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Dilated Cardiomyopathy Induced by Chronic Starvation and Selenium Deficiency


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Protein energy malnutrition (PEM) has been rarely documented as a cause of cardiovascular abnormalities, including dilated cardiomyopathy. Selenium is responsible for antioxidant defense mechanisms in cardiomyocytes, and its deficiency in the setting of PEM and disease related malnutrition (DRM) may lead to exacerbation of the dilated cardiomyopathy. We report a rare case of a fourteen-year-old boy who presented with symptoms of congestive heart failure due to DRM and PEM (secondary to chronic starvation) along with severe selenium deficiency. An initial echocardiogram showed severely depressed systolic function consistent with dilated cardiomyopathy. Aggressive nutritional support and replacement of selenium and congestive heart failure medications that included diuretics and ACE inhibitors with the addition of carvedilol led to normalization of the cardiac function within four weeks. He continues to have significant weight gain and is currently completely asymptomatic from a cardiovascular standpoint.
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Case Report
Dilated Cardiomyopathy Induced by Chronic Starvation and
Selenium Deficiency
Soham Dasgupta1and Ashraf M. Aly2
1Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA
2Department of Pediatric Cardiology, University of Texas Medical Branch, Galveston, TX 77555, USA
Correspondence should be addressed to Ashraf M. Aly;
Received  July ; Accepted  November 
Academic Editor: Bibhuti Das
Copyright ©  S. Dasgupta and A. M. Aly. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
Protein energy malnutrition (PEM) has been rarely documented as a cause of cardiovascular abnormalities, including dilated
cardiomyopathy. Selenium is responsible for antioxidant defense mechanisms in cardiomyocytes, and its deciency in the setting
of PEM and disease related malnutrition (DRM) may lead to exacerbation of the dilated cardiomyopathy. We report a rare case
of a fourteen-year-old boy who presented with symptoms of congestive heart failure due to DRM and PEM (secondary to chronic
starvation) along with severe selenium deciency.An initial echocardiogram showed severely depressed systolic function consistent
with dilated cardiomyopathy. Aggressive nutritional support and replacement of selenium and congestive heart failure medications
that included diuretics and ACE inhibitors with the addition of carvedilol led to normalization of the cardiac function within four
weeks. He continues to have signicant weight gain and is currently completely asymptomatic from a cardiovascular standpoint.
1. Introduction
e World Health Organization (WHO) denes malnutrition
as “the cellular imbalance between the supply of nutrients and
energy and the body’s demand for them to ensure growth,
maintenance, and specic functions [].” e term protein
energy malnutrition (PEM) applies to a group of related dis-
orders that include marasmus, kwashiorkor, and intermediate
states of marasmus-kwashiorkor. Marasmus involves inade-
emaciation while kwashiorkor involves normal caloric intake
but inadequate protein intake. We report a rare case of dilated
cardiomyopathy caused by severe malnutrition combined
with selenium deciency in a teenager. e malnutrition seen
in this patient can be more accurately dened as “disease
or injury related malnutrition” and is commonly seen in the
setting of major infection, burns, or trauma [].
2. Case Report
A fourteen-year-old boy from South America was transferred
to the burn unit at our institution for severe malnutrition.
e patient had sustained second-degree burns (>% BSA)
two years prior to admission. He did not receive adequate
nutrition and medical care because of poverty and limited
resources in his home country. He was noted to be severely
cachectic and malnourished at a local hospital and was
transferred to the United States by a charity organization for
higher level of care.
Initial assessment was signicant for a weight of
 kg (<rd percentile on WHO growth chart), height of
 cm (BMI . kg/m2,𝑧score .), blood pressure of
/ mmHg, and a heart rate of  bpm. He experienced
shortness of breath with minimal physical activity. Physical
examination revealed severe cachexia with atrophy of all
muscles without peripheral edema. He was also noted
to be moderately dehydrated. Initial investigations were
signicant for mild hyponatremia [ mmol/L (NL –
 mmol/L)], severe hypoalbuminemia [. g/dL (NL
.–. g/dL)], hypocalcemia [ionized calcium . mg/dL
(NL .–. mg/dL)], severe iron deciency anemia
[hemoglobin/hematocrit . gm/dL/.%, MCV . FL],
and selenium deciency [ ug/L]. e reported normal
serum selenium levels in the United States ranges from 
Hindawi Publishing Corporation
Case Reports in Pediatrics
Volume 2016, Article ID 8305895, 4 pages
Case Reports in Pediatrics
1 4 7 10 15 90 120
Number of days
Weight (kg)
F : A diagram showing the increase in body weight with time.
his country of origin is reported to be .– ug/L []. e
carnitine level was normal.
Immediate intravenous uid resuscitation was initiated.
