Increase of 25-hydroxyvitamin D levels after initiation of combination antiretroviral therapy.

Although vitamin D deficiency in HIV patients reported worldwide, the mechanisms and the effect of combination antiretroviral therapy (cART) on vitamin D levels are unclear. Patients were 50 male Japanese with HIV who visited Teikyo University Hospital, Tokyo, Japan. Patients were divided into those receiving cART (cART-experienced group, n = 30) and those who had not received cART (cART-naïve group, n = 20). Patients in the cART-experienced group had received treatment with cART for more than one year and those in the cART-naïve group were just about to start cART at study entry. Patients underwent measurement of serum 25-hydroxyvitamin D (25(OH)D) levels and assessment of clinical factors twice at one year intervals. At study entry, 23 (76.7%) in the cART-experienced group and 19 (95.0%) in the cART-naïve group had vitamin D insufficiency or deficiency. Mean 25(OH)D values were significantly higher in the cART-experienced group (25.2 ng/ml vs. 19.3 ng/ml, p = 0.01). However, levels of 25(OH)D at one year increased more in the cART-naïve group (-1.1 ng/ml vs. 5.0 ng/ml, p = 0.01), with mean 25(OH)D values in the cART-naïve group increasing to match those in the cART-experienced group. HIV infected patients who initiated cART showed increases in vitamin D levels in one year.

Maternal vitamin D deficiency and fetal programming--lessons learned from humans and mice.

BACKGROUND/AIMS: Cardiovascular disease partially originates from poor environmental and nutritional conditions in early life. Lack of micronutrients like 25 hydroxy vitamin D3 (25OHD) during pregnancy may be an important treatable causal factor. The present study explored the effect of maternal 25OHD deficiency on the offspring. METHODS: We performed a prospective observational study analyzing the association of maternal 25OHD deficiency during pregnancy with birth outcomes considering confounding. To show that vitamin D deficiency may be causally involved in the observed associations, mice were set on either 25OHD sufficient or insufficient diets before and during pregnancy. Growth, glucose tolerance and mortality was analyzed in the F1 generation. RESULTS: The clinical study showed that severe 25OHD deficiency was associated with low birth weight and low gestational age. ANCOVA models indicated that established confounding factors such as offspring sex, smoking during pregnancy and maternal BMI did not influence the impact of 25OHD on birth weight. However, there was a significant interaction between 25OHD and gestational age. Maternal 25OHD deficiency was also independently associated with low APGAR scores 5 minutes postpartum. The offspring of 25OHD deficient mice grew slower after birth, had an impaired glucose tolerance shortly after birth and an increased mortality during follow-up. CONCLUSIONS: Our study demonstrates an association between maternal 25OHD and offspring birth weight. The effect of 25OHD on birth weight seems to be mediated by vitamin D controlling gestational age. Results from an animal experiment suggest that gestational 25OHD insufficiency is causally linked to adverse pregnancy outcomes. Since birth weight and prematurity are associated with an adverse cardiovascular outcome in later life, this study emphasizes the need for novel monitoring and treatment guidelines of vitamin D deficiency during pregnancy.

Cross-sectional and prospective cohort study of serum 25-hydroxyvitamin D level and obesity in adults: the HUNT study.

Experimental studies suggest that vitamin D modulates the activity of adipocytes. The authors examined baseline serum 25-hydroxyvitamin D (25(OH)D) level in relation to prevalent and cumulative incident obesity in Norway. A cohort of 25,616 adults aged 19-55 years participated in both the second and third surveys of the Nord-Trøndelag Health Study (HUNT 2 (1995-1997) and HUNT 3 (2006-2008)). Serum 25(OH)D levels measured at baseline and anthropometric measurements taken at both baseline and follow-up were available for a random sample of 2,460 subjects. Overall, 40% of the 2,460 subjects had a serum 25(OH)D level less than 50.0 nmol/L, and 37% had a level of 50.0-74.9 nmol/L. The prevalence and cumulative incidence of obesity, defined as body mass index (weight (kg)/height (m)(2)) ≥30, were 12% and 15%, respectively. Lower serum 25(OH)D level was associated with a higher prevalence of obesity. In the 2,165 subjects with baseline BMI less than 30, a serum 25(OH)D level less than 50.0 nmol/L was associated with a significantly increased odds ratio for incident obesity during follow-up (adjusted odds ratio = 1.73, 95% confidence interval: 1.24, 2.41). When prevalent and incident obesity were classified according to waist circumference (≥88 cm for women, ≥102 cm for men), similar results were obtained. In addition to prevalent obesity, a serum 25(OH)D level less than 50.0 nmol/L was significantly associated with new-onset obesity in adults.

