Hematopoietically Active Adrenal Myelolipoma Mimicking Breast Cancer Metastasis
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Abstract:
A 66-year old woman had a left breast mass. Biopsy showed invasive ductal carcinoma. A PET/CT scan demonstrated hypermetabolism in the left breast and atypical heterogeneously increased uptake throughout the skeleton as well as a minimally FDG-avid right adrenal myelolipoma. PET/CT 4 months later after 6 cycles of neoadjuvant chemotherapy demonstrated increased size and FDG avidity of this adrenal mass concerning for metastasis and uniformly increased skeletal FDG avidity. Biopsy demonstrated adrenal myelolipoma. The growth and increased FDG avidity of the adrenal myelolipoma were due to the action of colony-stimulating factors on the tumor's hematopoietic component.Keywords:
Avidity
Hypermetabolism
Myelolipoma
Hypermetabolism is one of the remarkable characteristics of burn injury. Prolonged hypermetabolism causes insufficient energy supply, which leads to delayed wound healing, immune system dysfunction, increased infection rate, and multi-organ failure. In recent years, it is concerned that the activation of brown or beige adipose tissue may be related to hypermetabolism in severe burn patients. Brown or beige adipose tissue could be regulated by stress hormones and some cytokines which increase and persist in high level for several months after severe burn. This paper reviews the current knowledge of brown or beige adipocytes developmental lineages, molecular regulation mechanism, and regulation of brown or beige adipocytes activation after severe burn.
Hypermetabolism
Severe burn
Burn out
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When one is interpreting clinical 18F-FDG PET scans of the brain (excluding tumors) in children, the typical abnormality seen is hypometabolism of various brain regions. Focal areas of hypermetabolism are noted occasionally, and the usual interpretation is that the hypermetabolic region represents a seizure focus. In this review, I discuss and illustrate the multiple causes of hypermetabolism on 18F-FDG PET studies that should not be interpreted as seizure activity, as such an interpretation could potentially be incorrect. Various conditions in which focal hypermetabolism can be encountered on 18F-FDG PET studies include interictal hypermetabolism, Sturge–Weber syndrome, changes associated with brain plasticity after injury, Rett syndrome, hypoxic–ischemic brain injury, various inborn errors of metabolism, and autoimmune encephalitis. The radiologist or nuclear medicine physician interpreting clinical 18F-FDG PET studies should be aware of these circumstances to accurately assess the findings.
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Abnormality
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Hypermetabolism and insulin resistance are prominent features of trauma including burn injury, surgery, and infection. Hypermetabolism results in insufficiency in energy supply, which induces organ function lesion, immune suppression, high infection rate, and wound healing delay, thus exerting a strong impact on patients' quality of life and prognosis. The molecular mechanism in the occurrence and development of hypermetabolism is very complicated, and it has not been fully elucidated. Recently, brown adipose tissue (BAT) was found to be present not only in rodents but also in humans, and its activity was associated with resting metabolic rate. BAT may become the new target of research in prevention and control of metabolic disorder.
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Metabolic disorder
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Hypermetabolism is a prominent feature of burn injury, and altered mitochondria function is presumed to contribute to this state. Recently, brown adipose tissue (BAT) was found to be present not only in rodents but also in humans, and its activity is associated with resting metabolic rate. In this report, we elucidate the relationship between burn injury-induced hypermetabolism and BAT activity and the possible role of the mitochondria-targeted peptide SS31 in attenuating burn injury-induced hypermetabolism by using a rat burn injury model. We demonstrate that burn injury induces morphological changes in interscapular BAT (iBAT). Burn injury was associated with iBAT activation, and this effect was positively correlated with increased energy expenditure. BAT activation was associated with augmentation of mitochondria biogenesis, and UCP1 expression in the isolated iBAT mitochondria. In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria. Our results suggest that BAT plays an important role in burn injury-induced hypermetabolism through its morphological changes and expression of UCP1.