Since he was severely malnourished and had limited ability
for oral intake, high calorie enteral nutrition was admin-
istered via a nasogastric tube. An initial echocardiogram
(echo) showed a globular dilated le ventricle with a severely
depressed systolic function [ejection fraction (EF) <%]
consistent with dilated cardiomyopathy. He was initially
treated with furosemide and enalapril, and carvedilol was
added a week later since there was minimal improvement
in cardiac function in addition to selenium replacement
[ mcg (. umol) twice daily intravenously]. He received
two blood transfusions and repeated albumin infusions
within the rst ve days. One week later, his cardiac function
dramatically improved [EF %]. His selenium level, as well
as other labs, normalized within two weeks. e cardiac
function normalized within four weeks. His weight continued
to increase and reached  kg [BMI . kg/m2,𝑧score
.] within four months (Figure ). All cardiac medications
were then discontinued. e patient’s stamina continues to
3. Discussion
Malnutrition is a signicant cause of morbidity and mortality
in developing countries. It is the direct cause of over ,
deaths annually and is indirectly responsible for about half of
all deaths in children []. e median prevalence of under-
weight children worldwide in the year  was % with
% of them having severe muscle wasting []. Malnutrition
may be secondary to a variety of reasons including poverty,
pathologic states, political situations in certain countries, and
even acts of rebellion in order to achieve certain goals. Speci-
cally, “disease related malnutrition” is dened as malnutrition
in the setting of severe inammation and is commonly seen
in the setting of major infection, burns, or trauma. Critical
illness or injury promotes an acute inammatory response
that has a rapid catabolic eect on lean body mass []. e
inammatory condition in most diseases is chronic in nature
and loss of muscle mass and function may occur over months
to years. is form of malnutrition is partially attributable
to a decrease in nutrient intake and to the eect of the
inammatory state on metabolism. e malnutrition seen in
this case was both disease related and secondary to starvation
Children suering from severe malnutrition may exhibit
cardiovascular abnormalities including hypotension, cardiac
arrhythmias, cardiomyopathy, cardiac failure, and even sud-
den death []. e cardiac myocytes atrophy during star-
vation similar to other muscles in the body []. Kerpel-
heart in an autopsy study []. Ultrastructural features of rats
with PEM showed hyalinization and vacuolization of cardiac
muscle bers, loss of cross striations and myobrils, small
foci of necrosis, interstitial brosis, and mononuclear cell
inltration []. Histological studies of human myocardium
in patients with PEM show atrophy of the muscle bers with
interstitial edema. e heart has also been reported to be
thin-walled, pale, and abby on gross examination in other
autopsy studies of children with malnutrition [].
Echocardiographic studies have shown decreased le
ventricular (LV) mass in patients with PEM. Singh et al.
reported that LV systolic functions were reduced especially
in children with a loss in bodyweight of more than % of
expected weight []. A recent study showed that parameters
of LV systolic function were signicantly reduced in patients
with PEM as compared to controls []. PEM has been
established as an independent risk factor for mortality in
patients with heart failure [].
Chinese investigators rst showed that selenium de-
ciency is one of the principal factors responsible for Keshan
disease, a dilated cardiomyopathy that aects people living
in rural areas where selenium is decient []. Selenium
mediates its eects via incorporation into selenoproteins
(Figure ). Selenium-dependent enzymes mediate a wide
range of biological functions such as regulation of the
inammatory response and proliferation/dierentiation of
several immune cells.
Selenium is also important in the body’s antioxidant
defense mechanism []. When incorporated into the various
selenoenzymes, selenium increases antioxidant capacity and
suppresses the production of interleukins and tumor necrosis
factor alpha (TNF-𝛼). Lu et al. provided the rst evidence
that selenoproteins contribute to the antioxidant defense
mechanisms in cardiomyocytes. Venardos and colleagues
demonstrated that selenium deciency leads to myocardial
injury secondary to increased protein and lipid peroxidation
in a rat model. ese data were supported by the experiments
of Tanguy et al., who showed that selenium deciency in rats
lead to myocardial damage and altered recovery of cardiac
Given these ndings, various experimental studies have
aimed to limit myocardial injury through selenium supple-
mentation. e Venardos group showed signicantly more
myocardial injury in rats fed with a low selenium diet.
Furthermore, Tanguy and colleagues conrmed selenium’s
protective characteristics by demonstrating (a) an improved
cardiac function recovery, (b) a signicantly reduced infarct
Case Reports in Pediatrics
Prevents LDL oxidation, vascular inammation,
and atherogenesis
Protects cellular lipids from oxidation
Reduces hypertrophy
and oxidative stress
Decreases intracellular ROS
F : A diagram showing the actions of various selenoproteins on the cardiac myocytes. SelK: selenoprotein K. GP-: glutathione
peroxidase-. Trx-: thioredoxin reductase-. GP-: glutathione peroxidase-. ROS: reactive oxygen species. LDL: low density lipoprotein.
T : A comparison between marasmus and kwashiorkor.
