Diagnostic, and therapeutic challenges In HIV+ patient, presented with left-sided Haemiparesis and MRI changes

Neurological features occur during the later stages of HIV infection. The most common manifestations are opportunistic infections like cerebral toxoplasmosis and progressive multifocal leukoencephalopathy, as well as malignant lymphomas like primary EBV associated CNS lymphoma. We present a case of a 21-yearold man, diagnosed as HIV+ in 2010. The patient receives HAART (kivexa/kaletra) from 13.08.2013 to date with poor adherence. The current complaints began two weeks ago with weakness in the lower extremities, gait disturbances and headache. The neurological examination at the admission time showed no meningeal signs, weakened tendon reflexes in left limbs, absent abdominal reflexes, central facial palsy on the left, positive Babinski sign. Upon admission to the hospital the patient presented with CD 4-34c/mm³, VL- 2180 c/ml. Cerebral spinal fluid viral load was <20 c/ml. The results of the serological and virological tests from cerebral spinal fluid were: PCR EBV (-); PCR CMV (-); IgM EBV (-); IgG CMV (-); T.gondii IgM (-); IgG(-); PCR for pathogenic free-living amoeba (-). MRI: space occupying lesion, interpreted as a lymphoma, MRI after 6 months: progression of the lesion. A biopsy of peripheral lymph node showed nonspecific finding. The patient was put on patogenetic treatment against cerebral edema, treatment against T. gondii infection (clindamycin, co-trimoxazole), and gancyclovir, meronem, fungolon, ART as well. The patient was without precise, laboratory confirmed diagnosis, but the general condition is better

Maternal Iodine Status During Pregnancy Is Not Consistently Associated with Attention-Deficit Hyperactivity Disorder or Autistic Traits in Children

BACKGROUND: Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood. OBJECTIVES: We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits. METHODS: This was a collaborative study of 3 population-based birth cohorts: Generation R (n = 1634), INfancia y Medio Ambiente (n = 1293), and the Avon Longitudinal Study of Parents and Children (n = 2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 and 7.7 y for ADHD symptoms and 4.5 and 7.6 y for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) <150 μg/g-in all mother-child pairs, and in those with a urinary-iodine measurement at ≤18 weeks and ≤14 weeks of gestation-with the risk of ADHD or a high autistic-trait score (≥93rd percentile cutoff), using logistic regression. The cohort-specific effect estimates were combined by random-effects meta-analyses. We also investigated whether UI/Creat modified the associations of maternal free thyroxine (FT4) or thyroid-stimulating hormone concentrations with ADHD or autistic traits. RESULTS: UI/Creat <150 μg/g was not associated with ADHD (OR: 1.2; 95% CI: 0.7, 2.2; P = 0.56) or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6, 1.1; P = 0.22). UI/Creat <150 μg/g in early pregnancy (i.e., ≤18 weeks or ≤14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P = 0.017) was not modified by iodine status. CONCLUSIONS: There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits

Association of maternal iodine status with child IQ: a meta-analysis of individual-participant data

Dataset, supplement to the article (to be added later

Iodine status during pregnancy: a series of studies investigating the determinants, assessment methods and effects of maternal iodine deficiency

Adequate iodine intake during pregnancy is essential to maintain optimal maternal thyroid function which is crucial for fetal neurodevelopment. Though, globally, iodine deficiency is considered to be the single, most important, preventable cause of brain damage, many pregnant women are still iodine-deficient. The research work presented in this thesis aimed to investigate several aspects of maternal iodine nutrition, including: (i) the determinants of iodine status in pregnancy; ii) the effect of advancing gestation on urinary-iodine concentration which is the most commonly-used biomarker of population iodine-status; iii) the usefulness of serum thyroglobulin as a functional biomarker of longer-term iodine nutrition in pregnancy; iv) the effect of maternal iodine deficiency in pregnancy, as measured in multiple spot-urine samples, on child cognition; v) the effect of iodine supplementation of mildly-to-moderately iodine-deficient pregnant women on thyroid function and child cognition. In the first study, data from three European birth-cohorts were used. Milk and dairy products were found to be an important, common, dietary determinant of iodine status in pregnancy; cohort-specific determinants were also identified. In the second study, three spot-urine iodine measurements from each trimester were used in longitudinal analysis which showed an increase in urinary-iodine concentration across pregnancy. The third study showed that thyroglobulin was negatively associated with urinary-iodine concentration in an iodine-sufficient and a mildly iodine-deficient pregnant population; this suggested that thyroglobulin could be used as a complementary indicator of population iodine status. In the fourth study, iodine deficiency at multiple gestational time-points was associated with lower non-verbal intelligence quotient in children at 8 years. In the final study, evidence of the effects of iodine supplementation of mildly-to-moderately iodine-deficient pregnant women on thyroid function and child cognition was reviewed systematically; the results highlighted the lack of good-quality evidence from randomised-controlled trials to support recommendations for iodine supplementation in pregnancy in these areas. Public-health strategies aimed at educating pregnant women and women of childbearing age on the importance of iodine and the ways that they can meet iodine requirements through diet are needed. An accurate assessment of iodine status in pregnancy would be valuable for public-health monitoring and future research