Longitudinal vitamin D status in pregnancy and the risk of pre-eclampsia.

OBJECTIVE: Whether vitamin D deficiency in pregnancy is a cause of pre-eclampsia remains controversial. Most previous studies to date have assessed exposure at only one time-point in pregnancy. We assessed longitudinal vitamin D status during pregnancy and the risk of pre-eclampsia. DESIGN: Prospective cohort study. SETTING: Seventeen urban obstetric hospitals, Canada. POPULATION: Pregnant women who were participants in a trial of vitamin C and E supplementation for the prevention of pre-eclampsia. Canadian participants who consented to participate in a biobank with plasma specimens available at the baseline visit were included (n = 697). METHODS: Maternal plasma 25-hydroxyvitamin D (25(OH)D) concentrations were measured at 12-18 and 24-26 weeks of gestation using chemiluminescence immunoassay. MAIN OUTCOME MEASURES: Pre-eclampsia. RESULTS: Of the women, 39% were vitamin D deficient (25(OH)D <50 nmol/l). A strong positive correlation was observed in maternal 25(OH)D concentrations between the two gestational age windows (r = 0.69, P < 0.0001). Mean maternal 25(OH)D concentrations at 24-26 weeks of gestation were significantly lower in women who subsequently developed pre-eclampsia compared with those who did not (mean ± SD: 48.9 ± 16.8 versus 57.0 ± 19.1 nmol/l, P = 0.03). Women with 25(OH)D < 50 nmol/l at 24-26 weeks gestation experienced an increased risk of pre-eclampsia (adjusted odds ratio 3.24, 95% confidence interval 1.37-7.69), whereas the association was not statistically significant for maternal 25(OH)D level at 12-18 weeks of gestation. CONCLUSIONS: Lower maternal 25(OH)D levels at late mid-trimester were associated with an increased risk of pre-eclampsia.

Anaemia, lead poisoning and vitamin D deficiency in low-income children: do current screening recommendations match the burden of illness?

OBJECTIVE: Low-income children are routinely screened for anaemia and elevated blood lead levels (EBLL) but not for vitamin D deficiency. We sought to determine the relative prevalence of and the relationship among vitamin D deficiency, anaemia and EBLL among healthy low-income paediatric clinic patients. DESIGN: Retrospective chart review. SETTING: Paediatric outpatient clinic in an urban safety net hospital in a northern US state. SUBJECTS: Healthy toddlers and children under 6 years of age (n 127) who were seen for a routine well child check-up (WCC). RESULTS: The prevalence of vitamin D insufficiency (25-hydroxyvitamin D (25(OH)D) < 30 ng/ml) was 62 %; the prevalence of vitamin D deficiency (25(OH)D < 20 ng/ml) was 29 %. These rates were far higher than those for anaemia (Hb < 11·0 g/dl) at 10 %, EBLL (Pb > 9 µg/dl) at 1 % or even mildly EBLL (Pb 5-9 µg/dl) at 4 % (range: 1-11). There was no relationship among any of the following: vitamin D status, anaemia or EBLL. The vast majority of children with vitamin D deficiency had both normal Hb (86 %) and Pb level (100 %). After controlling for child's age, gender and race/ethnicity, there was no association between Hb (continuous, g/dl) and vitamin D deficiency (adjusted OR (aOR) = 0·97, 95 % CI 0·64, 1·47; P = 0·88). The only significant predictor of vitamin D deficiency was increasing age in years (aOR = 1·39, 95 % CI 1·03, 1·86; P = 0·03). None of these associations changed materially when deficiency was defined as <15 ng/ml. CONCLUSIONS: Vitamin D deficiency was far more common than anaemia or EBLL, and Hb and Pb status were not predictors of vitamin D status.

Vitamin D, race, and cardiovascular mortality: findings from a national US sample.

