Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 29  |  Issue : 2  |  Page : 252-258

Serum leptin level as a marker of neonatal sepsis


Department of Pediatrics, Faculty of Medicine, Menoufia University Nefia, Tanta, Gharbia, Egypt

Date of Submission17-Aug-2014
Date of Acceptance24-Sep-2014
Date of Web Publication18-Oct-2016

Correspondence Address:
Osama H Salem
Nefia, Tanta, Gharbia, 31511
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.192427

Rights and Permissions
  Abstract 

Objectives:
For evaluation of serum leptin level in neonates with sepsis to aid early and accurate diagnosis and treatment.
Background:
Leptin is a polypeptide hormone that is mainly, but not exclusively, produced in adipose tissue and plays an important role in the innate immune defense. This study was designed to evaluate the level of serum leptin in cases of neonatal sepsis.
Materials and methods:
This study was carried out on 50 neonates divided into a case group (30 neonates with sepsis) and a control group (20 healthy neonates). All patients in the study were subjected to adequate assessment of history, full clinical examination, complete blood cell, C-reactive protein with titer, blood culture, and serum leptin assay by ELISA at the time of diagnosis and after recovery from sepsis.
Results:
The study showed that neonates who developed sepsis had significantly higher serum leptin levels than those of the control group and leptin levels were significantly higher in patients before antimicrobial therapy than after antimicrobial therapy.
Also, there were no significant correlations between serum leptin and complete blood cell parameters or C-reactive protein, but there was a significant positive correlation with the sepsis score.
A significantly higher level of serum leptin was found in patients with positive blood cultures compared with those with negative blood cultures, but there was no difference in the serum leptin level between survivors and nonsurvivors.
The study showed that the best cut off value for serum leptin in the detection of sepsis was 2.75 ng/ml with a sensitivity of 75% and a specificity of 70%.
Conclusion:
Serum leptin plays a role in neonatal sepsis.

Keywords: leptin in sepsis, leptin marker, neonatal sepsis, neonatal septicemia, sepsis markers


How to cite this article:
El-Mashad GM, El-Sayed HM, Salem OH. Serum leptin level as a marker of neonatal sepsis. Menoufia Med J 2016;29:252-8

How to cite this URL:
El-Mashad GM, El-Sayed HM, Salem OH. Serum leptin level as a marker of neonatal sepsis. Menoufia Med J [serial online] 2016 [cited 2020 Jul 2];29:252-8. Available from: http://www.mmj.eg.net/text.asp?2016/29/2/252/192427


  Introduction Top


Despite improved neonatal care over the past decades, infections remain common and sometimes life-threatening in neonates admitted to the neonatal intensive care units (NICU).

For many years, a search has been ongoing to find predictors for neonatal sepsis that identify effectively patients who are at risk of infection.

Leptin is an important immunoregulatory hormone as it enhances a number of immune responses, including macrophage effector functions [1].

The leptin level increases in response to infection and inflammatory stimuli [2].

The aim of this study was to evaluate serum leptin level in neonates with sepsis to aid early and accurate diagnosis and to provide an effective treatment.


  Materials and Methods Top


This study was carried out on 50 neonates delivered in the Obstetrics and Gynecology Department, El Menshawy Hospital, and followed up at the neonatal intensive care unit in the same hospital. The study was carried out from April 2013 to December 2013.

The neonates were divided into two groups.

Group 1 was the case group, which included 30 neonates diagnosed with neonatal sepsis on the basis of clinical and laboratory data.

Group 2 was the control group, which included 20 apparently healthy neonates with no clinical signs or laboratory evidence of sepsis.

This study was carried out on full-term neonates and preterm neonates.

Exclusion criteria

  1. Severe congenital anomalies.
  2. Chromosomal abnormalities.
  3. Intrauterine growth retardation.
  4. Perinatal asphyxia.
  5. Infant of a diabetic mother.


For all neonates, the following were performed:

  1. Assessment of history (to detect risk factors for sepsis).

    1. Obstetric history (death of a previous sibling, previous admission to NICU, etc.).
    2. Prenatal history [diabetes mellitus, maternal fever >38°C, maternal antibiotics, maternal urinary tract infection (UTI), etc.].
    3. Natal history [premature rupture of membrane (PROM), maternal fever, prolonged second stage of labor, etc.].
    4. Postnatal history (low Apgar score at 1 and 5 min, aggressive resuscitation, respiratory distress, cyanosis, fever, jaundice, etc.).
    5. Current history, which includes most common symptoms of sepsis.


  2. Thorough clinical examination:

    1. Assessment of gestational age using the new Ballard score.
    2. Birth weight measurement.
    3. Detection of clinical signs of sepsis:


    1. Temperature instability (<37 or >38.5°C).
    2. Respiratory dysfunction (apnea, intercostal retraction, increased oxygen requirement, signs of respiratory distress).
    3. Circulatory dysfunction (poor peripheral circulation, hypotension, tachycardia, shock, prolonged capillary refill).
    4. GIT dysfunction (abdominal distension, bloody stool, feeding intolerance, hepatomegaly, jaundice).
    5. Neurological dysfunction (irritability, hypotonia, lethargy).
    6. Hypoglycemia or hyperglycemia.
    7. Petechiae, bleeding (with thrombocytopenia), or DIC.