Marasmus (PEM) Kwashiorkor
Severe deciency of all
nutrients and inadequate
caloric intake
Severe protein deciency
but normal caloric intake
Peripheral edema is absent Peripheral edema is present
Hair changes absent
Hair changes common
(sparse and easily pulled
Skin is dry and wrinkled
but no dermatosis
Dermatosis, aky paint
appearance of skin
Voracious appetite Poor appetite
Absent subcutaneous fat Reduced subcutaneous fat
Fatty liver uncommon Fatty liver common
Better prognosis Worse prognosis
size, and (c) a decreased incidence of postischemic ventric-
ular arrhythmias in rats that received the highest selenium
e patient we described had some features consistent
with marasmus (Table ). He also had evidence of dilated
and echocardiographic ndings. He responded well to stan-
dard therapy for dilated cardiomyopathy with furosemide
(preload reduction), enalapril (aerload reduction), and
carvedilol (antioxidant eects). Carvedilol is a nonselective
beta blocker which suppresses reactive oxygen species and
has antioxidant and anti-inammatory eects []. Selenium
supplementation was added for its documented deciency
in addition to providing adequate nutritional support. ere
was a remarkable weight gain from  kg to  kg in just
 weeks and he continues to gain more weight. He is
currently asymptomatic from a cardiovascular standpoint
and is tolerating complete oral intake.
4. Conclusion
Cardiac injury leading to dilated cardiomyopathy in cases of
severe malnutrition is rare but documented in the literature.
During the treatment of patients with malnutrition, levels
of trace elements (specially selenium) should be checked.
Adequate nutrition and replacement of decient elements
failure and dilated cardiomyopathy in these patients seem
addition of carvedilol as an antioxidant.
WHO: World Health Organization
PEM: Protein energy malnutrition
BSA: Body surface area
BMI: Body mass index
LV: Le ve ntricular
TNF-𝛼: Tumor necrosis factor-𝛼.
Competing Interests
e authors have no conict of interests relevant to this article
to disclose.
[] M. de Onis, C. Monteiro, and G. Clugston, e Worldwide
Magnitude of Protein-Energy Malnutrition: An Overview from
the WHO Global Database on Child Growth,vol.,no.,World
Health Organization, Geneva, Switzerland, .
[] G. L. Jensen, J. Mirtallo, C. Compher et al., “Adult starvation
and disease-related malnutrition: a proposal for etiology-based
diagnosis in the clinical practice setting from the International
Consensus Guideline Committee,Journal of Parenteral and
Enteral Nutrition,vol.,no.,pp.,.
[] R.E.LitovandG.F.CombsJr.,“Seleniuminpediatricnutrition,
[] F. Semp´
ertegui, B. Estrella, W. Vallejo et al., “Selenium serum
concentrations in malnourished Ecuadorian children: A Case-
Control Study,International Journal for Vitamin and Nutrition
[] O. M¨
uller and M. Krawinkel, “Malnutrition and health in
developing countries,Canadian Medical Association Journal,
vol. , no. , pp. –, .
[] Joint UNICEF—WHO—e World Bank Child Malnutrition
Database: Estimates for  and Launch of Interactive Data D
ashboards, unicef
who wb.pdf.
Case Reports in Pediatrics
[] A. A. Hill, L. D. Plank, P. J. Finn et al., “Massive nitrogen loss
in critical surgical illness: eect on cardiac mass and function,
Annals of Surgery,vol.,no.,pp.,.
[] B. ¨
Ocal, S. ¨
diographic evaluation of cardiac functions and le ventricular
mass in children with malnutrition,Journal of Paediatrics and
Child Health,vol.,no.,pp.,.
[] F. Kerpel-Fronius and F. Varga, “Dynamics of circulation in
infantile malnutrition,Pediatrics,vol.,no.,pp.,
[] M. A. Rossi and S. Zucoloto, “Ultrastructural changes in
nutritional cardiomyopathy of protein-calorie malnourished
rats,British Journal of Experimental Pathology,vol.,no.,
pp. –, .
[] B. D. Gelb and J. Abdenur, “Metabolic heart disease,” in e
Science and Practice of Pediatric Cardiology,A.Garson,T.J.
Bricker, D. J. Fisher, and J. R. Neish, Eds., p. , Williams &
Wilkins, Baltimore, Md, USA, nd edition, .
[] G. R. Singh, K. E. Malathi, R. R. Kasliwal, A. Ommar, S.
Padmavati, and S. Ramji, “An evaluation of cardiac function
in malnourished children by non-invasive methods,Indian
Pediatrics, vol. , no. , pp. –, .
[] N.H.A.Faddan,K.I.E.Sayh,H.Shams,andH.Badrawy,
“Myocardial dysfunction in malnourished children,Annals of
Pediatric Cardiology,vol.,no.,pp.,.
[] J. Bergstr and B. Lindholm, “Malnutrition, cardiac disease and
mortality,Peritoneal Dialysis International,vol.,supplement
, .
[] R.A.Johnson,S.S.Baker,J.T.Fallonetal.,“Anoccidentalcase
of cardiomyopathy and selenium deciency,e New England
Journal of Medicine,vol.,no.,pp.,.
