. Pre-operatively, the duration of traction varied from a few days to weeks (mean 3 weeks). Post-operatively, the patients were given continuous skull traction for 2 1/2-3 months. This procedure yielded neurological improvement and a stable graft in all but two patients. On follow-up, recurrence of neurological complaints was seen in nine patients, in four due to a new slip at a lower level. Three of these cases were reoperated with good results. Twenty-three patients have died: four 'early' (one pre-operatively and three within 6 weeks post-operatively) and 19 'late'. The mean duration of follow-up was 4.5 years. In those who died 'late', the cause of death was due to the effects of an unstable graft in two cases and in the others the causes were not related to changes in the cervical spine. In the 10 patients who are still alive the mean duration of follow-up is 5 years. The nine patients who were not operated upon all died within a year, 4 of them due to consequences of cord compression. If cervical spondylodesis is feasible in an RA patient with myelopathy, the procedure is advocated.
A 33-year old Caucasian woman with SLE, who had been treated with chloroquine and non-steroidal anti-inflammatory drugs for one year, suddenly presented with a rapidly progressive exacerbation of SLE featuring fever, arthritis, cutaneous manifestations, cerebral dysfunction, pleuritis, pericarditis and pancreatitis. Clinical deterioration and a rise in the serum amylase occurred during a month of high dose prednisone treatment. Plasmapheresis, while maintaining prednisone at a constant dosage, resulted in a complete remission of all symptoms within four weeks. Plasmapheresis was discontinued and improvement was maintained whilst tapering off prednisone and adding azathioprine.
The number of various lymphocyte subpopulations in the peripheral blood of 28 patients with definite rheumatoid arthritis (RA) were studied. The results were correlated with the disease activity, as assessed by the Ritchie index, erythrocyte sedimentation rate and clinical impression. Patients with active RA showed decreased numbers of T mu lymphocytes, strongly increased numbers of Tnull lymphocytes and slightly increased percentages of Fc gamma lymphocytes as compared to 22 healthy donors. Patients with inactive RA had similar, less striking, but significant changes in T mu and Tnull lymphocytes, but in contrast to patients with active RA had Increased numbers of T gamma lymphocytes. The imbalances in T mu and Tnull cells in patients with RA might be explained by endogenous T mu cell activation, resulting in increased numbers of Tnull cells.
Immunological analysis of the mononuclear infiltrates in 12 rheumatoid synovial membranes was performed by means of modified peroxidase antiperoxidase technique using a panel of monoclonal antibodies, directed against T cell differentiation antigens and HLA-DR (Ia-like) antigens. Helper/inducer T lymphocytes (OKT4 +, Leu3a+) were found in large numbers in nodular lymphoplasmocellular infiltrates, whereas the number of cytotoxic/suppressor T lymphocytes (OKT8 +m Leu2a+) was very low, resulting in a high T4/T8 or Leu3a/Leu2a ratio (6á14:1). In diffusely localized lymphoplasmocellular infiltrates this ratio was only slightly increased as compared with the peripheral blood of patients with rheumatoid arthritis (2á4:1). Moreover, most of these T lymphocytes appeared to have Ia-like antigens and seemed to have contact with HLA-DR+, sometimes weakly OKT6+ dendritic nonlymphoid cells. The results showed a constant basic localization pattern of T lymphocyte subsets and suggest that interactions between dendritic nonlymphoid cells, T lymphocyte subsets and B lymphocytes determine the ultimate architecture of the inflammatory infiltrates in the rheumatoid synovial membrane.