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Thermogenin
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Hypermetabolism
Severe burn
Resting energy expenditure
Basal (medicine)
Catabolism
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The complex pathophysiologic response of hypermetabolism plays a central role for the acute and long term outcomes in severely burned patients. Burns encompassing greater than 20% total body surface area (TBSA) are characterized by stress, insulin resistance, hyperglycemia, lipolysis and catabolism. The objective of this review is to discuss landmark studies in the field of hypermetabolism postburn with regards to the current best practice for efficacious burn care and to investigate the pros and cons of those treatments. Different modalities were identified from the literature to ameliorate the hypermetabolic condition. These include early excision and closure of the burn wounds, external thermoregulation, adequate nutritional supplementation, exercise and the utilization of various pharmacologic treatments. Furthermore, we included future avenues of research with regards to treating the complex condition of hypermetabolism and determining how we can create personalized treatments for the unique set of hypermetabolic conditions presented in each patient.
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Severe burn
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Hypermetabolism proportional to wound size is the expected response in patients who sustain large burns. This metabolic response persists until wound closure is achieved. The value of this response to the injured host remains unproven. Between 1978 and 1991, 104 patients with burns covering 30% or more of the body surface area underwent partitional calorimetry as a component of various research protocols. Thirteen of these patients failed to demonstrate an increase in metabolic rate as compared with a control group. These patients without hypermetabolism were compared with case-matched patients who demonstrated the expected increase in metabolic rate. Although they were not hypermetabolic in response to the burn injury, five of these patients were exposed to a cold stress and were able to increase their metabolic rate appropriately. The failure to mount a hypermetabolic response did not impact the clinical course as measured by survival, length of hospital stay, or maximum weight loss.
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Body surface area
Severe burn
Wound Closure
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Hypermetabolism
Body surface area
Resting energy expenditure
Rectal temperature
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The pattern of metabolism changes obviously after severe burn trauma, and it is characterized by an immensely increase in energy consumption, persistent strengthening in catabolism, and impediment of utilization of nutrient substrate. It will lead to autophagy, continuous consumption, and progressive emaciation, etc. If these pathological phenomena can not be effectively corrected, the prognosis of patients with serious burn will be poor, with complications of organ damage, immune dysfunction, and delayed wound healing, etc. Hypermetabolism after burn has become one of the leading causes of multiple organ dysfunction and even death. After many years' research, we have a certain understanding of burn hypermetabolism, but it is still difficult to clearly explain the mechanism up to now. Moreover, the measures of regulating hypermetabolism are still not perfect, hampering the advance of treatment of serious burn trauma. The purpose of the article is to analyze and discuss the essential mechanism of hypermetabolism after burn, basing on the new literature and a series of our experimental and clinical studies. Meanwhile the regulation strategy concerning burn hypermetabolism is proposed. It focuses on regulation of endocrine and inflammatory mediators, as well as maintenance of gastrointestinal structure and function.
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Severe burn
Organ dysfunction
Immune Dysfunction
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In order to
evaluate the effect of the postburn per-sistent hypermetabolism
on
the emergence and evolutionof multiple organ failure(MOF),animal experimentalmodel of
hypermetabolism and MOF was established.16goats were burned(3rd degree,20%-25%of the
totalbody surface area) by using hot water. Parameters re-flecting oxygen dynamics and organ
function were stud-ied before and after burns. 11 out of the 16 goats devel-oped
hypermetabolism associated with hyperdynamic cir-culation. MOF occurred in 10 of the 11
goats with an in-cidence rate of 90.9%。 Among the five non-hyperme-tabolic animals, only one
goat developed MOF with anincidence of 20.0%. Hypermetabolism mostly occurredon the lst
day after burn and became obvious on the 2ndday.MOF developed 2-5 days after burn in most
ani-mals. It is suggested that persistent hypermetabolic statemay play an important role in the
emergence and evolu-tion of MOF.
Hypermetabolism
Organ system
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