RESUMO
Pancreatic polycystosis is one of rare causes of recurrent abdominal pain of pancreatic origin in children frequently associated with other organ's cysts which are to be searched. Association with pineal cyst is exceptional, and link between the two locations is to be elucidated. MRI is highly valuable to characterize cysts.
RESUMO
We report a 13-month-old immune-competent male child who was diagnosed with pneumococcal serotype 19A meningitis despite having received three PCV13 injections. Clinicians are reminded that bacterial meningitis can still occur, even in correctly vaccinated children. Investigations should include immune system screening along with abdominal ultrasound to exclude asplenia.
RESUMO
The purpose of our study was to systematically evaluate gastric acid output in children with long-lasting gastro-esophageal reflux (GER) in order to assess its mechanism and the need for anti-acid treatment. The investigation was carried out in 20 males and 10 females, aged 7.5 +/- 3.8 years, with prolonged (>15 months) clinical manifestations of GER. All underwent routine ambulatory 24-h esophageal pH-monitoring and measurement of gastric acid secretion including gastric basal (BAO) (micromol/kg/h), maximal (MAO) and peak acid outputs (PAO) after pentagastrin (6 microg/kg sec) stimulation. Children with heartburn or abdominal pain underwent upper fiber-endoscopy. In group A (moderate GER, n=12), patients had a normal reflux index (pH<4 below 5.2% of total recording time) despite abnormal Euler and Byrne scoring (median 57, 95% confidence interval 53.5-73.4). In group B (severe GER, n=18, among whom 5 were with grade III esophagitis), reflux index was >5.2%. When considering all children, esophageal pH (%) was significantly correlated with MAO and PAO, r=0.33, p=0.05 and r=0.37, p=0.04, respectively. Children of group B exhibited significantly higher BAO (75, 53.96-137.81), MAO (468, 394.1-671.3) and PAO (617, 518.8-782.3) than those of group A, BAO (27, 10.8-38.5), MAO (266, 243.2-348.2) and PAO (387, 322.5-452.7), p<0.05). The five children of group B with severe esophagitis exhibited significantly higher BAO, MAO and PAO than the other 13 children from the same group and those of group A, p<0.05. Children with long-lasting and severe GER hyper-secrete gastric acid. Individual variations in gastric acid secretion probably account for variations in gastric acid inhibitor requirements. Anti-secretory treatment is justified in children with long-lasting GER and high pH-metric reflux index.
Assuntos
Antiácidos/uso terapêutico , Ácido Gástrico/metabolismo , Refluxo Gastroesofágico/classificação , Adolescente , Criança , Pré-Escolar , Intervalos de Confiança , Feminino , Refluxo Gastroesofágico/tratamento farmacológico , Humanos , Concentração de Íons de Hidrogênio , Masculino , Índice de Gravidade de DoençaAssuntos
Ampola Hepatopancreática , Endoscopia por Cápsula , Doenças do Ducto Colédoco/diagnóstico , Hemangioma Cavernoso/diagnóstico , Enteropatias/diagnóstico , Adolescente , Doenças do Ducto Colédoco/complicações , Doenças do Ducto Colédoco/cirurgia , Feminino , Hemorragia Gastrointestinal/etiologia , Hemangioma Cavernoso/complicações , Hemangioma Cavernoso/cirurgia , Humanos , Enteropatias/complicações , Enteropatias/cirurgia , Intestino Delgado , SíndromeRESUMO
OBJECTIVE: To determine an association between magnesium (Mg) depletion and chondrocalcinosis, which has been reported but not investigated in a cross-sectional study. METHODS: Prevalence of chondrocalcinosis was investigated in 144 individuals: 72 patients receiving home parenteral nutrition (HPN) compared with 72 age- and sex-matched controls. Presence of chondrocalcinosis was assessed by knee radiographs. Blood serum and globular Mg levels and 24-hour urinary Mg content were compared. RESULTS: Mean +/- SD age for both patients and controls was 51 +/- 17 years, and 51% in both groups were women. Mean duration of HPN was 6.4 years. Prevalence of chondrocalcinosis was markedly higher in patients receiving HPN than controls (16.6% versus 2.7%; P = 0.006, odds ratio [OR] 7.0, 95% confidence interval [95% CI] 1.45-66.1). Mean +/- SD serum and globular Mg levels were significantly lower in patients than controls (serum: 0.75 +/- 0.09 mmoles/liter versus 0.81 +/- 0.08 mmoles/liter, P = 0.0006; globular Mg: 1.8 +/- 0.31 mmoles/liter versus 2.0 +/- 0.35 mmoles/liter, P = 0.0003). Twenty-four-hour urinary Mg level was lower in patients than controls (mean +/- SD 3.85 +/- 1.50 mmoles versus 5.37 +/- 3.71 mmoles; P = 0.001). Prevalence of chondrocalcinosis was significantly higher in patients with a low serum Mg level (OR 13.5, 95% CI 2.76-127.3, P < 0.0001), with a similarly high but not significant occurrence of chondrocalcinosis in patients with a low globular Mg level (OR 4.09, 95% CI 0.603-20.26, P = 0.08) and in patients with a low 24-hour urinary Mg level (OR 3.9, 95% CI 0.77-16.34, P = 0.05). CONCLUSION: Long-lasting Mg depletion is strongly associated with chondrocalcinosis.
Assuntos
Condrocalcinose/sangue , Condrocalcinose/complicações , Magnésio/sangue , Adulto , Idoso , Estudos de Casos e Controles , Condrocalcinose/etiologia , Estudos Transversais , Feminino , Humanos , Enteropatias/terapia , Masculino , Pessoa de Meia-Idade , Nutrição Parenteral no Domicílio/efeitos adversos , Prevalência , Estudos Prospectivos , Fatores de RiscoRESUMO
Chondrocalcinosis is a result of deposition of calcium pyrophosphate dihydrate (CPPD) crystals in cartilage and fibrocartilage. Chondrocalcinosis is usually sporadic but has also been associated with a variety of metabolic diseases including hypomagnesemia. Reported cases of hypomagnesemia associated chondrocalcinosis were mostly due to renal genetic disorders such as Bartter's or Gitelman's syndrome. We describe 3 patients with chronic hypomagnesemia induced by short bowel syndrome who developed symptomatic chondrocalcinosis. CPPD crystals were identified by polarizing light microscopy in one patient. The underlying intestinal pathology was radiation enteritis in 2 patients and mesenteric arterial thrombosis in the third. Our observations strengthen the hypothesis of a role for magnesium in CPPD crystal deposition disease.
Assuntos
Condrocalcinose/etiologia , Deficiência de Magnésio/sangue , Deficiência de Magnésio/etiologia , Síndrome do Intestino Curto/complicações , Idoso , Pirofosfato de Cálcio/metabolismo , Cartilagem Articular/metabolismo , Cartilagem Articular/patologia , Condrocalcinose/metabolismo , Condrocalcinose/patologia , Doença Crônica , Enterite/complicações , Enterite/etiologia , Feminino , Humanos , Articulação do Joelho , Masculino , Meniscos Tibiais/metabolismo , Meniscos Tibiais/patologia , Artérias Mesentéricas , Microscopia de Polarização , Pessoa de Meia-Idade , Lesões por Radiação/complicações , Síndrome do Intestino Curto/etiologia , Trombose/complicaçõesRESUMO
To assess the dynamics of taurine metabolism in vivo, two sets of studies were carried out in healthy volunteers. First, pilot studies were carried in a single human subject to determine the time course of plasma and whole blood isotope enrichment over the course of an 8-h, unprimed continuous infusion of [1,2-(13)C(2)]taurine. Second, five healthy adult males received two tracer infusions on separate days and in randomized order: 1) a 6-h continuous infusion of [1,2-(13)C(2)]taurine (3.1 +/- 0.2 micromol x kg(-1) x h(-1)) and 2) a bolus injection of [(13)C(2)]taurine (3.0 +/- 0.1 micromol/kg). Isotope enrichments in plasma and whole blood taurine were determined by gas chromatography-mass spectrometry. The pilot experiments allowed us to establish that steady-state isotope enrichment was reached in plasma and whole blood by the 5th h of tracer infusion. The plateau enrichment reached in whole blood was lower than that obtained in plasma taurine (P < 0.02). In the second set of studies, the appearance rate (R(a)) of plasma taurine, determined from continuous infusion studies was 31.8 +/- 3.1 micromol x kg(-1) x h(-1). After a bolus injection of tracer, the enrichment decay over the subsequent 2 h was best fitted by a two-exponential curve. Taurine R(a) was approximately 85% higher when determined using the bolus injection technique compared with continuous infusion of tracer. We conclude that 1) taurine R(a) into plasma is very low in healthy postabsorptive humans, and, due to taurine compartmentation between the extra- and intracellular milieus, may represent only interorgan taurine transfer and merely a small fraction of whole body taurine turnover; and 2) the bolus injection technique may overestimate taurine appearance into plasma. Further studies are warranted to determine whether alterations in bile taurine dynamics affect taurine R(a).