The prevalence of radiographic vertebral fractures in Mexican men.

SUMMARY: The prevalence of radiographically ascertained vertebral fractures in a random sample of 413 in Mexican men is 9.7% (95% CI 6.85-12.55). Increase of vertebral fracture rises with age from 2.0% in the youngest group (50-59 years) to 21.4% in the oldest group (80 years and over). INTRODUCTION: This is the first population-based study of vertebral fractures in Mexican men using a standardized methodology reported in other studies. METHODS: The presence of radiographic vertebral fractures increases with age. This same pattern was found in Mexican women with steady age increments, but the higher prevalence of fractures in women starts at age 70, whereas in men, the higher prevalence starts a decade later (80 years and over). RESULTS: The standardized prevalence per 1,000 men 50 years and over in the Mexican population for the year 2005 is 65.8 (95% CI 29.9-105.5), and it is 68.6 (95% CI 32.2-108.7) in the US population for the year 2000.

The prevalence of radiographic vertebral fractures in Latin American countries: the Latin American Vertebral Osteoporosis Study (LAVOS).

UNLABELLED: In the first population-based study of vertebral fractures in Latin America, we found a 11.18 (95% CI 9.23-13.4) prevalence of radiographically ascertained vertebral fractures in a random sample of 1,922 women from cities within five different countries. These figures are similar to findings from studies in Beijing, China, some regions of Europe, and slightly lower than those found in the USA using the same standardized methodology. INTRODUCTION: We report the first study of radiographic vertebral fractures in Latin America. METHODS: An age-stratified random sample of 1,922 women aged 50 years and older from Argentina, Brazil, Colombia, Mexico, and Puerto Rico were included. In all cases a standardized questionnaire and lateral X-rays of the lumbar and thoracic spine were obtained after informed consent. RESULTS: A standardized prevalence of 11.18 (95% CI 9.23-13.4) was found. The prevalence was similar in all five countries, increasing from 6.9% (95% CI 4.6-9.1) in women aged 50-59 years to 27.8% (95% CI 23.1-32.4) in those 80 years and older (p for trend < 0.001). Among different risk factors, self-reported height loss OR = 1.63 (95% CI: 1.18-2.25), and previous history of fracture OR = 1.52 (95% CI: 1.14-2.03) were significantly (p < 0.003 and p < 0.04 respectably) associated with the presence of radiographic vertebral fractures in the multivariate analysis. In the bivariate analyses HRT was associated with a 35% lower risk OR = 0.65 (95% CI: 0.46-0.93) and physical activity with a 27% lower risk of having a vertebral fracture OR = 0.73 (95% CI: 0.55-0.98), but were not statistically significant in multivariate analyses CONCLUSION: We conclude that radiographically ascertained vertebral fractures are common in Latin America. Health authorities in the region should be aware and consider implementing measures to prevent vertebral fractures.

Geographic differences in bone mineral density of Mexican women.

The aim of this study was to generate standard curves for normal spinal and femoral neck bone mineral density (BMD) in Mexican women using dual-energy X-ray absorptiometry (DXA), to analyze geographic differences and to compare these with 'Hispanic' reference data to determine its applicability. This was a cross-sectional study of 4460 urban, clinically normal, Mexican women, aged 20-90 years, from 10 different cities in Mexico (5 in the north, 4 in the center and 1 in the southeast) with densitometry centers. Women with suspected medical conditions or who had used drugs affecting bone metabolism, were excluded. Lumbar spine BMD was significantly higher (1.089 +/- 0.18 g/cm2) in women from the northern part of Mexico, with intermediate values in the center (1.065 +/- 0.17 g/cm2) and lower values (1.013 +/- 0.19 g/cm2) in the southeast (p < 0.0001). Similarly, femoral neck BMD was significantly higher in women from the north (0.895 +/- 0.14 g/cm2), intermediate in the center (0.864 +/- 0.14 g/cm2) and lower (0.844 +/- 0.14 g/cm ) in the southeast part of Mexico (p < 0.0001). Northern Mexican women tend to be taller and heavier than women from the center and, even more, than those from the southeast of Mexico (p < 0.0001). However, these differences in BMD remained significant after adjustment for weight (p < 0.0001). A significant loss (p < 0.0001) in BMD was observed from 40 to 69 years of age at the lumbar spine and up to the eighth decade at the femoral neck. Higher and lower lumbar spine values, as compared with the 'Hispanic' population, were observed in Mexican mestizo women from the northern and southeastern regions, respectively. In conclusion, there are geographic differences in weight and height of Mexican women, and in BMD despite adjustment for weight.