[] C. Benstoem, A. Goetzenich, S. Kraemer et al., “Selenium and
its supplementation in cardiovascular disease—what do we
know?” Nutrients,vol.,no.,pp.,.
[] D.Paresh,G.Husam,andB.David,“Antioxidantactivityof
carvedilol in cardiovascular disease,Journal of Hypertension,
vol. , no. , pp. –, .
... Several micronutrients such as carnitine, thiamine, selenium, taurine and niacin are essential co-factors of metabolic reactions in the myocardium and contribute to efficient and appropriate energy utilization. Thus, genetic or acquired deficits in any one of these micronutrients has the potential to lead to specific forms of cardiomyopathies (CMs) [4][5][6]. ...
... Keshan disease is the classical clinical presentation of cardiac disease due to selenium deficiency, often presenting with clinical features characteristic of DCM: cardiogenic shock, cardiac arrhythmias, ECG abnormalities, enlarged heart, and/or heart failure [117]. There is also echocardiographic evidence of biventricular enlargement and histologically defined oedema, mitochondrial swelling, hypercontraction bands, widespread myocytolysis and extensive fibrosis [6]. The possibility of selenium deficiency should be considered in all malnourished patients who receive parenteral nutrition. ...
The increasing recognition of deficiency of certain essential micronutrients in the failing heart suggests that they may be involved in the pathogenesis of nutritional deficiency cardiomyopathy (NDCM) and ultimately heart failure (HF). Chronic deficits in thiamine, carnitine, selenium, niacin, taurine and Coenzyme Q10 in the myocardial tissues have already been associated with alterations in myocardial energy production, calcium balance or oxidative defences. These pathologic changes may lead to metabolic or myocardial remodelling progressing into NDCM. Due to the severity of potential outcomes of untreated NDCM, it is important for cardiologists to have a good understanding of NDCM. More importantly, NDCM is a treatable phenotype of dilated or hypertrophic cardiomyopathy (CM). Early detection and prompt initiation of nutrient supplementation therapy (NST) has the potential to reverse pathologic myocardial changes and resolve cardiac symptoms. However, current expert consensus guidelines on the treatment of HF do not expressly recommend or are conspicuously silent about the use of NST possibly attributable to inconsistent findings by several small-scale trials and the lack of reliable data by large-scale randomized clinical trials. This review summarizes the existing published data about NDCM with an emphasis on the specific aetiologic micronutrients deficiencies, including their pathophysiology, manifestation, diagnosis and clinical management. This review also identifies gaps in current studies and areas of limited knowledge to move forward with research to fill these critical gaps in knowledge.
... Additionally, an inverse association between Se levels and atherosclerosis was found, such that low serum Se levels were more frequently associated with CVD. Moreover, Se deficiency has been reported in cardiomyopathy [24,25]. At the same time, the administration of high doses of glucocorticoids causes hypertension, hyperglycemia, and dyslipidemia, resulting in increased cardiovascular or cerebrovascular risk factors and initiating oxidative stress. ...
... At the end of this period, 100 mg/kg bw prednisolone was intramuscularly injected once a day for 3 d to all of the groups, except the first group, which was treated with serum physiologic to provide the same injection stress . Ten rats from each group were killed by decapitation at the indicated times (4,8,12,24, and 48 h after the last prednisolone administration) ( Figure 1). ...
Aim of this work was to determine the effects of dietary intake vitamin E and Se on lipid peroxidation (LPO) as Thiobarbituric acid reactive substances (TBARS) and on the antioxidative defense mechanisms in heart tissues of rats treated with high doses of prednisolone. 250 adult male Wistar rats were randomly divided into 5 groups and fed with normal diet. Additionally groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se (20 mg/ 0.3 mg), respectively, for 30 days. For 3 d subsequently, control group was treated with placebo, and remaining four groups were injected intramuscularly with 100 mg/kg prednisolone. After last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of antioxidant enzymes and the levels of GSH and TBARS were measured. GSH-Px, CAT activities and GSH levels decreased starting from 4th hour to 48% and 65% of control levels by 24th hour, respectively and it reincreased to control levels at 48th hour in the prednisolone group (p < 0.001, p < 0.001). In addition, prednisolone administration led 2-fold increase in heart TBARS levels at 24th hour (p < 0.001). E vitamins and Se inhibited the increase in heart TBARS and the decrease in antioxidative enzymes levels. Therefore, It is concluded that vitamin E and Se may have a preventive role in decreasing the increase of TBARS caused by prednisolone administration in our study.
... However, group VI showed significantly lower TNF-α and MDA levels and significantly higher CK and glycogen levels in stimulated right gastrocnemius if compared to group Ia and III. This could be explained by the fact that selenium supplementation is important for the body's antioxidant defense mechanism and suppresses the production of interleukins and TNF-α (Dasgupta & Aly, 2016). It is also important for the improvement of skeletal muscular dystrophy due to the down regulation of myogenin and related cytokines (Bodnar et al., 2016). ...
