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Purpose: To compare the correction of ocular aberrations between custom and standard LASIK retreatment., Methods: Prospective, randomized trial with paired eye control of 74 eyes from 37 patients who underwent LASIK retreatment. Each patient underwent retreatment using Zyoptix LASIK (Bausch & Lomb) in 1 eye and Planoscan LASIK (Bausch & Lomb) in the fellow eye. Correction of ocular aberrations was compared between custom and standard LASIK retreatments., Results: At 6 months, there was a statistically significant reduction in defocus, astigmatism, coma, spherical aberration, second, third, higher-order and total aberration in Zyoptix eyes. There was a statistically significant reduction in defocus, second-order and total aberration in Planoscan eyes., Conclusions: Custom retreatment was statistically superior than standard retreatment for correction of lower and higher ocular aberrations.

Purpose: To evaluate visual quality after wavefront-guided LASIK versus standard LASIK in retreatment of primary LASIK for myopia and myopic astigmatism., Methods: A prospective study was performed with paired eye control of 74 eyes with LASIK retreatment. Each patient underwent retreatment using custom ablation (Zyoptix, Bausch & Lomb) in 1 eye and standard ablation LASIK (PlanoScan, Bausch & Lomb) in the contralateral eye. A complete ophthalmologic examination was performed, including evaluation of glare test and contrast sensitivity test, with a follow-up of 6 months., Results: Zyoptix eyes showed better results of glare test and contrast sensitivity test than the contralateral eyes., Conclusions: Wavefront-guided LASIK produces better visual quality than standard LASIK in the retreatment of refractive errors after primary LASIK.

Purpose: To evaluate refractive outcomes of wavefront-guided LASIK (Zyoptix, Bausch & Lomb) versus standard LASIK (PlanoScan, Bausch & Lomb) in retreatment of primary LASIK for myopia and myopic astigmatism., Methods: A prospective, randomized trial with paired eye control of 74 eyes from 37 patients who underwent LASIK retreatment was performed. Each patient underwent retreatment using Zyoptix LASIK in 1 eye and Planoscan LASIK in the contralateral eye. A complete ophthalmologic examination was performed, including evaluation of high contrast visual acuity and manifest refraction, with a follow-up of 6 months., Results: Both Zyoptix and Planoscan groups had similar values of high contrast visual acuity, gain and loss of best spectacle-corrected visual acuity, safety and efficacy indexes, percentage of eyes with spherical equivalent within +/- 0,50 D and +/- 1,00 D in the postoperative period of 6 months. In the Zyoptix group, the values of spherical component and spherical equivalent of manifest refraction were more hyperopic than in the Planoscan group in the postoperative periods of 1 week, 1, 3 and 6 months. The predictability of spherical equivalent correction was better for the Zyoptix group than for the Planoscan group at 6 months., Conclusions: Wavefront-guided LASIK with Zyoptix produces superior refractive outcomes than standard LASIK with Planoscan in retreatment of refractive errors after primary LASIK. High contrast visual acuity measures are not sensitive in showing the best technique.

Intravesical administration of Calmette-Guérin bacillus (BCG) is effective in the treatment of superficial bladder carcinoma. Transient arthritis or migratory arthralgia has been reported in 0.5% of cases. The authors report on four men (mean age 65 years), who developed an oligoarthritis in three cases after the 2nd, 5th, and 6th weekly instillation of Pasteur BCG, respectively, and symmetrical polyarthritis in one after 48 BCG instillations over a three-year period. Joints involved were the knees (3/4), ankles (3/4), shoulders (1/4), wrists, and hands (1/4). Features included morning stiffness and local evidence of inflammation. All four patients had an elevated erythrocyte sedimentation rate and negative tests for rheumatoid factor. Neutrophils were the main cell type in synovial fluid. Synovial biopsy performed in two cases revealed non-specific inflammation. Erosions of the metatarsophalangeal joints were observed in one patient. Locoregional or systemic symptoms included transient fever (3/4), cystitis (4/4), urethritis (1/4), epididymoorchitis (2/4), conjunctivitis (1/4), and pleural effusion with pericarditis (1/4). The BCG was recovered from an epididymal specimen in one patient. Two patients were positive for the HLA B27 antigen. Outcome was favorable in every case (range: 15 days-6 months) after discontinuation of BCG therapy and administration of isoniazid, rifampin, and prednisone (3 patients) or NSAID (1 patient). Various pathogenic hypotheses for BCG-induced arthritis are discussed, including infection, immune responses to heat shock proteins, and reactive arthritis.