Serum antibodies to distinct epitopes of the tissue-type plasminogen activator (t-PA) in patients with systemic lupus erythematosus.

Defective fibrinolysis due to decreased tissue-type plasminogen activator (t-PA) activity is a well-established finding in patients with systemic lupus erythematosus (SLE). The possibility that this decrease in t-PA activity may be related to the presence of autoantibodies directed against t-PA, and the possible role of these autoantibodies in the pathophysiology of fibrinolysis in SLE, were investigated. Serum samples from 115 SLE patients and 63 normal volunteers were analyzed for the presence of such antibodies. The search for antibodies to t-PA was performed by means of several systems, allowing for the identification of epitopes presented in different conformational physical states of t-PA: free or associated to its inhibitor (PAI-1) in plasma, specifically bound to fibrin surface, or passively adsorbed to solid supports. Antibodies in variable amounts were detected by all systems used; however, t-PA activity was not inhibited by the IgG fraction of the positive sera in a fibrin-agar fibrinolysis system. Moreover, the demonstration of serum anti-t-PA antibodies was not associated with clinical or laboratory abnormalities related to vasoocclusive episodes. These results indicate that, as in the case of other autoantibodies, their detection in serum does not imply their direct participation in the pathophysiology of thrombosis in SLE.

Presence of serum antibodies to coagulation protein C in patients with systemic lupus erythematosus is not associated with antigenic or functional protein C deficiencies.

Antibodies directed to immunopurified coagulation protein C (PC) were investigated in serum samples from 108 patients with systemic lupus erythematosus (SLE) and found in 12 of them. However, their presence was not associated with antigenic or functional deficiencies of PC, which were documented in 6 and 17 patients, respectively.

Natural anticoagulants in systemic lupus erythematosus. Deficiency of protein S bound to C4bp associates with recent history of venous thromboses, antiphospholipid antibodies, and the antiphospholipid syndrome.

The association of thrombosis with antiphospholipid antibodies (aPL) in patients with systemic lupus erythematosus (SLE) could be due to their interference with natural phospholipid dependent anticoagulant mechanisms. We studied antigenic protein C (APC), functional protein C (FPC), free protein S (FPS), protein S bound to C4 binding protein (C4bp-S), antithrombin III (ATIII), as well as IgG and IgM anticardiolipin antibodies (aCL) in 38 patients with SLE with a history of thromboses and 70 patients with SLE without such history. We found a high frequency of deficiencies of natural anticoagulants in both groups of patients with SLE but, because of patient selection, we could not determine the actual prevalence of these defects. Patients having had a venous thrombosis in the previous year had low C4bp-S more frequently than patients with older or no thromboses. When we divided our patients with SLE into those who had a definite, probable, questionable or no antiphospholipid syndrome (aPS) we found the frequency of C4bp-S deficiency to be significantly higher in those with definite aPS than in those without aPS. Intermediate proportions were found in patients with probable and questionable aPS. The levels of C4bp-S decreased as the levels of aCL, particularly IgG, increased. Stepwise discriminant analysis of natural anticoagulants selected deficiencies of C4bp-S and FPC with increased ATIII as a set of variables with highest predictive power for classification of patients with and without aPS. Thus, deficiencies of natural anticoagulants may occur frequently in patients with SLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiphospholipid antibodies and the antiphospholipid syndrome in systemic lupus erythematosus. A prospective analysis of 500 consecutive patients.