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Skeletal muscle is metabolically and functionally flexible and contractile under normal conditions. Obesity is a risk factor that causes metabolic disorders and reduces muscle contractility. Sleeve gastrectomy (SG) has been used for surgical correction of obesity. This work aimed to investigate how obesity and its surgical correction affects skeletal muscle and the possible role of nutritional supplementation and physical exercise. Adult male albino rats were randomly divided into five groups, 8 rats per group: group Ia (control non-obese), group Ib (control obese), group II (post-operative, SG), group III (post SG + nutritional supplementation) and group IV (post SG + nutritional supplementation + physical exercise). SG resulted in cellular and metabolic degenerative disorders in the muscle including wasting, weakness and fibrosis with elevated inflammatory, oxidative and injury markers. Nutritional supplementation induced the post SG muscle regeneration indicated by high expression of insulin growth factor-1 (IGF-1) and myogenin and low expression of transforming growth factor beta 1 (TGF-β1). Interestingly, it improved the metabolic state of the muscle by reducing the oxidative stress, inflammatory and muscle injury markers and delaying the onset of fatigue. What is more, physical exercise along with nutritional supplementation resulted in further improvement of the muscle metabolic state and function. In conclusion, nutritional supplementations together with physical exercise after SG are essential for preserving muscle mass and contractility and improving its metabolic and functional status.
... SE deficiency can also lead to other cardiomyopathies, such as dilated cardiomyopathy (DCM) (57). In 2016, a Galveston (TX) investigator reported a rare case of DCM caused by severe malnutrition combined with Se deficiency in a 14-year-old boy (58 ...
Full-text available
Keshan disease (KD) as an endemic, highly lethal cardiomyopathy, first reported in northeast China's Keshan County in 1935. The clinical manifestations of patients with KD include primarily congestive heart failure, acute heart failure, and cardiac arrhythmia. Even though some possible etiologies, such as viral infection, fungal infection, microelement deficiency, and malnutrition, have been reported, the exact causes of KD remain poorly known. The endemic areas where KD is found are remote and rural, and many are poor and mountainous places where people are the most socioeconomically disadvantaged in terms of housing, income, education, transportation, and utilization of health services. To date, KD is a huge burden to and severely restricts the economic development of the local residents and health systems of the endemic areas. Although efforts have been made by the government to control, treat, and interrupt disease transmission, the cure for or complete eradication of KD still requires global attention. For this reason, in this review, we systematically describe the etiological hypothesis, clinical manifestations, incidence characteristics, and treatment of KD, to facilitate the better understanding of and draw more attention to this non-representative cardiovascular disease, with the aim of accelerating its elimination.
... However, group VI showed significantly lower TNF-α and MDA levels and significantly higher CK and glycogen levels in stimulated right gastrocnemius if compared to group Ia and III. This could be explained by the fact that selenium supplementation is important for the body's antioxidant defense mechanism and suppresses the production of interleukins and TNF-α (Dasgupta & Aly, 2016). It is also important for the improvement of skeletal muscular dystrophy due to the down regulation of myogenin and related cytokines (Bodnar et al., 2016). ...
... Severe acute malnutrition is associated with 1 of 2 classic syndromes, marasmus (wasting syndrome, or total calorie malnutrition) and kwashiorkor (protein calorie malnutrition), and sometimes a combination of the 2 (marasmic kwashiorkor). 245 Children with kwashiorkor have mild DCM and a precarious fluid balance. Saline infusions may increase venous pressure and lead to acute HF, whereas a decrease in blood volume can compromise tissue perfusion. ...
Full-text available
In this scientific statement from the American Heart Association, experts in the field of cardiomyopathy (heart muscle disease) in children address 2 issues: the most current understanding of the causes of cardiomyopathy in children and the optimal approaches to diagnosis cardiomyopathy in children. Cardiomyopathies result in some of the worst pediatric cardiology outcomes; nearly 40% of children who present with symptomatic cardiomyopathy undergo a heart transplantation or die within the first 2 years after diagnosis. The percentage of children with cardiomyopathy who underwent a heart transplantation has not declined over the past 10 years, and cardiomyopathy remains the leading cause of transplantation for children >1 year of age. Studies from the National Heart, Lung, and Blood Institute-funded Pediatric Cardiomyopathy Registry have shown that causes are established in very few children with cardiomyopathy, yet genetic causes are likely to be present in most. The incidence of pediatric cardiomyopathy is ≈1 per 100 000 children. This is comparable to the incidence of such childhood cancers as lymphoma, Wilms tumor, and neuroblastoma. However, the published research and scientific conferences focused on pediatric cardiomyopathy are sparcer than for those cancers. The aim of the statement is to focus on the diagnosis and classification of cardiomyopathy. We anticipate that this report will help shape the future research priorities in this set of diseases to achieve earlier diagnosis, improved clinical outcomes, and better quality of life for these children and their families.
