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Hypermetabolism is the physiological state of increased rate of metabolic activity and is characterized by an abnormal increase in the body’s basal metabolic rate.^{[citation needed]} Hypermetabolism is accompanied by a variety of internal and external symptoms, most notably extreme weight loss, and can also be a symptom in itself. This state of increased metabolic activity can signal underlying issues, especially hyperthyroidism or fatal familial insomnia. The drastic impact of the hypermetabolic state on patient nutritional requirements is often understated or overlooked as well.

Hypermetabolism typically occurs after significant injury to the body. In hospitals and institutions, the most common causes are infections, sepsis, burns, multiple traumas, fever, long-bone fractures, hyperthyroidism, prolonged steroid therapy, surgery and bone marrow transplants. Hypermetabolism may occur in particular in the brain after traumatic brain injury. The cause and location of hypermetabolic symptoms within the body can be accurately detected by PET scan. Symptoms will usually subside once the underlying illness or injury is treated.

Signs and symptoms

Symptoms may last for days... weeks, or months until injury is healed. The most apparent sign of hypermetabolism is an abnormally high intake of calories followed by continuous weight loss. Internal symptoms of hypermetabolism include but are not limited to: peripheral insulin resistance, elevated catabolism of protein, carbohydrates and triglycerides, and a negative nitrogen balance in the body.^[1] Outward symptoms of hypermetabolism may include:

Sudden weight loss
Anemia
Fatigue
Elevated heart rate
Irregular heartbeat
Insomnia
Dysautonomia
Shortness of breath
Muscle weakness
Excessive sweating

Detection

Positron emission tomography (PET scan) is the primary means of detection for hyperthyroidism. This technique identifies both the location and the cause of hypermetabolic activity within the body. The resolution of PET scans, however, are limited and inconsistent in detecting the details of cortical alterations.^[2]

Pathophysiology

During the acute phase, the liver redirects protein synthesis, causing up-regulation of certain proteins and down-regulation of others. Measuring the serum level of proteins that are up- and down-regulated during the acute phase can reveal extremely important information about the patient's nutritional state. The most important up-regulated protein is C-reactive protein, which can rapidly increase 20- to 1,000-fold during the acute phase. Hypermetabolism also causes expedited catabolism of carbohydrates, proteins, and triglycerides in order to meet the increased metabolic demands.

Differential diagnosis

Hypermetabolism is one symptom of Astrocytoma. Shown above is a PET scan of hypermetabolic Astrocytoma in the brain.

Many different illnesses can cause an increase in metabolic activity as the body combats illness and disease in order to heal itself. Hypermetabolism is a common symptom of various pathologies. Some of the most prevalent diseases characterized by hypermetabolism are listed below.

Hyperthyroidism: Manifestation: An overactive thyroid often causes a state of increased metabolic activity.^[1]
Friedreich's ataxia: Manifestation: Local cerebral metabolic activity is increased extensively as the disease progresses.^[3]
Fatal familial insomnia: Manifestation: Hypermetabolism in the thalamus occurs and disrupts sleep spindle formation that occurs there.^[4]
Graves' disease: Manifestation: Excess hypermetabolically-induced thyroid hormone activates sympathetic pathways, causing the eyelids to retract and remain constantly elevated.^[5]
Anorexia and bulimia: Manifestation: The prolonged stress put on the body as a result of these eating disorders forces the body into starvation mode. Some patients recovering from these disorders experience hypermetabolism until they resume normal diets.^[6]
Astrocytoma: Manifestation: Causes hypermetabolic lesions in the brain^[7]

Treatment

Since hypermetabolism itself is a symptom and not an independent disease, treatment first and foremost requires attention to the underlying disease. Usually once the underlying cause is remedied, the symptoms will subside. The duration of symptoms depends upon the severity of the illness or trauma. Although hypermetabolism is a potentially dangerous condition that usually signals an underlying issue, it is one of the body’s strongest defenses against illness and injury.

