PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12160680

Barlow's disease.

C A B Clemetson
View original source ↗Export metadata ↓

Abstract

The classical form of Barlow's disease or infantile scurvy, with bruises, broken bones and sores that will not heal, is rarely seen today, but it seems to be reappearing under a different guise, when infants with borderline vitamin C depletion are assaulted with too many inoculations at one time.Moreover, it is now sometimes mistakenly diagnosed as child abuse.

Explore related subjects

Ascorbic Acid DeficiencyHumansInfantInfant Nutritional Physiological PhenomenaScurvyVaccinationJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C A B Clemetson. 2002. Barlow's disease.. https://doi.org/10.1016/s0306-9877(02)00114-7

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2005

Musculoskeletal manifestations of scurvy.

Scurvy occurs in individuals who eat inadequate amounts of fresh fruit or vegetables, often because of dietary imbalances related to advanced age or homelessness. Asthenia, vascular purpura, bleeding, and gum abnormalities are the main symptoms. In 80% of cases, the manifestations of scurvy include musculoskeletal symptoms consisting of arthralgia, myalgia, hemarthrosis, and muscular hematomas. Vitamin C depletion is responsible for structural collagen alterations, defective osteoid matrix formation, and increased bone resorption. Imaging studies may show osteolysis, joint space loss, osteonecrosis, osteopenia, and/or periosteal proliferation. Trabecular and cortical osteoporosis is common. Children experience severe lower limb pain related to subperiosteal bleeding. Laboratory tests show nonspecific abnormalities including anemia and low levels of cholesterol and albumin. The finding of a serum ascorbic acid level lower than 2.5 mg/l confirms the diagnosis. Vitamin C supplementation ensures prompt resolution of the symptoms.

Ascorbic Acid Deficiency↗
PubMed2005

Possible interplay between vitamin C deficiency and prolactin in pregnant women with premature rupture of membranes: facts and hypothesis.

The precise etiologic mechanisms involved in the premature rupture of membranes (PROM) during pregnancy, the main cause of preterm delivery worldwide, are unknown. Previous studies have shown that: (a) the rupture of chorioamniotic membranes is related to an imbalance between synthesis and degradation of collagen induced by the overexpression/activity of various matrix metalloproteinases (MMP); (b) during human labor and delivery the expression of prolactin receptors (PRL-R) increases in chorioamniotic membranes, decidua and placenta; (c) prolactin (PRL) can influence the synthesis of prostaglandins, the expression of some MMP (MMP-2, MMP-9 and decysin) and tissue inhibitors of MMP in general; (d) vitamin C deficiency induces the expression/activity of extracellular MMP and is considered a risk factor for PROM; and (e) vitamin C potentiates the dopamine-mediated inhibition of PRL in rats. The present hypothesis proposes that a decreased hypothalamic dopaminergic tone-and thus an increased synthesis/release of pituitary PRL - is induced by vitamin C deficiency below a critical threshold (<18 microg/10(8) leukocytes) and that both factors, in turn, would cause upregulation of the expression/activity of several MMP. The increased PRL concentrations (acting like a Th1-type cytokine) along with the overexpression of other proinflammatory cytokines would induce a premature switch from a favorable Th2-type immune response to a noxious Th1-type immune response in the intrauterine environment. This change, in conjunction with the upregulation of MMP-2 and MMP-9, would cause a premature imbalance between synthesis/degradation of collagen in chorioamniotic membranes (an "anticipation" of the normal parturition cascade?), which favors extracellular matrix degradation, proposed as the most relevant event in the genesis of PROM. This hypothesis represents a new dimension in the study of the etiology of PROM.

Ascorbic Acid Deficiency↗