PURPOSE: Findings are conflicting about the relationship between vitamin D levels and cardiovascular mortality. We wanted to determine the contribution of vitamin D levels to black-white disparities in cardiovascular mortality. METHODS: We examined the association of serum 25(OH)D levels with cardiovascular mortality and its contribution to elevated risk among blacks through a retrospective cohort using baseline data from the third National Health and Nutrition Examination Survey 1988-1994 and cause-specific mortality through 2001 using the National Death Index. Using piecewise Poisson regression models, we examined the risk of cardiovascular death (coronary heart disease, heart failure, and stroke) by sample 25(OH)D quartile, adjusting for cardiovascular risk factors, and compared models of adjusted race-related cardiovascular mortality with and without further adjustment for 25(OH)D levels. RESULTS: Participants with 25(OH)D levels in the lowest quartile (mean = 13.9 ng/mL) compared with those in the 3 higher quartiles (mean = 21.6, 28.4, and 41.6 ng/mL) had higher adjusted risk of cardiovascular death (incident rate ratio [IRR] = 1.40; 95% confidence interval [CI], 1.16-1.70). The higher age- and sex-adjusted cardiovascular mortality observed in blacks vs whites (IRR = 1.38; 95% CI, 1.13-1.70) was attenuated (IRR = 1.14; 95% CI, 0.91-1.44) by adjustment for 25(OH)D levels and fully eliminated with further adjustment for income (IRR=1.01; 95% CI, 0.82-1.24). CONCLUSIONS: Low serum levels of 25(OH)D are associated with increased cardiovascular mortality in a nationally representative US sample. Black-white differences in 25(OH)D levels may contribute to excess cardiovascular mortality in blacks. Interventional trials among persons with low vitamin D levels are needed to determine whether oral supplementation improves cardiovascular outcomes.

The synergistic effects of vitamin D and estradiol deficiency on metabolic syndrome in Chinese postmenopausal women.

OBJECTIVE: Recent studies show that vitamin D (VitD) deficiency is associated with metabolic syndrome (MetS). Current evidence suggests that estrogen and VitD have similar physiological functions and potentially interact with bone health. We investigated the association between estradiol (E2) and 25-hydroxyvitamin-D [25(OH)D] with MetS and its components in Chinese postmenopausal women. METHODS: In this cross-sectional study, we examined 616 postmenopausal women (aged 49-86 y) from southern China who were not taking estrogen and VitD/calcium supplements. At the end of data collection, serum E2 and 25(OH)D were measured for each participant. MetS was defined according to the 2006 International Diabetes Federation standard. RESULTS: There was a positive correlation between 25(OH)D and E2. Higher 25(OH)D was associated with a favorable lipid profile, blood pressure, and glucose level. E2 was negatively associated with cholesterol, triglycerides, and blood pressure. The odds ratio for MetS was 2.19 (95% CI, 1.19-4.01, P value for trend=0.009) for deficient compared with sufficient women after multivariable adjustment. This association remained unchanged after further adjusting for E2 levels. After stratified analysis by VitD status, low E2 increased MetS risk in women with VitD deficiency (odds ratio = 3.49, 95% CI, 1.45-8.05 for the lowest vs the highest tertile). CONCLUSIONS: These results suggest a synergistic role of VitD and E2 deficiency in MetS in Chinese postmenopausal women.

Occurrence of metabolic osteopathy in patients with chronic pancreatitis.

INTRODUCTION: Chronic pancreatitis is an inflammatory disease manifested by maldigestion and, in an advanced stage, by malabsorption. The aim of our research was to monitor the occurrence of metabolic osteopathies (osteopenia, osteoporosis and osteomalacia) in patients with chronic pancreatitis. PATIENTS AND METHODS: The group consisted of 73 patients (17 women and 56 men) in different stages of chronic pancreatitis. In all patients we determined serum concentrations of Ca, P, 25-OH vitamin D, 1,25-(OH)(2) vitamin D, alkaline phosphatase and its bone isoenzyme. Bone mineral density was measured by dual-energy X-ray absorptiometry (DXA) in the lumbar spine (L(1)-L(4)) and in the proximal femur. When bone pathology was identified by DXA, we determined the other to exclude other causes of secondary osteopathy and the 24-hour loss of calcium and phosphorus in the urine. RESULTS: Osteopathy was found in 39% of patients, i.e. osteopenia in 26%, osteoporosis in 5% and osteomalacia in 8% of cases. CONCLUSION: The occurrence of relatively high percentages of metabolic osteopathies in patients with chronic pancreatitis may correlate, namely in advanced stages of the disease, with the malabsorption of vitamin D to the enterohepatic circulation. In initial forms of pancreatitis, it is not possible to exclude progression of osteopathy due to changes of the intestinal flora, with disturbance of vitamin D absorption to the intestinal mucosa.