We studied glomerulonephritis in a child with a deficiency of the second component of complement (C2) who was without clinical or serologic evidence of systemic disease. The clinical course was severe, with malignant hypertension and terminal renal failure when the child was 14 years old. Results of histologic studies were typical of membranoproliferative glomerulonephritis with subendothelial deposits. Immunofluorescence microscopy showed diffuse and intense localization of IgG, C1q, and C4 as granular deposits along the glomerular capillary walls and within the mesanguim. Diffuse deposits of C3 were also found along the capillary walls. Nine months after transplantation, the graft biopsy specimen showed glomerular lesions with IgG, C1q, C4, and C3 deposits, which suggests the possibility of a recurrence. The analysis of the previously reported cases of glomerulonephritis with C2 deficiency showed variable, but generally mild, glomerular lesions. Progression of the glomerulonephritis to severe renal insufficiency, as in the present case, is exceptional.

A direct in vitro reaction between complement system and cell nuclei of human leucocytes and of cryostat sections of rat liver or kidney, has been demonstrated by an indirect immunofluorescence technique. The first step of this reaction involves a fixation of C1q to the nuclear DNA as shown by the peripheral distribution of the fluorescence and by the extinction of the fluorescence when the tissue-slices are pretreated by DNase but not by RNase or trypsin. This fixation gives rise to an activation of C1 which can be demonstrated by the capacity of the fixed C1 to induce a fixation of C4 of the same distribution. Although the sequential fixation experiments have not allowed to establish directly the fixation of the following components of the complement system (C2 and C3), the positive results obtained using whole fresh normal human serum as a source of complement and a fluorescent anti-human C3 serum clearly indicate that the activation of the classical pathway by whole cells DNA can go as far as the C3 step. All these results were obtained at physiological pH and molarity: this can suggest a physiopathological meaning for this reaction.

The authors studied the correlations between renal histology and specific antinuclear antibodies of soluble nuclear antigens (anti-Sm, anti-RNP, anti-protein) in 44 patients with such auto-antibodies. They were mostly patients with lupus erythematosus (35/44), more rarely mixed collagen disease or Sjögren's disease. The presence of any one of the specific antibodies of nuclear antigens is not associated with any special renal prognosis; thus the presence of anti-RNP does not mean that there are no histological renal lesions. The renal prognosis depends in fact on the presence of anti-ADN native antibodies. Among the other laboratory parameters (rheumatoid factors, complement levels, cryoglobulinemia) only hypocomplementemia seems to be associated with a poor renal prognosis, the presence of rheumatoid factor has perhaps a protective role.

Studies of platelet C1 have been performed in 11 patients with chronic lymphocytic leukemia (CLL). The platelet C1 level evaluated by the hemolytic method was very low and the platelet aggregation induced by aggregated IgG or anti C1q antisera was significantly reduced. "In vitro", the lymphocytes from CLL were capable of inhibiting platelet C1 and platelet aggregation induced by aggregated IgG and anti C1q to a greater extent than normal lymphocytes. These results lead the authors to discuss the role of platelet C1 in the interaction platelet/immunoglobulins and the nature of the inhibition.

A case of human complete C6 deficiency is reported. The patient, a 31 year old white male, was seen on the occasion of an isolated episode of meningococcal meningitis. Serum complement hemolytic and bactericidal activities were lacking and could be restored to normal by addition of appropriate amounts of purified C6. No hemostatic abnormalities were observed.

The soluble ribonucleoprotein nuclear antigen reactive with specific antibodies present in sera from patients with Mixed Connective Tissure disease has alpha 2-beta 1 electrophoretic mobility, thus enabling its reaction with specific serum antibodies to be studied by counter-immunoelectrophoresis. Its molecular weight determined by elution from a calibrated Sephadex G-200 gel column is about 175,000. Its purification has been attempted by successive DEAE cellulose chromatography, Sephadex G-200 gel filtration and Hydroxyapatite chromatography. Polyacrylamide gel electrophoresis of RNP antigen-containing fractions showed persistent heterogeneity which could be due either to inadequate purification or to dissociation of the RNP-antigen during electrophoresis.

A patient with non-systemic idiopathic glomerulonephritis was found to have a complete deficiency of C2, the second component of complement. The clinical course, histological findings and serological abnormalities are reported in detail. The renal disease was a mild glomerulonephritis with mesangial and subendothelial immune deposits comprising IgG, IgM and C3, increased mesangial matrix without significant cell proliferation. An immunogenetic analysis of the patient's family was carried out. It was demonstrated that the homozygous C2 deficiency was associated with heterozygotism for HLA-A, B and D. Only one of the C2 deficient genes was associated with the expected HLA-A10, B18 haplotype and the propositus was HLA-D2 negative. This report confirms the fact that non-systemic glomerulonephritis should be included in the variety of immunological disorders associated with a complement deficient state. However, C2 deficiency does not seem to be related specifically to a given histological variety of glomerulonephritis.