Five hundred consecutive patients with systemic lupus erythematosus (SLE) were entered into a prospective study of anticardiolipin antibodies (ACLA) in their 3 major immunoglobulin isotypes and followed thereafter with repeated testing for a mean period of nearly 8 months. Manifestations of SLE that were strongly associated with ACLA included venous thrombosis (particularly when recurrent), thrombocytopenia, hemolytic anemia, recurrent fetal loss, and leg ulcers. Other manifestations found to be associated with ACLA were arterial occlusions, transverse myelitis, and pulmonary hypertension. Conversely, we found no relationship between ACLA and migraine, convulsions, transient ischemic attacks, psychoses, or avascular necrosis of bone. No relationship was found between the presence of ACLA and that of anti-DNA antibodies studied in the same serum sample. Association with ACLA grew stronger and titers became higher in patients with several of the associated manifestations. Statistical analyses revealed the existence of a syndrome, the antiphospholipid syndrome, comprising 2 or more manifestations in conjunction with ACLA titers 5 standard deviations above the mean of normal control subjects, particularly if ACLA had been positive on at least 2 occasions. We propose that such criteria could be applied to the definition of the antiphospholipid syndrome. The presence and the titers of these antibodies related to disease activity and titer decreased by treatment, particularly when they were of the IgM isotype. Patients in whom a thrombotic episode occurred during the course of the study were observed to have a coincident decrease in ACLA titers, a finding that might indicate consumption of the antibody during the event. Treatment and the resulting inactivation of disease appear to have independent effects on ACLA titers. Physicians should therefore be cautious in prescribing high doses of corticosteroids or immunosuppressants to patients with SLE solely because they have high titers of ACLA.

Hemocytopenia in systemic lupus erythematosus. Relationship to antiphospholipid antibodies.

We studied 500 consecutive patients with systemic lupus erythematosus (SLE) for antibodies to phospholipids (APLA) by an ELISA method using cardiolipin as antigen and antiimmunoglobulins G, M and A to determine their isotype. Once entered into this prospective study the patients were followed for up to 16 months (mean 7.7 +/- 4.72 SD) with periodic determinations of APLA. Of the 500 patients with SLE, 88 had had thrombocytopenia, 25 had had hemolytic anemia, 25 had had both, and 362 had no history of these hemocytopenias. If we considered the odds ratio of these 362 patients for having high titer APLA as 1, patients with a history of thrombocytopenia, hemolytic anemia or both had significantly higher odds ratios of having APLA than did those without hemocytopenia. Patients with thrombocytopenia had significantly higher levels of IgG APLA, those with hemolytic anemia had significantly higher titers of IgM APLA and patients with both had significantly higher titers of both of these APLA isotypes, than did patients without hemocytopenias. A correlation between positive direct Coombs' tests and IgM APLA was also found. We conclude that APLA is associated with these hemocytopenias in SLE. This might be due to their interaction with negatively charged phospholipids in the cell walls of the respective cells.

Relationship between antiphospholipid antibodies and recurrent fetal loss in patients with systemic lupus erythematosus and apparently healthy women.

We studied 199 patients with systemic lupus erythematosus (SLE) who had been at risk for recurrent fetal loss. Thirty-six had had recurrent fetal loss. These patients, plus a group of 38 healthy women with history of recurrent fetal loss and a group of healthy women who had had at least 3 pregnancies, were tested for antiphospholipid antibodies (APLA) of the 3 major immunoglobulin isotypes using an ELISA method with cardiolipin as antigen. Thirty of the 36 patients with SLE with recurrent fetal loss, 23 of the 163 patients with SLE without recurrent fetal loss, 3 of the 38 healthy women with recurrent fetal loss and no healthy woman with normal obstetric histories had APLA. In all but 3 of the patients with SLE with recurrent fetal loss these included APLA of the IgG isotype. Considering the odds ratio of having recurrent fetal loss as 1 for those patients with SLE without APLA, we found it to be 10.54 times higher in patients with SLE with high titer APLA. Titers of IgG APLA were also 3.2 times higher in patients with SLE with recurrent fetal loss than in those without. We conclude that recurrent fetal loss associates strongly with APLA of the IgG isotype.

Acquired protein C deficiency in a patient with primary antiphospholipid syndrome. Relationship to reactivity of anticardiolipin antibody with thrombomodulin.

A 16-year-old boy had recurrent venous thromboses and pulmonary thromboembolism that caused him pulmonary hypertension. He also had livedo reticularis, thrombocytopenia and high titer IgG antiphospholipid (cardiolipin) antibodies. In the absence of clinical and laboratory evidence of SLE, he was considered to have a primary antiphospholipid syndrome. Coagulation studies revealed a functional deficiency of protein C although it was present in normal antigenic amounts. Since both his parents had normal functional and antigenic protein C findings, his deficiency was considered acquired. The reactivity of the anticardiolipin antibodies could be decreased in a dose dependent fashion when preincubated with increasing amounts of thrombomodulin, a protein required for protein C activation at the endothelial cell membrane. This interaction of antiphospholipid antibodies with thrombomodulin may help explain the occurrence of thrombosis in some patients with antiphospholipid antibodies, despite the behavior in vitro of these antibodies as circulating anticoagulants.