... Clinically malnutrition in the elderly is either when the dietary intake is insufficient with essential nutrients or when a disturbance in the intake of protein and calories, which resulted in what is called protein-energy malnutrition (PEM). Three common disorders constitute the PEM; namely "marasmus, kwashiorkor, and intermediate states of marasmus-kwashiorkor." Marasmus occurs when the intake of both protein and calories is inadequate, while kwashiorkor occurs when the protein intake is inadequate, but the caloric intake is regular [4,5]. Weight loss with marked depletion in both fat stores and muscle mass are the characteristic features of Marasmus; however, the visceral organs remain function well with normal serum albumin [6]. ...
... A recent study showed that parameters of left ventricular systolic function were significantly reduced in patients with protein energy malnutrition as compared to that in controls (9). Starvation and food deprivation caused our patient's malnutrition, as confirmed by his anthropometric and biochemical evaluation findings, which could have increased his systolic dysfunction. ...
Full-text available
Severe accidental hypothermia has been demonstrated to affect ventricular systolic and diastolic functions, and rewarming might be responsible of cardiovascular collapse. Until now, there have been only a few reports on severe accidental hypothermia, none of which involved children. Herein, we describe here a rare case of heart failure in a 6-year-old boy admitted to the emergency unit owing to severe hypothermia and malnutrition. After he was warmed up (core temperature of 27.2°C at admission), he developed cardiac arrest, requiring vasoactive amines administration, and veno-arterial extracorporeal membrane oxygenation. Malnutrition and refeeding syndrome might have caused the thiamine deficiency, commonly known as beriberi, which contributed to heart failure as well. He showed remarkable improvement in heart failure symptoms after thiamine supplementation. High-dose supplementation per os (500 mg/day) after reconstitution of an adequate electrolyte balance enabled the patient to recover completely within 2 weeks, even if a mild diastolic cardiac dysfunction persisted longer. In conclusion, we describe an original pediatric case of heart failure due to overlap of severe accidental hypothermia with rewarming, malnutrition, and refeeding syndrome with thiamine deficiency, which are rare independent causes of cardiac dysfunction. The possibility of beriberi as a cause of heart failure and adequate thiamine supplementation should be considered in all high-risk patients, especially those with malnutrition. Refeeding syndrome requires careful management, including gradual electrolyte imbalance correction and administration of a thiamine loading dose to prevent or correct refeeding-induced thiamine deficiency.
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Selenium (Se) is an essential trace element that is necessary for various metabolic processes, including protection against oxidative stress, and proper cardiovascular function. The role of Se in cardiovascular health is generally agreed upon to be essential yet not much has been defined in terms of specific functions. Se deficiency was first associated with Keshan’s Disease, an endemic disease characterized by cardiomyopathy and heart failure. Since then, Se deficiency has been associated with multiple cardiovascular diseases, including myocardial infarction, heart failure, coronary heart disease, and atherosclerosis. Se, through its incorporation into selenoproteins, is vital to maintain optimal cardiovascular health, as selenoproteins are involved in numerous crucial processes, including oxidative stress, redox regulation, thyroid hormone metabolism, and calcium flux, and inadequate Se may disrupt these processes. The present review aims to highlight the importance of Se in cardiovascular health, provide updated information on specific selenoproteins that are prominent for proper cardiovascular function, including how these proteins interact with microRNAs, and discuss the possibility of Se as a potential complemental therapy for prevention or treatment of cardiovascular disease.
Malawi is one of the poorest nations in the world, ranked 151st among 195 countries by the World Bank, with an under-5-year mortality rate of 63 per 1000 live births. There are no previous studies describing the spectrum of inpatient pediatric cardiology consultations in sub-Saharan Africa. A descriptive cohort study was performed at Kamuzu Central Hospital (KCH), a tertiary care hospital in Lilongwe, Malawi. Demographic, anthropometric, and clinical information for all cardiology consults patients aged 0–18 years admitted to the children's wards over a period of 1 month was reviewed. Seventy-three consults and 69 echocardiograms were performed on 71 patients (35 males, 38 females). The median (IQR) age was 3.1 years (9 months–10.5 years). About 53% (39/73) had failure to thrive, 4.1% (3/73) were sero-reactive for HIV and 100% (73/73) were fully immunized for age per the Expanded Program on Immunization schedule. Seventy-four percent of the echocardiograms were abnormal, with 34.8% (24/69) having congenital heart disease (CHD) and 18.8% (13/69) having acquired heart disease (AHD) with preserved cardiac function. Among CHD, 10.1% (7/69) had cyanotic CHD and 24.6% (17/769 had acyanotic CHD. Among AHD, 10.1% (7/69) had rheumatic heart disease with preserved cardiac function. Symptomatic systolic heart failure (HF) with ejection fraction <50%, was found in 20.3% (14/69), and pulmonary hypertension was diagnosed in 10.1% (7/69). Overall admission mortality was 5.5% (4/73). Three patients left the hospital against medical advice. None of the patients with systolic HF had CHD. There was no significant association of HIV, gender, or failure to thrive on presence of systolic HF. This is the first report describing the spectrum of pediatric cardiology consults in an inpatient setting in Malawi. There was an unexpectedly high proportion of CHD and systolic HF. Further studies should be conducted to explore the implications and potential causes of these findings.