A direct reaction between the complement system and DNA in nuclei was demonstrated in vitro by an indirect immunofluorescence technique using cryostat-cut sections of rat liver as a substrate. This reaction occurred at physiological conditions of pH and molarity and was abolished by pre-treatment of the tissue sections by DNase. It begins by the fixation of C1q and involves the fixation and probably the activation of apparently all the components of the classical pathway of the complement system. The pattern of fluorescence given by this reaction was similar to the pattern given by anti-DNA antibodies present in sera from systemic lupus erythematosus (SLE) patients.

Mac Duffie's syndrome includes a hypocomplementaemic allergic vasculitis with essentially cutaneous and articular manifestations. Its pathogenesis, still incompletely elucidated, involves the precipitation of immune complexes in the walls of the all vessels. The problem remains as to whether the alteration in the complement system is merely a reflection of this formation of immune complexes, or if it is primary, favourising the chronic infections which produce such complexes. The significance of the presence of low molecular weight precipitins reacting with C1g in the serum of a number of patients remains uncertain. The case reported, with its new clinical features, does not provide an answer to these questions but emphasises the possible role of chronic infections in the origin of this syndrome.

This study involved 10 patients having, in direct immunofluorescence, with covered healthy skin, a speckled IgG (+/-IgM) staining of the epidermal nuclei. The chief clinical signs seen and their respective percentages were: Raynaud's syndrome (80%), arthralgia (80%), diffuse or localised alopoecia (60%), muscular disease (40%), swollen fingers (40%), sclerodactylie (20%), cutaneous sclerosis extending beyond the extremities (30%), cutaneous signs of lupus erythematosus (30%), renal involvement (10%). In nine cases out of ten there were circulating anti-ENA antibodies at high levels, divided into anti-RNP antibodies (7/10), anti-Sm antibodies (1/10) and anti-RNP and anti-Sm antibodies (1/10). Diagnoses were divided into: lupus erythematosus (3/10), systemic scleroderma (3/10), Sharp's mixed connective tissue disease (MCTD) (3/10) and non-classified connective tissue disease (1/10). The combination of speckled staining of epidermal nuclei and circulating anti-ENA antibodies cannot be considered to be specific of any particular type of connective tissue disease and the prognosis of the disease does not appear to differ from that of the usual prognosis of connective tissue disease with anti-ENA antibodies.

The authors present 4 patients who had suffered for several years from isolated systemic scleroderma and in whom, after 3, 10, 19 and 22 years, clinical, biological and histological signs of DLE appeared. There was no current further progression of the scleroderma in two cases, at the time of onset of DLE. In the oter two cases, it had disappeared. All four patients had a serum cryoglobulin. In all cases the kidneys were involved histologically : extra membranous glomerulitis in one, segmental glomerulitis in a second, and diffuse progressive glomerulitis in the last two. The authors analyse the biological changes which accompanied the clinical transformation. One of the patients had anti-ribonucleoprotein antibodies. She died from severe renal involvement which would be against the good prognosis usually associated with the presence of this type of antibody.

We study the consumption kinetic of the fourth and second component of complement by the C1 esterase in different systems with EA or EAC1 and fresh NHS, or functionally purified C4 and C2 preparations. The results show that the two kinetics are similar with a comparable decrease in both C4 and C2 activities till 90 seconds (the mean residual values are from 21 to 34% at this time). The results show moreover that the consumption of the C2 component requires necessarily the presence of the C4 component. The C4 reaction kinetic compared with the C2 "in vitro" one refutes the hypothesis of a greater sensitivity of the C4 component compared with the C2, for the enzymatic action of the C1 esterase. So, a discrepancy in the reaction speed cannot be evoked in order to explain the obvious C4 depression in the consumption hypocomplementemia, and different hypothesis have to be investigated, such as, for instance, a lower synthesis rate of the C4 component compared with the C2 one.

