The impact of 10-valent pneumococcal vaccine introduction on invasive disease in Fiji.

BACKGROUND: In 2012, Fiji introduced the 10-valent pneumococcal conjugate vaccine (PCV10). We assessed the impact of PCV10 on invasive pneumococcal disease (IPD), probable bacterial or pneumococcal meningitis (PBPM), meningitis and sepsis 3-5 years post-introduction. METHODS: Laboratory-confirmed IPD and PBPM cases were extracted from national laboratory records. ICD-10-AM coded all-cause meningitis and sepsis cases were extracted from national hospitalisation records. Incidence rate ratios were used to compare outcomes pre/post-PCV10, stratified by age groups: 1-23m, 2-4y, 5-9y, 10-19y, 20-54y, ≥55y. To account for different detection and serotyping methods in the pre-and post-PCV10 period, a Bayesian inference model estimated serotype-specific changes in IPD, using pneumococcal carriage and surveillance data. FINDINGS: There were 423 IPD, 1,029 PBPM, 1,391 all-cause meningitis and 7,611 all-cause sepsis cases. Five years post-PCV10 introduction, IPD declined by 60% (95%CI: 37%, 76%) in children 1-23m months old, and in age groups 2-4y, 5-9y, 10-19y although confidence intervals spanned zero. PBPM declined by 36% (95%CI: 21%, 48%) among children 1-23 months old, and in all other age groups, although some confidence intervals spanned zero. Among children <5y of age, PCV10-type IPD declined by 83% (95%CI; 70%, 90%) and with no evidence of change in non-PCV10-type IPD (9%, 95%CI; -69, 43%). There was no change in all-cause meningitis or sepsis. Post-PCV10, the most common serotypes in vaccine age-eligible and non-age eligible people were serotypes 8 and 23B, and 3 and 7F, respectively. INTERPRETATIONS: Our study demonstrates the effectiveness of PCV10 against IPD in a country in the Asia-Pacific of which there is a paucity of data. FUNDING: This study was support by the Department of Foreign Affairs and Trade of the Australian Government and Fiji Health Sector Support Program (FHSSP). FHSSP is implemented by Abt JTA on behalf of the Australian Government.

Effects of bicarbonate supplementation on urinary mineral excretion during very low energy diets.

Metabolic acidosis is associated with increased calciuria and ammoniagenesis. This study evaluated the effects of oral sodium bicarbonate (NaHCO3) or combined potassium bicarbonate-calcium carbonate supplementation on urinary mineral excretion during the ketoacidosis of a very-low-energy protein diet. Seventeen healthy obese subjects (BMI: 37.5 +/- 3.2 kg/m2, weight: 100 +/- 3 kg) were given a 1.72 MJ all protein (93 g) liquid formula and a multivitamin-mineral supplement daily for 3 weeks. Subjects in groups 1 (n = 6) and 2 (n = 5) received 16 mmol KCl. In addition, subjects in group 1 received 60 mmol Na+ daily as sodium chloride, subjects in group 2, 60 mmol Na+ as NaHCO3. The subjects in group 3 (n = 6) were given 32 mmol K+ as bicarbonate and 16 mmol Ca++ as carbonate daily. Metabolic acidosis was prevented in groups 2 and 3 with bicarbonate and bicarbonate-carbonate administration. This was reflected in significant curtailment of the augmented ammonium nitrogen excretion found in group 1. The additional oral K+ in group 3 improved K+ balance and probably also inhibited ammoniagenesis. Urine calcium was greater (p less than 0.04) in group 1 subjects, but similar in groups 2 and 3, despite higher calcium intake in group 3. Urinary phosphorus decreased with time in all groups, but more so in the group 2 subjects who received NaHCO3. Acidosis was associated with the reverse effect on urinary magnesium, which decreased in group 1 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sodium bicarbonate on nitrogen metabolism and ketone bodies during very low energy protein diets in obese subjects.