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The trace element selenium is of high importance for many of the body's regulatory and metabolic functions. Balanced selenium levels are essential, whereas dysregulation can cause harm. A rapidly increasing number of studies characterizes the wide range of selenium dependent functions in the human body and elucidates the complex and multiple physiological and pathophysiological interactions of selenium and selenoproteins. For the majority of selenium dependent enzymes, several biological functions have already been identified, like regulation of the inflammatory response, antioxidant properties and the proliferation/differentiation of immune cells. Although the potential role of selenium in the development and progression of cardiovascular disease has been investigated for decades, both observational and interventional OPEN ACCESS Nutrients 2015, 7 3095 studies of selenium supplementation remain inconclusive and are considered in this review. This review covers current knowledge of the role of selenium and selenoproteins in the human body and its functional role in the cardiovascular system. The relationships between selenium intake/status and various health outcomes, in particular cardiomyopathy, myocardial ischemia/infarction and reperfusion injury are reviewed. We describe, in depth, selenium as a biomarker in coronary heart disease and highlight the significance of selenium supplementation for patients undergoing cardiac surgery.
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Malnourished children suffer several alterations in body composition that could produce cardiac abnormalities. The aim of the present study was to detect the frequency of myocardial damage in malnourished children as shown by echocardiography and cardiac troponin T (cTnT) level. Forty-five malnourished infants and young children (mean±SD of age was 11.24 ±7.88 months) were matched with 25 apparently healthy controls (mean±SD of age was 10.78±6.29 months). Blood sample was taken for complete blood picture, liver and kidney function tests, serum sodium, potassium, calcium levels and cTnT. All the malnourished children were subjected to echocardiographic evaluation. Malnourished children showed a significantly lower left ventricular (LV) mass than the control group. The LV systolic functions were significantly impaired in patients with severe malnutrition. The cTnT level was higher than the upper reference limits in 11 (24.44%) of the studied malnourished children and all of them had a severe degree of malnutrition. The cTnT level was significantly higher in patients with anemia, sepsis and electrolyte abnormalities and it correlated negatively with LV ejection fraction (EF). Six of the studied children with high cTnT levels (54.5%) died within 21 days of treatment while only one case (2.9%) with normal level of cTnT died within the same period. LV mass is reduced in malnourished children. Children with severe malnutrition have a significant decrease in LV systolic functions. Elevated cTnT levels in malnourished children has both diagnostic and prognostic significance for cardiomyocyte damage.
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Multiple definitions for malnutrition syndromes are found in the literature resulting in confusion. Recent evidence suggests that varying degrees of acute or chronic inflammation are key contributing factors in the pathophysiology of malnutrition that is associated with disease or injury. An International Guideline Committee was constituted to develop a consensus approach to defining malnutrition syndromes for adults in the clinical setting. Consensus was achieved through a series of meetings held at the A.S.P.E.N. and ESPEN Congresses. It was agreed that an etiology-based approach that incorporates a current understanding of inflammatory response would be most appropriate. The Committee proposes the following nomenclature for nutrition diagnosis in adults in the clinical practice setting. "Starvation-related malnutrition", when there is chronic starvation without inflammation, "chronic disease-related malnutrition", when inflammation is chronic and of mild to moderate degree, and "acute disease or injury-related malnutrition", when inflammation is acute and of severe degree. This commentary is intended to present a simple etiology-based construct for the diagnosis of adult malnutrition in the clinical setting. Development of associated laboratory, functional, food intake, and body weight criteria and their application to routine clinical practice will require validation.
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Using the WHO Global Database on Child Growth, which covers 87% of the total population of under-5-year-olds in developing countries, we describe the worldwide distribution of protein-energy malnutrition, based on nationally representative cross-sectional data gathered between 1980 and 1992 in 79 developing countries in Africa, Asia, Latin America, and Oceania. The findings confirm that more than a third of the world's children are affected. For all the indicators (wasting, stunting, and underweight) the most favourable situation--low or moderate prevalences--occurs in Latin America; in Asia most countries have high or very high prevalences; and in Africa a combination of both these circumstances is found. A total 80% of the children affected live in Asia--mainly in southern Asia--15% in Africa, and 5% in Latin America. Approximately, 43% of children (230 million) in developing countries are stunted. Efforts to accelerate significantly economic development will be unsuccessful until optimal child growth and development are ensured for the majority.