Presence of 25(OH) D deficiency in a rural North Indian village despite abundant sunshine.

BACKGROUND AND OBJECTIVE: Several studies have shown wide prevalence of vitamin D deficiency with serum 25(OH)D <49.9 nmol/L in urban Indians related to their poor sunshine exposure and skin pigmentation. However, there is limited information in rural Indians. We hypothesized presence of higher 25(OH)D in rural subjects as compared to urban because of farming related abundant sunshine exposure. DESIGN AND METHODS: We assessed serum 25(OH)D levels in residents of a North Indian village with 200 families, located 90 km East of Delhi during February (winter). Fifty seven subjects (32 males and 25 females) from 50 families consented for the study. RESULTS: The mean 25(OH)D values of all subjects in the rural area was 36.4 +/- 22.5 nmol/l/L. Males had significantly higher 25(OH)D values than females. When compared to urban subjects, the mean 25(OH)D value of rural males and females was six and three folds higher, respectively. However even with five hours of daily sunshine exposure only 31.5% had serum 25(OH)D levels > or = 50 nmol/L. CONCLUSIONS: Thus, with longer sunshine exposure subjects residing in rural area had better mean 25(OH)D values than that of urbans. However, 70% of them were still vitamin D deficient. These facts indicate the need for the countrywide vitamin D food fortification program irrespective of rural or urban setting.

Osteomalacia due to 1alpha,25-dihydroxycholecalciferol deficiency. Association with a giant cell tumor of bone.

Oncogenic osteomalacia is a syndrome in which unexplained osteomalacia remits after resection of a coexisting mesenchymal tumor. We have investigated the mechanism by which a giant cell tumor of bone caused biopsy-proved osteomalacia in a 42-yr-old woman. The biochemical abnormalities were: hypophosphatemia; decreased renal tubular maximum for the reabsorption of phosphate per liter of glomerular filtrate; negative calcium and phosphorus balance; hyperaminoaciduria; and subnormal calcemic response to exogenously administered parathyroid hormone. Malabsorption, hypophosphatasia, fluorosis, and acidosis were excluded as causes of the osteomalacia. Serum 25-hydroxycholecalciferol was normal (27+/-1 ng/ml). However, the serum concentration of 1alpha,25-dihydroxycholecalciferol was low (1.6+/-0.1 ng/100 ml). Oral administration of physiological amounts of 1alpha,25-dihydroxycholecalciferol resulted in resolution of the biochemical abnormalities of the syndrome and healing of the bone pathology. We suggest that tumor-induced inhibition of 1alpha,25-dihydroxycholecalciferol synthesis caused the osteomalacia. The causal role of the tumor was proved by demonstrating that resection was accompanied by roentgenographic evidence of bone healing and maintenance of normal serum phosphorus; renal tubular maximum for the reabsorption of phosphate; calcium and phosphorus balance; aminoaciduria; and calcemic response to exogenous parathyroid hormone.

Neonatal vitamin D status at birth at latitude 32 degrees 72': evidence of deficiency.

OBJECTIVE: With vitamin D deficiency as a serious public health problem, vitamin D status at birth was measured in neonates at latitude 32 degrees 72' (southeastern United States). STUDY DESIGN: In umbilical cord blood, vitamin D status, demonstrated by circulating 25-hydroxyvitamin D, was measured and related to race and season of birth. RESULT: The mean+/-standard deviation of 25-hydroxyvitamin D in 100 cord blood samples was 13.5+/-8.3 ng/ml for the cohort. African-American infants, with a mean+/-standard deviation of 10.5+/-6.0 ng/ml, demonstrated significantly lower vitamin D status than Caucasian infants, with a mean+/-standard deviation of 19.5+/-9.6 ng/ml (P<0.0001). By season, the mean 25-hydroxyvitamin D level at birth in November-March compared to April-October was 11.3 ng/ml lower in Caucasian infants (from 29.0 to 17.7 ng/ml) and 3 ng/ml lower in African-American infants (from 13.1 to 10.1 ng/ml). CONCLUSION: The prevalence of vitamin D insufficiency is high in this cohort. African-American infants demonstrate significantly lower vitamin D status at birth than Caucasian infants. Seasonality, while significant in both groups, had a greater impact on the vitamin D status of Caucasian newborns.