This study evaluated the effects of oral sodium bicarbonate (NaHCO3) supplementation on ammonium (NH4+) nitrogen (N) and urea N excretion and on ketone bodies during the metabolic acidosis of a very low energy protein diet. Ten healthy obese female subjects (BMI, 38.4 +/- 1.5 kg/m2;weight, 100 +/- 4 kg) were given a 1.72 MJ (412 kcal) all protein (16.8 g N) liquid formula, 16 mmol KCl and a multivitamin-mineral supplement daily for 4 weeks. In addition, the five subjects in group 1 received 60 mmol Na+ daily as sodium chloride (NaCl) for 3 weeks and as NaHCO3 during week 4. The subjects in group 2 were given 40 mmol/d NaHCO3 during the first week, 60 mmol/d during weeks 2 and 3, and 60 mmol/d NaCl during week 4. Nitrogen balance was achieved in both groups by the end of week 3. The subjects in group 1 at week 2 showed an increase in blood [H+] of 0.41 +/- 0.06 x 10(-8) mol/L and a decrease in blood bicarbonate from 26.0 +/- 0.8 to 23.8 +/- 1.2 mmol/L. The subsequent NaHCO3 curtailed NH4+ N excretion by one half, without significant change in ketone body levels or excretion. Administration of NaHCO3 from the start of the diet to the subjects in group 2 prevented both the metabolic acidosis and the increase in NH4+ N excretion and attenuated the increase in blood and urine 3-hydroxybutyrate. When NaCl replaced NaHCO3 during week 4, ammonium N excretion doubled. Urea N excretion was comparable in both groups and was unaffected by bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium chloride supplementation and urinary calcium excretion in postmenopausal women.

It was hypothesized that variations within the range of usual salt intakes of North Americans influence urinary excretion of calcium in healthy postmenopausal women. The effects of sodium chloride supplements of 0.51, and 102 mmol/d, randomly assigned to 17 healthy, noninstitutionalized, postmenopausal women consuming their usual diets were compared. Diets and discretionary salt intake were repeated exactly for three experimental periods of 4 d each for 3 consecutive weeks. Supplementing with 51 mmol NaCl/d increased average daily urinary excretion of Ca, Na, and Cl by 0.5, 51.0, and 48.9 mmol respectively, urine pH by 0.1, and serum Cl by 1.5 mmol/L (p less than 0.05). Supplementing with 102 mmol/d induced additional increases in these variables (p less than 0.05). Assuming a total body mass of 900 g Ca and no decrease in renal or fecal losses, additions of 51 and 102 mmol/d NaCl to the diet for 10 y would mobilize Ca stores of 7.5% and 10%, respectively, and could thus constitute a risk factor for osteoporosis.

Comparison of daily diets containing 400 kcal (1.67 MJ) of either protein or glucose, and their effects on the response to subsequent total fasting in obese subjects.

Eleven obese subjects (body mass index, 41.3 kg/m2) were examined to determine their metabolic and acid-base responses during two hypoenergetic diets, and the diets' influence on subsequent responses to prolonged total fasting. Subjects were first treated for 2 wk with 400-kcal/d (1.67-MJ/d) diets of either protein (13.2 g nitrogen, 23 mmol potassium) or glucose with 16 mmol potassium chloride and a multivitamin supplement. Mild acidosis developed during the protein diet as well as greater excretions of urinary ammonium and urea N, a greater degree of ketosis, and significantly better N balance (-42.7 vs -80.4 g, p less than 0.05) than during the glucose diet. The subsequent fast was associated with greater negative N balance after protein (-129 vs 83 g), mainly as urea N, but despite similar ketosis there was a greater acidosis after glucose and greater ammonium N excretion and cumulative K losses. These data support the concept of a labile N pool, depleted during a glucose diet and resulting in a decreased loss with the subsequent fast. We suggest a role for K depletion in augmenting fasting ammonium excretion.