Se is an essential nutrient that provides antioxidant protection in concert with vitamin E. Several selenoproteins have been identified, but only one, SeGSHpx, has a known function, that of neutralizing toxic hydroperoxides. Plasma Se concentration, being responsive to changes in Se intake, is the most practical and widely used measure of nutritional Se status. The plasma Se concentrations of the majority of healthy infants and children fall within the range of 50 to 150 micrograms/L. Although SeGSHpx activity measures the metabolically functional form of Se, the lack of a standardized analytical method has limited its usefulness as an index of nutritional Se status. Se deficiency was first observed in animals, but it is now recognized to occur in humans. Two human diseases associated with severe nutritional Se deficiency have been reported from China: a juvenile cardiomyopathy named Keshan disease and a chondrodystrophy named Kaschin-Beck disease. Long-term TPN, which provides negligible amounts of intrinsic Se, has been demonstrated in some cases to result in biochemical and clinical impairment. Although there are no consistent signs and symptoms characteristic of TPN-associated Se deficiency in addition to the low blood selenium levels, some patients will experience leg muscle pain and altered serum transaminase and creatine kinase activities. These manifestation of Se deficiency usually take years to develop. Recent information about the amount of dietary Se needed to maximize plasma SeGSHpx activity in adult men has allowed for better estimates of the Se requirement for humans. Recommended daily dietary allowances published recently by the National Academy of Sciences have been revised for infants and children in this paper by making appropriate adjustments for the protein requirements of these age-groups. These recommended intakes for Se can generally be met by consuming adequate amounts of cereals, meat, eggs, dairy products, human milk, and infant formula, which are good sources of highly available Se and are of low risk of providing excess amounts of Se. Suboptimal Se intakes by pregnant women may predispose their infants to low Se status at birth, which in turn may affect the infants ability to maintain adequate Se status during the first few months of life. In those situations where protein intake is restricted, such as in phenylketonuria and maple syrup urine disease, Se-supplemented formulas should be used. The most critical situation for Se supplementation is in pediatric patients receiving long-term TPN therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
Forty-six malnourished children between 3-48 mo with varying grades of malnutrition (PEM) were evaluated for left ventricular function by echocardiography. None of these children had any pre-existing cardiac disease, chronic illness or significant anemia. Children with Grades III and IV PEM had significantly smaller cardiac chamber size and ventricular wall thickness as compared to normally nourished children. Cardiac output as well as other indices of left ventricular function (percentage fractional shortening, mean rate of circumferential fibre shortening and ejection fraction) were also significantly decreased in severe PEM. The atrophic PEM heart does appear to show left ventricular dysfunction in moderately severe malnutrition.
Selenium is a trace element that until recently has been considered unimportant in human nutrition, except when ingested in excessive amounts. during the past decade, Chinese investigators have shown that selenium deficiency is one of the principal factors responsible for Keshan disease, a 'dilated' (congestive) cardiomyopathy that affects persons (mainly children and young women) living in rural areas of a selenium-deficient zone in China. This report describes an Occidental patient in whom selenium deficiency became associated with dilated cardiomyopathy.
In this investigation, the ultrastructural features of the nutritional cardiomyopathy of protein-calorie-malnourished rats were examined. Protein-calorie malnutrition was induced in young rats by feeding them a low-protein diet (4% protein) for 6 weeks. Control animals were fed a high-protein diet (16% protein). The deficient rats showed severe restriction of body-weight gain, fatty liver and hypoproteinaemia. The results of the present study clearly demonstrated that the experimentally induced protein-calorie malnutrition brings about striking morphological changes in the heart of the rat. On light microscopy hyalinization an vacuolization of muscle fibres, loss of cross striations and myofibrils, small foci of necrosis, interstitial fibrosis and mononuclear-cell infiltration could be detected. The ultrastructural lesions were characterized by myofibrillar degeneration, contraction-band formation, dilatation of sarcoplasmic reticulum, mitochondrial swelling, dehiscence of intercalated discs, and widened interstitial spaces, especially around vessels, due to oedema fluid and cellular infiltration by mononuclear cells an activated fibroblasts with collagen fibres and microfibrils. In addition, an increase in relative heart weight was also observed. The potential role of catecholamines in the pathogenesis of this cardiomyopathy is discussed.
The authors measured cardiac mass and function to determine whether these changed in patients who were critically ill who were losing large amounts of nitrogen from the body. The large losses of body nitrogen that occur in patients with protein-energy malnutrition are associated with a loss of cardiac mass and function. It is not known if this also occurs in patients who were critically ill who are losing massive amounts of nitrogen. Once hemodynamically stable, 13 patients who were critically ill underwent sequential measurements of left ventricular mass (LVM) and function, total body nitrogen (TBN), total body potassium, body weight, fat-free mass, and limb muscle mass. Over a 21-day study period, there was no change in LVM or function despite falls of 14% and 21% in TBN and total body potassium, respectively, a 21% fall in limb muscle mass, and a deterioration in skeletal muscle function by approximately 40%. In patients who were critically ill, cardiac mass does not decrease and function does not deteriorate after hemodynamic stability has been achieved despite massive losses of protein from the body.