Occurrence of both hemolytic anemia and thrombocytopenic purpura (Evans' syndrome) in systemic lupus erythematosus. Relationship to antiphospholipid antibodies.

Ten of 12 patients with systemic lupus erythematosus (SLE) who had hemolytic anemia and thrombocytopenic purpura (Evans' syndrome) during their course had evidence of antiphospholipid antibodies either because they had a false positive VDRL test (8 patients), a prolonged partial thromboplastin time (5 patients), a lupus anticoagulant (3/4 patients), and/or anticardiolipin antibodies as determined by an ELISA method (7 patients). Antibodies to cardiolipin were found in very high levels (up to 38 standard deviations above the mean of normal controls) and were of both IgG and IgM isotypes. The 2 patients with SLE and Evans' syndrome who did not have evidence of antiphospholipid antibodies were studied at the onset of SLE which occurred with Evans' syndrome. Although cardiolipin is not a constituent of the cell wall of either platelets or erythrocytes, other phospholipids that cross react antigenically with cardiolipin are and can be exposed through cell damage. This could be a mechanism whereby hemolytic anemia and thrombocytopenia could occur in the same patient with SLE. Whether absorption of the antiphospholipid antibody during the acute episode of hemocytopenia could occur, and thus prevent its detection at such time, remains undetermined.

Toxoplasma gondii encephalitis in systemic lupus erythematosus. A neglected cause of treatable nervous system infection.

Opportunistic infections are common in patients with systemic lupus erythematosus (SLE) and toxoplasmosis of the brain resembles central nervous system manifestations of active SLE. A case is described that illustrates the clinical and pathological features of this infection with discussion of the diagnostic procedures and treatment.

Cardiovascular manifestations in systemic lupus erythematosus. Prospective study of 100 patients.

One hundred consecutive female patients with active systemic lupus erythematosus (SLE) were studied from the cardiovascular point of view by means of non invasive methods. Seventy percent of the cases presented some type of cardiovascular anomaly. Seventy four percent of the resting electrocardiograms were abnormal as well as 72% of the M mode echocardiograms and 55% of the cardiac X ray series. The most frequent observed complications were: pericarditis and or pericardial effusion (39%), arterial hypertension (22%), ischemic heart disease (16%), myocarditis (14%), congestive heart failure (10%), pulmonary hypertension (9%), valvular heart disease (9%), pleural effusion (7%) and cerebro vascular accident (3%). We analyzed each one of these complications and found of special interest the high incidence of ischemic heart disease which is more frequent than has been hitherto reported. Ischemic heart disease was observed in two types of patients: a) Those with long term steroid therapy. In these, the mechanism seems to be an atherosclerotic disease probably induced by the chronic use of steroids. The management of these cases do not differ from other types of coronary heart disease due to atherosclerosis. b) Those with frank episodes of vasculitis in whom the basic mechanism is an inflammatory process of the coronary arteries and its treatment is fundamentally that of the vasculitis. We consider necessary to study routinely all patients with SLE through non invasive cardiological methods.

Contraception with progestagens in systemic lupus erythematosus.

To test the efficacy and tolerance of progestagens as contraceptives in systemic lupus erythematosus (SLE), 200 mg IM norethisterone enanthate was administered to 10 patients, 0.03 mg/day oral levonorgestrel to 15 patients and they were compared with 18 control patients. There were 4 episodes of active SLE in 48 patient-months on norethisterone enantate and 6 episodes in 122 patient-months on levonorgestrel as compared with 9 episodes of active disease in 298 control patient-months (p = ns). There were no pregnancies and intermenstrual bleeding led to discontinuation of medication in 30% of patients. Progestagens may be an alternative contraceptive method in SLE.

PIP: To test the efficacy and tolerance of progestagens as contraceptives in systemic lupus erythematosus (SLE), 200 mg intramuscular norethisterone enanthate was administered to 10 patients, .03 mg/day oral levonorgestrel to 15 patients; they were compared with 18 controls. There were 4 episodes of active SLE in 48 patient-months on norethisterone enanthate and 6 in 122 patient-months on levonorgestrel as compared with 9 episodes of active disease in 298 control patient-months (p=ns). There were no pregnancies, and intermenstrual bleeding led to discontinuation of medication in 30% of the patients. Progestagens may be an alternative contraceptive method in SLE.