Vitamin D, bone metabolism and fracture risk.

Insufficient serum levels of 25OH vitamin D (25OHD) is a risk factor for osteoporosis. A new paradigm has emerged with the locally synthesized 1,25(OH)2D within osteoblasts and osteoclasts as the essential pathway for the effects of 25OHD in regulating bone remodeling via direct or indirect activation of the specific receptor VDR. Vitamin D has positive effects on fracture risk but these results have been consistently observed whenever daily doses were above 800 UI/d administered to compliant patients together with adequate calcium supplementation and with an achieved biological target of serum 25OHD levels above 30 ng/mL.

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Aim: The aim of this study was to assess the prevalence of hypovitaminosis D in candidates to bariatric surgery (BS) and its relationship with risk factors and components of the metabolic syndrome. Material and methods: Clinical, anthropometric and biochemical parameters were measured in 56 Caucasian patients included in a protocol of BS between January and June 2014. Patients were stratified into three groups according to their vitamin D status: sufficiency (≥ 40 ng/ml), insufficiency (40-20 ng/ml) and deficiency (< 20 ng/ml). Results: Data showed vitamin D deficiency in 75% of patients. These patients had greater BMI (p = 0.006) and lower PTH concentrations in plasma (p = 0.045). In addition, there were more patients with diabetes mellitus type 2 (DM2) and dyslipidemia (DLPM) in the group with 25 (OH) D < 20 ng/ml levels. Another finding was that 25(OH) D levels were observed to be negatively correlated with fat mass (r = -0.504; p = 0.009), BMI (r = -0.394; p = 0.046) and hypertension (r = -0.637; p = 0.001). Conclusion: We conclude that vitamin D deficiency is extremely common among candidates to BS, who are associated with DM2 and DLPM. Although there are limited data regarding the best treatment for low Vitamin D status in BS candidate patients, screening for vitamin D deficiency should be regularly performed in cases of morbid obesity

Objetivo: el objetivo de este estudio fue evaluar la prevalencia de hipovitaminosis D en los candidatos a cirugía bariátrica (CB) y su relación con factores de riesgo y los componentes del síndrome metabólico. Material y métodos: los parámetros clínicos, antropométricos y bioquímicos se midieron en 56 pacientes caucásicos incluidos en un protocolo de cirugía bariátrica entre enero y junio de 2014. Los pacientes fueron estratificados en tres grupos de acuerdo al status de vitamina D: suficiencia (≥ 40 ng/ml), insuficiencia (40-20 ng/ml) y deficiencia (< 20 ng/ml). Resultados: se observó deficiencia de vitamina D en el 75% de los pacientes. Estos pacientes tenían mayor índice de masa corporal (p = 0,006) y concentraciones plasmáticas mas bajas de PTH (p = 0,045). Además, hubo más pacientes con diabetes mellitus tipo 2 (DM2) y dislipemia (DLPM) en el grupo con niveles de 25 (OH) D < 20 ng/ml. Asimismo la 25 (OH) D se correlacionó negativamente con la masa grasa (r = -0,504; p = 0,009), el IMC (r = -0,394; p = 0,046) y la hipertensión arterial (r = -0,637; p = 0,001). Conclusión: De nuestros hallazgos concluimos que la deficiencia de vitamina D es muy común entre los candidatos a CB y que la misma está asociada con DM2 y DLPM.Aunque hay pocos datos sobre el mejor tratamiento para el bajo nivel de vitamina D en los pacientes candidatos CB, la detección de la deficiencia de vitamina D debe realizarse de forma rutinaria en estos casos.

1,25-Dihydroxycholecalciferol deficiency: the probable cause of hypocalcemia and metabolic bone disease in pseudohypoparathyroidism.

Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.

Serum 25-hydroxyvitamin D concentrations in sudden infant death syndrome.

Among the many theories put forth to explain sudden infant death syndrome (SIDS) is a theory of vitamin D deficiency. 25-Hydroxyvitamin D (25-OHD) serum concentrations were measured in 31 SIDS and 24 postmortem control infants. 25-OHD was 19.0 +/- 7.9 mg/ml in SIDS, 16.9 +/- 5.2 ng/ml in acute death control infants, and 11.9 +/- 4.4 ng/ml in in-hospital deaths. For four "near miss" infants the mean serum 25-OHD concentration was 21.1 +/- 4.1 ng/ml. The mean serum 25-OHD concentration of 39 living premature or small-for-gestational-age infants at 3 months of age was 26 +/- 9.9. Serum calcium and serum copper concentrations were also the same in SIDS and control infants. Parathyroid hormone was measured in ten and was detectable in five SIDS infants. These data eliminate a simple vitamin D deficiency or a 25-OHD deficiency as a significant contribution to the pathophysiology of SIDS.

Bone density, vitamin D nutrition, and parathyroid hormone levels in women with dementia.

OBJECTIVE: To determine whether patients with dementia have reduced bone mass, altered vitamin D, or parathyroid hormone status. DESIGN: Survey. SETTING: University hospital outpatient department. PARTICIPANTS: Twenty women with DSM-III-R mild dementia living in the community were compared with 40 cognitively normal community-dwelling women, matched for age, who had been recruited as part of studies in elderly twins. MEASUREMENTS: Bone density at the lumbar spine and neck of femur by dual-energy X-ray absorptiometry, intact serum PTH, and 25-hydroxyvitamin D levels. MAIN RESULTS: There was no significant difference in bone density between the subjects with mild dementia and the age- and sex-matched controls. The intact PTH (mean +/- SD) in the demented subjects was 4.9 +/- 2.1 pmol/L compared with 2.9 +/- 1.7 pmol/L in the twin controls (P < .01). The mean 25-hydroxyvitamin D in the demented subjects was 61 +/- 33 nmol/L, whereas it was 90 +/- 38 nmol/L in the twin controls (P < .01). CONCLUSIONS: We conclude that there were no significant differences in the bone density of community-dwelling women with mild dementia compared with normals. However, there were significant differences in parathyroid hormone and vitamin D levels between the two groups, suggesting that there is a high prevalence of subclinical hypovitaminosis D in demented women in the community.

Long-term nutritional and metabolic consequences of pancreaticoduodenectomy in children.

BACKGROUND: The long-term nutritional and metabolic consequences of pancreaticoduodenectomy in children are unknown. METHODS: Five children were evaluated in a clinical research center 2.5 to 10 years after pancreaticoduodenectomy to assess their nutritional status based on patterns of growth and to assess their gastrointestinal function. Investigation included vitamin levels, a bentiromide study, and serum immunoreactive trypsinogen levels to evaluate pancreatic function and a d-xylose absorption and a radionuclide gastric emptying scan for intestinal absorption and motility. RESULTS: Children were able to grow after pancreaticoduodenectomy. Three remained in low percentile groups for height/weight ratio, and two were near or above normal. Low normal levels of the fat-soluble vitamins were present. Very low levels of pancreatic function were found based on the bentiromide and trypsinogen studies, whereas intestinal absorption of d-xylose was normal except for one patient with extremely rapid gastric emptying. CONCLUSIONS: After pancreaticoduodenectomy children can grow and develop normally if given adequate levels of oral pancreatic supplements to replace the severely decreased level of endogenous pancreatic enzymes after operation. Routine supplementation of the fat-soluble vitamins should be considered.

Severe vitamin D deficiency in Auckland.