Studies have been performed with platelets using C1 haemolytic assays and platelet aggregation induced by anti-C1q, anti-C1s and aggregated IgG in the presence of C1 subcomponents C1q, C1r and C1s. C1q was removed by EDTA or modified by collagenase from human platelets while after the same treatment C1s remained bound to the platelets. EDTA treated platelets were no longer aggregated by aggregated IgG. The addition of C1q restored the reactivity of the platelets to aggregated IgG while the addition of C1r or C1s was without effect. Furthermore, the addition of C1r or C1s to C1q inhibited the action of C1q in platelet aggregation induced by IgG.The possible association between the different C1 subcomponents and human platelets is discussed.

Clinical and biological manifestations have been studied in 134 patients whose serum had antibodies to soluble extractable nuclear antigens (ENA). 85 of the patients had anti-RNP antibodies, 18 had anti-Sm antibodies, and 31 had antibodies to one or more soluble nuclear antigen. In all groups, the predominant clinical manifestations were polyarthritis, Raynaud's phenomenon, fever, and skin involvement. Renal disease was less common in those patients with anti-RNP antibodies than in the other patients. Most patients with definite renal disease (13 out of 15) also had circulating anti-DNA antibodies. The final diagnoses in these 134 patients were well defined connective tissue disease in 59; overlap syndromes in 34; a limited clinical syndrome made up of polyarthritis Raynaud's phenomenon--often with swollen fingers--and/or hypergammaglobulin-aemia in 31, and various other clinical conditions in 10.

Fifty sera containing antinucleolar antibodies were o gathered in a routine laboratory during testing for antinuclear antibodies with indirect immun-fluorescence over a five-year period. The patients involved were suffering from sclerodermia (13 cases), rheumatoid arthritis (7 cases), polymyositis (3 cases), lupus (2 cases), various rhumatismal disease (59 cases) and non rhumatismal diseases in 16 cases, including 5 malignant diseases. In 80 per cent of the cases nucleolar fluorescence was combined with nuclear fluorescence of another type. The antibodies were almost always of the IgG category and belonged in 2/3 of cases to several immunoglobulin categories, most often IgG-IgA. Pretreatment of the liver cuttings with RNase always modifies the nucleolar fluorescence, most often making it negative, and pretreatment with DNase using a combination of enzymes 10 times higher also modifies it (more often decreasing it than making it negative), which indicates that the nucleolar antigen, probably an ARN with a low molecular weight, also depends upon the ADN.

In a patient suffering from rheumatoid arthritis thorough investigations led to the discovery of complete deficiency in the 7th component of the complement. A study of the patient's family tree confirmed the hereditary, codominant autosomal character of the deficiency, unrelated to the HLA system. The complement-dependent serum functions were investigated: the opsonizing and chemotactic activities were preserved, but bactericidal properties were lacking. Coagulation studies showed disorders in platelet aggregation in the presence of thrombin, and these were corrected by the addition of C7. The association of a dysimmune disease with C7 deficiency is probably not fortuitous; it might result from a common gene abnormality or, in some cases, from repeated infections.

Sharp and coworkers have coined the name "Mixed connective tissue disease" to an association of symptoms seen in different connective tissue diseases. Those symptoms are associated with a special antibody directed against ribonucleoproteins (RNA-P). The presence of this antibody accounts for a high titer of antinuclear fluorescent antibody, of the speckled type. The most frequents symptoms in the association described by Sharp are Raynaud's phenomenon, swollen fingers, non deforming arthritis. We have observed those symptoms without any further symptoms of connective tissue disease, but with the presence of anti-RNA-P antibody. We suggest to coin the name of Sharp's syndrome to that clinical association. The significance of anti-RNA-P, and their correlation with a remarkable benignity of the disease, is discussed.

A previously healthy 14-year-old boy presented with fulminant meningococcemia. He was found to have a total deficiency of C7. His serum totally lacked bactericidal activity against Neisseria meningitidis. Addition of purified C7 restored the serum hemolytic and bactericidal activity. Susceptibility to disseminated Neisseria infections has previously been reported in 3 patients with C7 deficiency, as well as in a few patients with deficiency of C5, C6 and C8. These findings emphasize the importance of intact complement mediated bactericidal activity in host defense against disseminated Neisseria infections. Evaluation of the complement system in individuals with Neisseria infections appears mandatory.

Among 23 patients with Sharp's disease, 14 initially had only polyarthritis, Raynaud's syndrome and anti-ribonucleoprotein antibodies. During a mean 5.6 years (range: 1-7 years) follow-up these 14 patients, 2 cases of pericarditis, 1 case of trigeminal neuralgia, 2 cases of nephropathy and 1 case of pulmonary arterial hypertension were observed. The 9 remaining patients had symptoms of multiple collagen disease. They were followed up for a mean of 4.3 years (range: 3-7 years) and 3 developed pericarditis. We discuss the prognostic significance of anti-DNA antibodies (7 cases) and low serum complement (3 cases) which, when combined, seem to be associated with severe visceral lesions.

