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Human T-cell lymphotrophic virus type I (HTLV-I), is a member of the oncogenic retroviruses family endemic in several parts of the world and also recently identified in the Jewish Mashhadi population who immigrated from Iran to Israel. The virus is the causative agent of adult T-cell leukemia (ATL) and a chronic myelopathy known both as tropical spastic paraparesis (TSP) or HTLV-I associated myelopathy (HAM). The known modes of HTLV-I transmission are by sexual intercourse, from mother to child in breast milk, via blood transfusion, and by sharing of needles by parenteral drug users. In the present study we examined the presence of HTLV-I provirus genomic DNA by nested polymerase chain reaction (PCR) and by DNA hybridization in mouthwash samples obtained from 13 Mashhadi-born Iranian Jews with spastic paraparesis associated with HTLV-I, 4 Mashhadi-born Iranian Jews asymptomatic carriers for HTLV-I and 21 healthy controls. Proviral HTLV-I DNA was detected by mouthwash PCR in 12 of 17 HTLV-I infected subjects (71%) but in none of 21 controls. Proviral DNA was also detected in mouthwash samples using HTLV-I probe by dot blot hybridization assay. The presence of HTLV-I proviral DNA in whole saliva may suggest a possible transmission of the virus via saliva and explain the increased rate of infection in elderly Mashhadi-Jewish population.

To assess linear growth in patients with persistent oligoarticular juvenile idiopathic arthritis (JIA) treated by intra-articular corticosteroid injections (IACSI).Data were obtained from a retrospective review of the charts of 95 patients with persistent oligoarticular JIA (69 females). The mean age at first visit was 4.9 ± 3.4 years, with follow-up of 6 ± 3.7 years. The height SDS for chronologic age (z-score) was correlated with the clinical course of the disease and compared among patients treated by IACSI alone (group I) or by a combination of disease-modifying antirheumatic drugs (DMARDs) (group II).Growth retardation was found in 35.8% of patients (Δ z-score-0.3), including 11.6% with severe growth retardation (Δ z-score-1.0). Growth retardation was found in a smaller proportion of patients in group I (any growth retardation, 30.6%; severe growth retardation, 6.5%) than in patients in group II (any growth retardation, 44.4%; severe growth retardation, 21.2%; P.05). Elevated erythrocyte sedimentation rate values (≥ 40 mm/1sth) indicated a significantly higher risk for growth retardation. All other clinical variables had no association with growth retardation.A significant proportion of patients with persistent oligoarticular JIA have growth retardation and a minority have severe growth retardation. Only elevated erythrocyte sedimentation rate values were proven to be a good predictor of risk for growth retardation.

Objective To identify physical, behavioral, and environmental features of adolescents (aged 11-17 years) with type 2 diabetes mellitus and their families to define the involvement of known risk factors and to define a profile of at-risk individuals. Design and Methods A total of 42 subjects from 11 families with an adolescent in whom type 2 diabetes was previously diagnosed participated. All subjects underwent anthropometric measurement and completed food frequency and eating disorder questionnaires, and were classified according to theDiagnostic and Statistical Manual of Mental Disorders, Fourth Edition. In addition, laboratory tests to determine levels of hemoglobin A1c, fasting glucose, C peptide, insulin, and proinsulin were performed. Results Type 2 diabetes had been diagnosed in 5 of 11 mothers and 4 of 11 fathers before the study. Type 2 diabetes was diagnosed in 3 of the remaining 7 fathers during the study. In 3 families, both parents were affected with type 2 diabetes. As a group, participants were obese, with a body mass index higher than the 95th percentile for probands and fathers, and higher than the 85th percentile for mothers and siblings. The sum of skin fold measurements was above the 95th percentile for the probands, their siblings, and the parents. All groups had high fat intake and low fiber intake. None of the subjects participated in a structured or routine exercise program, and most reported no regular physical activity. Three of the probands met the criteria for binge-eating disorder, and 6 additional patients had notable characteristics of the disorder. Mothers affected with type 2 diabetes had markedly abnormal hemoglobin A1clevels, indicating poor control. There were no group differences in fasting concentrations of insulin, proinsulin, or C peptide. However, a third of the mothers with type 2 diabetes, and all but 1 of the siblings, had evidence of insulin resistance. Conclusions Adolescents in whom type 2 diabetes has been diagnosed, as well as their first-degree family members, are obese. In addition, the incidence of diagnosed and undiagnosed type 2 diabetes or of insulin resistance in the families of adolescents with type 2 diabetes is striking. Probands and other family members have lifestyles characterized by high fat intake, minimal physical activity, and a high incidence of binge eating. These findings indicate that the families of adolescents with type 2 diabetes share many anthropometric and lifestyle risk factors. The design of treatment programs for adolescents with type 2 diabetes will need to address the lifestyle and health habits of the entire family.