References

^ ^a ^b "What is Hypermetabolism?". Wise Geek. Retrieved 29 November 2012.
^ Bar, M.D., Karl-Jurgen. "Serial Positron Emission Tomgraphic Findings in an Atypical Presentation of Fatal Familial Insomnia". Archives of Neurology. University of Illinois Urbana-Champaign. Retrieved 29 November 2012.
^ Gilman et al. "Cerebral Glucose Hypermetabolism in Friedreich's Ataxia Detected with Positron Emission Tomography" (PDF). Annals of Neurology. American Neurological Association. Retrieved 29 November 2012.
^ Cortelli, Pietro. "Pre-symptomatic diagnosis in fatal familial insomnia: serial neurophysiological and FDG-PET studies" (PDF). Brain. Oxford Journal. Retrieved 29 November 2012.
^ Trobe, M.D., Jonathan. "Graves' Disease: Proptosis, Lid Retraction, Strabismus, Optic Nerve Compression". The Eyes Have It. University of Michigan Kellogg Eye Center. Retrieved 29 November 2012.
^ "Re-Feeding". Families Empowered and Supporting Treatment of Eating Disorders. Retrieved 29 November 2012.
^ Mirzaei et al. "Diagnosis of Recurrent Astrocytoma with Fludeoxyglucose F18 PET Scanning". The New England Journal of Medicine. Retrieved 29 November 2012.

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Early hemorrhage triggers metabolic responses that build up during prolonged shock.

D'Alessandro A1, Moore HB2, Moore EE3, Wither M4, Nemkov T4, Gonzalez E2, Slaughter A2, Fragoso M2, Hansen KC4, Silliman CC5, Banerjee A2.
American journal of physiology. Regulatory, integrative and comparative physiology.Am J Physiol Regul Integr Comp Physiol.2015 Jun 15;308(12):R1034-44. doi: 10.1152/ajpregu.00030.2015. Epub 2015 Apr 15.
Metabolic staging after trauma/hemorrhagic shock is a key driver of acidosis and directly relates to hypothermia and coagulopathy. Metabolic responses to trauma/hemorrhagic shock have been assayed through classic biochemical approaches or NMR, thereby lacking a comprehensive overview of the dynamic
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The Janus faces of acquired angioedema: C1-inhibitor deficiency, lymphoproliferation and autoimmunity.

Wu MA, Castelli R.
Clinical chemistry and laboratory medicine : CCLM / FESCC.Clin Chem Lab Med.2015 Jun 12. pii: /j/cclm.ahead-of-print/cclm-2015-0195/cclm-2015-0195.xml. doi: 10.1515/cclm-2015-0195. [Epub ahead of print]
Several clinical and biological features of lymphoproliferative diseases have been associated with an increased risk of developing autoimmune manifestations. Acquired deficiency of C1-inhibitor (C1-INH) (AAE) is a rare syndrome clinically similar to hereditary angioedema (HAE) characterized by local
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[Understanding the pathophysiology of malnutrition for better treatment].

De Bandt JP1.
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Malnutrition results from an imbalance between intake and protein-energy requirements resulting in tissue losses with adverse functional consequences. However, it would be better to speak of "states of malnutrition" rather than "malnutrition". Indeed, the mechanisms involved associate, with varying
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Japanese Journal

負のエネルギーバランスを伴った第四胃左方変位乳牛の血中遊離アミノ酸濃度

浜名盛浩,大塚浩通,及川正明 [他],川村清市
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Obligatory Nitrogen Losses in Pregnant Rats with Special Reference to Estimation of Net Protein Utilization.

SAKAMOTO Sadaichi,MORI Masahiro,OHNAKA Masaharu,NIIYAMA Yoshiaki
Journal of Nutritional Science and Vitaminology 38(5), 493-499, 1992
… The endogenous urinary nitrogen excretions during early-mid and late pregnancies were significantly higher in pregnant rats (666mg/15 days and 234mg/6 days, respectively) than in nonpregnant animals (585mg/15 days and 153mg/6 days, respectively), indicating pregnancy-induced protein hypercatabolism. …
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Protein and Energy Metabolism in Patients with Progressive Muscular Dystrophy.

OKADA Kazuko,MANABE Sachinobu,SAKAMOTO Sadaichi,OHNAKA Masaharu,NIIYAMA Yoshiaki
Journal of Nutritional Science and Vitaminology 38(2), 141-154, 1992
… Thus, we conclude that the underweight of the DMD patients resulted from nu-trient deficiencies due to hypercatabolism, despite their considerably high intakes of energy and protein, expressed as per kg body weight. …
NAID 130001369349