AIMS: To study the presentation of severe vitamin D deficiency in Auckland and to determine if appropriate therapy was given. METHODS: Retrospective review of records of patients with very low plasma 25 hydroxyvitamin D concentrations (< or = 12.5 nmol/L or 5 micrograms/L). RESULTS: Fifty cases were identified over a two year period. 28 subjects had recognised risk factors for vitamin D deficiency (such as gastrointestinal disease or greatly reduced food intake). The majority of the other 22 subjects were elderly residents of rest homes or private hospitals. Low body weight and reduced mobility were common features of both groups. Increased plasma alkaline phosphatase activity and hypocalcaemia were the most frequent biochemical findings. Appropriate treatment with high dose calciferol had been given to only 28% of the subjects. CONCLUSIONS: Severe vitamin D deficiency does occur in Auckland despite its low latitude. Low body weight, reduced mobility and lack of sun exposure are particular risk factors. Appropriate therapy is cheap, safe and effective but many patients with severe vitamin D deficiency are being managed suboptimally.

Niveles de 25(oh)-vitamina D en pacientes con diabetes mellitus tipo 2 con y sin síndrome metabólico / 25(OH)-Vitamin D levels in type 2 diabetes with and without metabolic syndrome

Los bajos niveles de 25-hidroxivitamina D (25OHD) se han vinculado con el desarrollo de enfermedad cardiovascular, diabetes mellitus tipo 2, obesidad, dislipidemia e hipertensión arterial, todos componentes del síndrome metabólico (SM). Además, se ha reportado una asociación inversa entre 25OHD y el SM, resistencia a la insulina, deterioro de la función celular ß e intolerancia a la glucosa. El objetivo de este trabajo fue evaluar los niveles de 25OHD en pacientes diabéticos tipo 2 con y sin SM. Se llevó a cabo un estudio observacional de corte transversal. Se evaluaron 108 pacientes diabéticos tipo 2 (grupo DM2) y 89 pacientes sin DM2 (GC) con y sin SM, en los cuales se determinó la concentración de 25OHD total. Se calculó el cociente de probabilidad (OR) e intervalo de confianza del 95% (IC95) para la deficiencia de 25OHD (<20 ng/ml). Resultados: el grupo DM2 presentó niveles menores de 25OHD (19,8 ng/ml vs. 25,0 ng/ml) y mayor proporción de pacientes con deficiencia de 25OHD respecto del GC (50,9% vs. 28,1%, OR 2,7, IC95%: 1,5-4,8). No se halló una correlación entre 25OHD y HbA1c. Se halló asociación significativa entre deficiencia de 25OHD y presencia de diabetes, obesidad y SM. Sin embargo, en el análisis multivariado solo la presencia del SM presentó asociación negativa significativa con la deficiencia de 25OHD (OR=4,04, IC95% 1,48-11,68). En conclusión, nuestros datos demuestran una elevada prevalencia de hipovitaminosis D en pacientes con diabetes mellitus tipo 2 a expensas, principalmente, del elevado porcentaje de pacientes que padecen SM. El SM incrementa cuatro veces el riesgo de deficiencia de vitamina D independientemente de la presencia de diabetes mellitus tipo 2. (AU)

Low levels of 25-hydroxyvitamin D (25OHD) have been linked to cardiovascular disease, type 2 diabetes mellitus, obesity, dyslipidemia and hypertension, all components of the metabolic syndrome. An inverse association has been observed between 25OHD and metabolic syndrome, insulin resistance, impaired ß-cell function and glucose intolerance. The aim of this study was to evaluate the 25OHD levels in type 2 diabetic patients with and without metabolic syndrome. An observational cross-sectional study was carried out. We included 108 type 2 diabetic patients (DM2 group) and 89 patients without DM2 (CG) with and without metabolic syndrome, in which the total 25OHD levels were measured. The odds ratio (OR) and 95% confidence interval (95%CI) for 25OHD deficiency (<20 ng/ml) were estimated. Results: The DM2 group had lower 25OHD levels (19.8 ng/ml vs 25.0 ng/ml) and higher proportion of patients with a 25OHD deficiency compared to the CG (50.9% vs 28.1%, OR 2.7, 95%CI: 1.5-4.8). No correlation was found between 25OHD and HbA1c. A significant association was found between 25OHD deficiency and the presence of diabetes, obesity, and the presence of metabolic syndrome. However, in the multivariate analysis only the presence of metabolic syndrome had a significant negative association with the 25OHD deficiency (OR=4.04, 95%CI 1.48-11.68). In conclusion, we found a high prevalence of hypovitaminosis D in DM2 and the metabolic syndrome increases the risk of 25OHD deficiency by four times. (AU)