A C1 haemolytic activity was previously shown to be associated with platelets. The presence of C1 on human gel filtered platelets is confirmed by Ouchterlony analysis, and platelet aggregation induced by anti-c1 q antisera. After cleavage of C1 by EDTA, platelet aggregation induced by aggregated was decreased and was restored by the addition of C1. The possible role of C1 in human platelet aggregation induced by aggregated immunoglobulins or immune complexes is discussed.

The author reviews the present state of knowledge of value in rheumatology concerning serum immunoglobulins, their structure, their cellular biosynthesis, and their relation to membrane immunoglobulins of the B lymphocytes. He then examines the concept of dysglobulinaemia and explains why the terms monoclonal immunoglobulin and monoclonal immunoglobulinopathy are preferable to dysglobulinaemia and paraprotein. The clinical and immunochemical classification of monoclonal immunoglobulins, the problem of amylosis, and the relationship with plasmocytic dyscrasias and with the cryoglobulins are then discussed. Afterwards the pathogeny of these affections is briefly considered.

The clinical and laboratory features of rheumatoid arthritis (RA) with antinuclear factor (ANF) were prospectively analyzed in 50 patients and compared with those of another series of 50 patients of similar age, sex and duration of disease, but without ANF. The severity of articular lesions was about the same in both series, but systemic symptoms and Gougerot-Sjögren syndrome occurred more frequently in patients with ANF. Gold compounds and D-penicillamine appeared to be well tolerated by all patients. RA patients with ANF had more strongly positive responses to latex and Waaler-Rose tests. Farr's radioimmunoassay was sometimes positive (11/49), but as a rule, the degree of positivity was inferior to 50%.

Three methods of determination of anti-DNA antibodies were compared. The indirect immunofluorescence method after exposure to animal DNA (IF) and Farr's radio-immunological method with bacterial DNA labelled with C14, gave highly similar results, although there were some cases in which Farr's method gave a negative and the IF method a positive result. In part, this discordance appears to be accounted for by the variable affinity of the anti-DNA antibodies for DNA. The counter-immuno-electrophoresis method (CIEP) on the other hand, gave very different results: positive reactions in a large proportion of normal sera and a considerable proportion of false-positive and false-negative results in disseminated lupus erythematosus. It is concluded that until the CIEP method is made more reliable by technical refinement, determination of anti-DNA antibodies may be carried out by either the IF or the radio-immunological method, but a double-check, by application of the two methods at the same time, is highly advisable.

A 22 year old woman having disseminated discoid L.E. with alopecia, photosensitivity and normal renal function is presented. Speckled FANA type R.N.P. was found; L.E. cells and anti-DNA were not present. Direct IF of involved skin revealed deposits of IgG and C3 forming a band at the dermo-epidermal junction. In normal skin there was speckled epidermal nuclear staining with IgG. The study of the patient's complement revealed a selective defect of the C2 component (0 p.100) with a drop in total complement (6 p. 100). The father probably has a heterozygote deficit of C2 (55 p. 100); the mother, however, is within the normal range (119 p. 100). The HLA investigation of the patient and her immediate family did not demonstrate haplotype A10, B18, DW2 as is frequently seen in cases of L.E. associated with a C2 deficiency. The patient is A1, B18, DW--/A10 (W26), BW15, DW--.

An ultrastructural immunoperoxidase study of human synovial membrane biopsies performed in 16 patients with rheumatoid synovitis and in 14 control patients showed that: (1) plasma immunoglobulins have an intercellular distribution and seem to diffuse mainly by an intercellular rather than by a transcellular pathway; and (2) there is a difference in the distribution of plasma IgG and IgM. IgG was found in intravascular and extravascular spaces in all biopsies. IgM was found only in intravascular spaces in control biopsies, but in rheumatoid synovitis it was present in both intravascular and extravascular spaces. This difference in distribution may be due to increased vascular permeability in inflammatory synovitis.

The aim of the study is to compare two methods for the measurement of the fourth human complement component through its hemolytic activity and immunodiffusion properties in 35 healthy subjects and 35 patients with immunological complement depletion. For the healthy subjects, the results show a highly significant correlation between the two methods (the coefficient of correlation is + 0.80). On the contrary, there is no correlation between the two assays for the patients suffering from consumption hypocomplementemia. The reasons of this discrepancy are discussed.