We hypothesized that type 2 diabetes among adolescents occurs within families in which known diabetes risk factors are prevalent. Therefore,we investigated these families in order to define the presence of known risk factors and to determine whether a profile of the at-risk family can be identified. A total of 42 subjects from 11 families with adolescent previously diagnosed with type 2 diabetes participated. All subjects underwent anthropometric measurements, as well as determination of fasting glucose, HbA1c C-peptide, pro-insulin, and insulin. Subjects also completed food frequency and DSMIV eating disorder questionnaires. Results: Forty-five percent of mothers and 36% of fathers had been diagnosed with type 2 diabetes prior to the study. An additional 40% of the fathers were diagnosed with type 2 diabetes as part of their participation. Mothers affected with type 2 diabetes had markedly abnormal hemoglobin A1c values indicating poor control. As a group, participants were obese, with BMI above the 95%ile for probands and fathers, and at the 85%ile for mothers and siblings. The sum of skin folds was above the 95% percentile for the patients, their siblings and the parents. All groups had high fat intake and low fiber intake. None of the subjects participated in a structured or routine exercise program and the vast majority reported no regular physical activity. Three (27%) of the probands met the criteria for Binge Eating Disorder and six additional patients had significant characteristics of the disorder. None of the siblings (mean age 14±0.3 yrs) had elevated glucose or HbA1c levels. However, siblings had markedly elevated fasting C-peptide (0.69 ± 0.13 nmol/L vs normal 0.46± 0.03) and proinsulin levels (20.1 ± 5.1 pmol/L vs normal 8.6± 0.64). Previously undiagnosed mothers also displayed signs of insulin resistance, with C-peptide of 0.85 ± 0.12 nmnol/l and proinsulin of 18.8 ± 8.6 pmol/l. CONCLUSIONS: Probands, as well as other family members, are centrally obese and have lifestyles characterized by high fat intake, minimal physical activity and a high incidence of binge eating disorders. Furthermore, the incidence of diagnosed and undiagnosed type 2 diabetes and insulin resistance in these families is striking. Taken together, these findings suggest that adolescent type 2 diabetes frequently occurs in a high-risk family setting and indicate that screening of family members for diabetes may be appropriate. Furthermore, treatment programs for adolescents with type 2 diabetes will need to address the lifestyle and health habits of the entire family.

Haemophilus influenzae infections of the genitourinary tract are rare. A case of a life-threatening Haemophilus influenzae bacteremia associated with a septic abortion is presented. Sexual transmission of bacteria after orogenital contact is proposed as a possible source of this uncommon infection.

Benign familial leukopenia (BFL) has been described in various ethnic groups around the world; in Israel it is found among Yemenites and Ethiopians. Neuroleptics infrequently cause acute leukopenia. We described nine Ethiopian subjects who were treated with conventional antipsychotics for four weeks. In three subjects probable BFL was demonstrated prior to treatment. By the end of four weeks of treatment 6/9 subjects developed leukopenia with neutropenia. Reduction in mean WBC counts and neutrophil counts was significant (p=0.014 and p=0.001, respectively).None of the subjects developed an acute illness or an infection during the studied period. We tentatively suggest that in subjects belonging to ethnic groups where BFL is common antipsychotics may induce its expression without significant clinical symptomatology.