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Background: Human T-lymphotropic virus type 1 (HTLV-1) is known to cause HTLV-associated myelopathy (HAM)/tropical spastic paraparesis and adult T cell leukemia. A growing body of evidence links HTLV-1 infection with an increasing spectrum of disease, including uveitis, periodontal disease, arthropathy, sicca syndrome, and neurologic deficits., Objectives: Despite recent findings, the natural history of HTLV-1 infection remains poorly defined. This study was designed to better characterize initial clinical and neurological findings in individuals diagnosed with HTLV-1 infection., Study Design: We conducted a cross-sectional study of 71 individuals recently diagnosed with HTLV-1 and 71 uninfected age- and sex-matched blood donors in Salvador, Brazil. Subjects were administered a standardized questionnaire and underwent physical exam., Results: HTLV-1 infected subjects were significantly more likely than controls to report complaints of hand and foot numbness (OR=5.3; 95% CI: 1.8-15.3; p=0.002 and OR=4.0; 95% CI: 1.3-12; p=0.013 respectively), difficulty running (OR=4.0; 95% CI: 1.1-14.2; p=0.032), nocturia (OR=5.0; 95% CI: 1.1-22.8; p=0.038), arthralgia (OR=3.3; 95% CI: 1.4-7.7; p=0.006), and photophobia (OR=3.3; 95% CI: 1.4-7.7; p=0.006)., Conclusions: Neurologic, ocular and rheumatologic complaints may be the first manifestations of HTLV-1 infection. Therefore, all patients presenting with initial diagnosis should be rigorously screened for these symptoms., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Human T lymphotropic virus (HTLV)-I is known to cause HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and other pronounced disease in less than 4% of those infected. However, evidence is accumulating that a proportion of HTLV-I carriers have neurological and urological symptoms without fulfilling criteria for HAM/TSP. Brain white matter (WM) lesions on magnetic resonance imaging (MRI) are frequently seen in HAM/TSP. HTLV-I carriers with MRI scans for other neurological diagnoses have WM lesions more frequently than expected. We studied 10 patients with HAM/TSP and 20 HTLV-I carriers without overt neurological disease and evaluated clinical characteristics, viral load, total, small, large, confluent WM lesion number, and lesion volume on MRI. Cerebral WM lesions were found in of 85% of HTLV-I carriers and 80% of HAM/TSP patients. Lesion number, size or location was no different between carriers and HAM/TSP. Cognitive function was lower in HAM/TSP (p = 0.045) but did not correlate with WM lesion number. Viral load and peripheral blood mononuclear cell interferon production correlated positively (p = 0.001) but did not correlate with lesion number or volume. Conventional brain MRI frequently shows WM lesions in HTLV-I-infected individuals suggesting potential early central nervous system inflammation with rare development of progressive disease.

Human T-lymphotropic virus type I (HTLV-I) causes HTLV-I-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia in a small percentage of infected individuals. HTLV-I infection is increasingly associated with clinical manifestations. To determine the prevalence of clinical manifestations in HTLV-I infected individuals, we conducted a cross-sectional study of 115 HTLV-I-infected blood donors without myelopathy and 115 age- and sex-matched seronegative controls. Subjects answered a standardized questionnaire and underwent physical examination. Compared with controls, HTLV-I-infected subjects were more likely to report arm or leg weakness (OR = 3.8, 95% CI: 1.4-10.2; OR = 4.0, 95% CI: 1.6-9.8, respectively), hand or foot numbness (OR = 2.1, 95% CI: 1.1-3.9; OR = 4.8, 95% CI: 2.0-11.7, respectively), arthralgia (OR = 3.3, 95% CI: 1.7-6.4), nocturia (OR = 2.7, 95% CI: 1.04-6.8), erectile dysfunction (OR = 4.0, 95% CI: 1.6-9.8), and to have gingivitis (OR = 3.8, 95% CI: 1.8-7.9), periodontitis (OR = 10.0, 95% CI: 2.3-42.8), and dry oral mucosa (OR = 7.5, 95% CI: 1.7-32.8). HTLV-I infection is associated with a variety of clinical manifestations, which may occur in patients who have not developed myelopathy.

Sickle cell disease (SCD) is the most prevalent inherited monogenic pathology in South America. Although children with SCD have normal birthweight, weight deficit is often seen from early childhood. On the other hand, paradoxically, normal final height associated with delayed puberty has been reported from Brazil and Jamaica. This cross-sectional study describes the growth pattern by age and sex in 76 children and adolescents with SCD in Sergipe, north-east Brazil with a median age of 110 months. Median weights and heights for age were below the NCHS standards. The weight and height deficits were statistically significant for boys of all ages, except for 7-year-olds. Most girls have median weights and heights below the NCHS standards but this only becomes statistically significant at 15 years of age. Family channels were calculated from the parents' heights. The observed height was lower than the expected percentile value for the family in seven (41%) children, equal to expected family height in six (35%) and above expected family height in four (24%) of 17 teenagers. Our findings suggest that Brazilian children with SCD do not attain normal height and weight. It is therefore likely that, although maximum height and weight velocity occur significantly later than normal due to delayed puberty, the magnitude of this spurt is less than normal.