Systematic review and meta-analysis of the effects of iodine supplementation on thyroid function and child neurodevelopment in mildly-to-moderately iodine-deficient pregnant women

Background: Mild-to-moderate iodine deficiency, particularly in pregnancy, is prevalent; this is of concern as observational studies have shown negative associations with child neurodevelopment. Though neither the benefits nor the safety of iodine supplementation in pregnancy in areas of mild-to-moderate deficiency are well researched, such supplementation is increasingly being recommended by health authorities in a number of countries. Objective: By reviewing the most recent published data on the effects of iodine supplementation in mildly-to-moderately deficient pregnant women on maternal and infant thyroid function and child cognition, we aimed to determine whether the evidence was sufficient to support such recommendations in these areas. Design: A systematic review of randomised controlled trials (RCTs), non-RCT interventions and observational studies was conducted. To identify relevant papers we searched the PubMed and Embase databases. We defined mild-to-moderate iodine deficiency as a baseline, median, urinary iodine-concentration (UIC) of 50-149 µg/L. Eligible studies were included in meta-analyses. Results: In total, 37 publications were included – ten RCTs, four non-RCT interventions and 23 observational studies. Most studies showed no effect of iodine supplementation on maternal or infant thyroid-stimulating hormone and free-thyroxine. Most RCTs found that supplementation reduced maternal thyroglobulin and in three RCTs, it prevented or diminished the increase in maternal thyroid volume during pregnancy. Three RCTs addressed child neurodevelopment; only one was adequately-powered. Meta-analyses of two RCTs showed no effect on child cognitive [mean difference (MD) (95%CI): -0.18 (-1.22, 0.87)], language [MD (95%CI): 1.28 (-0.28, 2.83)] or motor scores [MD (95%CI): 0.28 (-1.10, 1.66)]. 4 Conclusions: There is insufficient good-quality evidence to support current recommendations for iodine supplementation in pregnancy in areas of mild-to-moderate deficiency. Well designed RCTs with child cognitive outcomes are needed in areas of moderate deficiency (median UIC<100 µg/L). The maternal intra-thyroidal iodine stores should be considered in future trials by including appropriate measures of pre-conceptional iodine intake

Dairy as a Source of Iodine and Protein in the UK: Implications for Human Health Across the Life Course, and Future Policy and Research

This narrative review summarizes key concepts in dairy nutrition for supporting human health throughout the life course. Milk and dairy products have been a staple component of our diet for thousands of years and provide a wide range of important nutrients that are otherwise difficult to obtain from dairy-free diets. In this review, we provide a broad perspective on the nutritional roles of iodine and dairy protein in supporting human health during pregnancy and early life, childhood and adolescence, mid- and later-life. New methodologies to identify biomarkers of dairy intake via high-throughput mass spectrometry are discussed, and new concepts such as the role of the food matrix in dairy nutrition are introduced. Finally, future policy and research related to the consumption of dairy and non-dairy alternatives for health are discussed with a view to improving nutritional status across the lifespan

Maternal iodine status during pregnancy is not consistently associated with attention-deficit hyperactivity disorder or autistic traits in the child

Background: Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood. Objective: We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits. Methods: Collaborative study of three population-based birth cohorts: Generation R (N=1634), INMA (N=1293), and ALSPAC (N=2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 – 7.7 years for ADHD symptoms and 4.5 – 7.6 years for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) < 150 μg/g – in all mother-child pairs, and in those with a urinary-iodine measurement at ≤ 18 weeks and ≤ 14 weeks of gestation – with the risk of ADHD or a high autistic-trait score (≥ 93rd percentile cut-off), using logistic regression. The cohort-specific effect estimates were combined by random effects meta-analyses. We also investigated whether UI/Creat modified the association of maternal free thyroxine (FT4) or thyroid stimulating hormone (TSH) concentrations with ADHD or autistic traits. Results: UI/Creat <150 μg/g was not associated with ADHD [odds ratio (OR): 1.2; 95% CI: 0.7, 19 2.2; P=0.56] or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6-1.1; P=0.22). UI/Creat <150 20 μg/g in early pregnancy (i.e., ≤ 18 weeks or ≤ 14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P=0.017) was not modified by iodine status. Conclusion: There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits