What Causes Calcium Deposits In Baby's Heart – A preterm infant presented to the emergency department several weeks after birth for evaluation of a mass on the right arm that had been present for several days (Figure 1). The infant had a slight fever and was on high alert. The mass was located in the right antecubital fossa and was erythematous, nodular, and firm. Laboratory test results upon arrival showed no leukocytosis or neutrophilia. The newborn had been discharged from the neonatal intensive care unit (NICU) several days before the mass appeared. In the NICU, the patient was treated for hypocalcemia with peripheral intravenous calcium gluconate placed in the right antecubital fossa.
Ultrasound images showed a well-circumscribed, heterogeneous mass containing calcifications with posterior opacities and no abnormal internal vascularity (Figure 2). The cephalic and basilar veins were hyperechoic with posterior opacities consistent with complete calcification, and the right subclavian vein showed a small, partially calcified, nonocclusive thrombus. Right humerus radiography shows dense calcification in the antecubital region, with dense material flowing along a path suggestive of venous structures, and ultrasound findings of calcified cephalic and basilar veins. was confirmed (Figure 3).
- 1 What Causes Calcium Deposits In Baby's Heart
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- 1.2 Why Studies Say White Spots On A Child’s Nails Show Signs Of Emotional Imbalance & Behavior Issues
- 2 Brain Mri Features Of Methylmalonic Acidemia In Children: The Relationship Between Neuropsychological Scores And Mri Findings
What Causes Calcium Deposits In Baby's Heart
Iatrogenic neonatal cutaneous calcinosis. Differential diagnosis based on imaging findings includes neonatal subcutaneous fat necrosis, subepidermal calcified nodules, dermal osteoma, pilarisoma (Malherbe calcific epithelioma), and pseudoxanthoma elasticum.
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Cutaneous calcinosis is caused by the deposition of insoluble calcium salts in the skin and subcutaneous tissues. It can be divided into five subtypes: dystrophic calcification, metastatic calcification, calciphylaxis, idiopathic calcification, and iatrogenic calcification.
Dystrophic calcification refers to ectopic calcified masses in the skin composed of hydroxyapatite and calcium phosphate. Necrotic cells with denatured phosphate-binding proteins serve as foci of calcification, and altered collagen and elastin also promote calcification.
High mitochondrial calcium and phosphate levels lead to subsequent crystal deposition and necrosis, making the environment more acidic. The increase in acidity then interferes with the action of calcification inhibitors.
Dystrophic calcifications are classically seen in connective tissue diseases. However, it can also occur after local tissue damage or within a tumor. Focal dystrophic calcifications are seen in scleroderma, whereas widespread calcifications are seen in juvenile dermatomyositis and are called generalized calcifications.
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Metastatic calcifications are caused by abnormally elevated serum calcium or phosphate levels, causing precipitation of calcium salts in normal tissues. Milk-alkali syndrome, excessive intake of calcium-containing foods and antacids, and hypervitaminosis D can lead to metastatic calcification with regression of skin lesions when serum calcium levels return to the normal range.
Calciphylaxis is primarily characterized by small vessel calcification of the wall within the subcutaneous fat or dermis, leading to vascular damage and ultimately ischemia or infarction of the supplied tissue. Calcium may also be deposited outside the blood vessels.
Calciphylaxis most often occurs in patients with end-stage renal disease. However, it has also been reported in patients with primary hyperparathyroidism and normal renal function.
The absence of identifiable metabolic disturbances, tissue damage, or treatment characterizes the idiopathic subtype. An example of idiopathic cutaneous calcinosis is calcinosis tumefaciens, a condition typified by deposits of calcium around major joints in adolescents without underlying disease or altered calcium metabolism.
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The iatrogenic subtype is usually seen as a side effect of treatment and has been reported to occur after intravenous administration of calcium gluconate for hypocalcemia.
In our patient, further testing revealed that the mother had vitamin D deficiency. Vitamin D deficiency is a risk factor that predisposes newborns to neonatal hypocalcemia.
Damaged subcutaneous tissue and resulting cellular necrosis at the site of extravasation create a more acidic environment lacking mineralization inhibitors, promoting precipitation.
Within 3 weeks of the initial soft tissue injury, multiple whitish-yellow skin papules or nodules with erythema or necrosis develop.
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Calcification can also develop along the vascular sheath from extravasated material. Our patient’s thrombosis was attributed to venous stasis due to calcification. Intravenous therapeutic calcium solutions are not highly radioactive. Therefore, radiographs usually do not show subcutaneous calcification until approximately 2 weeks after extravasation. Treatment options include elevation, cold compresses, local surgery, the topical glucocorticoid triamcinolone, and the calcium channel blocker diltiazem. In most cases, calcifications begin to disappear by 8 weeks and resolve by 6 months.
Subcutaneous fat necrosis of the newborn (SCFN) is one of the targets in the differential diagnosis of subcutaneous lesions in newborns. It is a transient disease of the subcutaneous adipose tissue, most commonly occurring in infants with hypoxia or perinatal stress, and is characterized by hard subcutaneous nodules.
The mechanism of SCFN is currently unknown. However, SCFN is hypothesized to occur due to a combination of local tissue hypoxia and mechanical stress and/or enrichment of saturated fatty acids that increase tissue crystallization propensity.
Although the proposed mechanism of SCFN is different from iatrogenic cutaneous calcinosis, the lesions may appear similar on ultrasound. Additionally, subepidermal calcified nodules are a different consideration than solitary nodules within this demographic. However, the former usually occurs on the head or neck and is classified as idiopathic calcinosis cutis. A clinical history is essential to make the correct diagnosis in these cases.
Why Studies Say White Spots On A Child’s Nails Show Signs Of Emotional Imbalance & Behavior Issues
Cutaneous calcinosis occurs when insoluble calcium salts are deposited in the skin and subcutaneous tissue. Neonatal iatrogenic calcinosis cutis is rare but may be seen in neonates with a history of intravenous calcium gluconate administration and may be suspected by appropriate medical history findings, such as a history of neonatal hypocalcemia .
© Anderson Publishing, Ltd. 2023 All rights reserved. Reproduction in whole or in part without express written permission is strictly prohibited. Calcinosis, the deposition of insoluble calcium salts in the skin, subcutaneous tissue, fascia, tendons, and muscles, is a concerning complication of juvenile dermatomyositis. Calcinosis is estimated to affect up to 40% of patients with juvenile dermatomyositis, contributing to significant disease morbidity. Calcinosis can be difficult to treat, and the most effective treatment remains unclear due to the lack of comparative studies. We aim to review the literature published over the past 5 years to summarize the latest information on the pathogenesis and treatment of calcinosis in juvenile dermatomyositis and to discuss areas for future research.
Juvenile dermatomyositis (JDM) is the most common inflammatory myopathy in children, affecting 2 to 4 children per million per year (1). Children usually present with proximal muscle weakness and a characteristic rash, particularly Gottron’s sign and heliotrope (2). Despite improvements in mortality, significant morbidity associated with JDM remains. Calcinosis is an intracellular deposit of insoluble calcium salts in the skin, subcutaneous tissue, fascia, tendons, and muscles that affects approximately 40% of patients and can lead to skin ulcers, recurrent infections, joint contractures, and nerve May cause strangulation. Calcinosis in JDM is dystrophic and occurs secondary to injury and in the presence of otherwise normal calcium and phosphate (3). Figure 1 shows calcification in the fingers of a child with JDM, and Figure 2 is her radiograph of calcification in the subcutaneous tissue near the knee. Previous studies have suggested that risk factors include late diagnosis of his JDM and prolonged disease activity, and early and aggressive treatment can minimize the risk of calcification. It has been suggested that this is possible (4). There is still no consensus regarding the appropriate treatment of calcification in JDM. This is probably due to unclear understanding of its etiology, rarity of the disease, and reliance on expert opinion via case reports and case series. This article is a review of the literature published over the past 5 years regarding calcification in JDM, highlighting the latest information on pathogenesis and treatment.
Figure 1. Photograph of calcific lesions on the fingers of a child with juvenile dermatomyositis. Permission has been obtained from the patient to publish this image.
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Figure 2. Plain radiograph of a calcific lesion in the subcutaneous tissue adjacent to the right knee of a child with juvenile dermatomyositis. Permission has been obtained from the patient to publish this image.
A 2022 review by Davuluri et al. (5) summarized the potential pathogenesis mechanisms of calcification in JDM, including the process of mitochondrial calcification (3) which is primarily driven by reactive oxygen species (ROS) generated secondarily by inflammation. I am. Calcified mitochondria have been found in skeletal muscle cells of patients with JDM (6), and once mineralized, mitochondria secrete inflammatory cytokines such as IL-1β and are secreted by upregulating type I interferon-regulated genes. Perpetuates inflammation (7). Furthermore, JDM patients had increased cell-free mitochondrial DNA in their peripheral blood, and even higher levels were found in patients with calcinosis. Autoantibodies against mitochondrial antigen (AMA) were present in 40% of her JDM patients and were significantly associated with calcinosis (odds ratio = 6.1). Interestingly, AMA is elevated before clinical diagnosis of calcification and may predict prognosis (8).
The role of neutrophils in JDM has also been studied, but they are not usually found in muscle biopsies. The researchers identified neutrophils within the injured muscle tissue using electron microscopy and showed that the neutrophils were phagocytosing calcium crystals. The crystals induced neutrophil extracellular traps (NETs), causing local tissue damage and inflammation. Macrophages have also been shown to phagocytose calcium crystals (9).
The reported incidence of calcification and associated risk factors vary. Recent North American reviews reported calcification in 2–5% of patients at the time of JDM diagnosis and 13–25% overall (10–13). International cohort studies have shown that high rates of 9 to 11% at diagnosis and 20 to 40% develop calcinosis throughout the course of the disease (14-21). A multinational, multicenter study of patients with the myositis-specific antibody (MSA) anti-nuclear matrix protein 2 (NXP2) reported calcification in 15% at diagnosis and 42% overall.
Brain Mri Features Of Methylmalonic Acidemia In Children: The Relationship Between Neuropsychological Scores And Mri Findings
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