  3. Laboratory investigations at diagnosis of sepsis including:

    1. Complete blood cell count with differential leukocytic count.
    2. C-reactive protein (CRP) quantitative assay.
    3. Blood culture.
    4. Serum leptin level was assessed by an enzyme-linked immunosorbent assay (ELISA) using a commercially available kit. This was repeated after successful antibiotic treatment indicated by CRP less than or equal to 6.
    5. Statistical presentation and analysis of the present study were carried out using the mean, SD, and χ2-test.




Neonates were followed up in the NICU for clinical symptoms and signs of sepsis, and laboratory evidence of sepsis.

An informed consent was obtained from the parents before their enrollment in the study. The study was approved by the Ethical Committee of Faculty of Medicine, Menoufia University.

Principle of the leptin test

The DRG Leptin (Sandwich) ELISA (EIA-2395) RUO in the USA is a solid-phase ELISA based on the sandwich principle. The microtiter wells are coated with a monoclonal antibody directed toward a unique antigenic site on a leptin molecule. An aliquot of sample containing endogenous leptin is incubated in the coated well with a specific biotinylated monoclonal antileptin antibody. A sandwich complex is formed. After incubation, the unbound material is washed off and a streptavidin peroxidase enzyme complex is added for detection of the bound leptin. On addition of the substrate solution, the intensity of color developed is proportional to the concentration of leptin in the sample.


  Results Top


This study showed that there was no significant difference between the case and the control group in the mean gestational age, sex, and mode of delivery. Birth weight and Apgar scores at 1 and 5 min. were highly significantly lower in the case group compared with the control group.

It was also found that in the case group, there was a highly significant increase in the occurrence of PROM more than 18 h, need for resuscitation, and maternal UTI, whereas there was no significant difference between both groups in the incidence of chorioamnionitis or mortality rate.

It was also observed that 56.7% of cases needed mechanical ventilation, 90% developed respiratory distress, 23.3% developed pallor, 16.7% developed bleeding, 26.7% developed jaundice, 46.7% developed hypotonia, 63.3% of cases had poor reflexes, 100% developed feeding intolerance, 83.3% had poor perfusion, 66.7% were lethargic, 56.7% developed hypotension, and 83.3% had temperature instability ([Figure 1]).
Figure 5: Receiver operating characteristic (ROC) curve.

Click here to view


In addition, there was a highly significant decrease in hemoglobin (Hb) and platelet count in the case group before treatment compared with the control group. Also, there was a highly significant increase in total leukocytic count (TLC), mature polymorphonuclear leukocytes (PMN) count, immature PMN count, immature to total neutrophil (I/T) ratio, CRP, and serum leptin level (before and after treatment) in the case group ([Table 1]).
Table 3: Comparison between survivors and nonsurvivors in the case group

Click here to view


Moreover, 23.3% had negative blood cultures and 76.6% of the case group (23 patients) had positive blood cultures; 36.7% of these were positive for Klebsiella spp., 16.7% were positive for Staphylococcus aureus, 13.3% were positive for  Escherichia More Details coli, 6.7% were positive for b-hemolytic streptococci, and 3.3% were positive for Candida albicans ([Figure 2]).
Figure 4: Comparison between serum leptin level in patients with positive and negative blood cultures in the case group.

Click here to view


There was also a highly significant decrease in serum leptin in the case group after successful management of neonatal sepsis ([Figure 3]).
Figure 3: Comparison between serum leptin level before and after treatment in the case group.

Click here to view


This study showed that serum leptin showed a significant positive correlation with the sepsis score (the higher the sepsis score, the higher the serum leptin level), whereas there were no significant correlations with the other parameters measured in the case group ([Table 2]).
Table 2: Correlation between serum leptin and other parameters measured in the case group

Click here to view


Serum leptin was significantly higher in patients with a positive blood culture compared with those with a negative blood culture ([Figure 4]).
Figure 2: Percentage of cases for results of blood culture.

Click here to view


There was no significant difference between survivors and nonsurvivors in the case group in the parameters presented in [Table 3].
Table 1: Comparison between the case group (before treatment) and the control group of laboratory data for neonatal sepsis

Click here to view


Finally, it was found that serum leptin level was reliable in the detection of sepsis (P<0.01). The cutoff value was 2.856 ng/ml with 76.1% sensitivity and 71.4% specificity ([Figure 5]).
Figure 1: Percentages of clinical manifestations of neonatal sepsis in the case group.

Click here to view



  Discussion Top


In the current study, it was found that lower birth weight was associated significantly with increased frequency of sepsis. This was also observed in several other studies [3],[4],[5],[6].

In the current study, it was found that Apgar scores at 1 and 5 min were highly significantly lower in the case group than in the control group. This was in agreement with a study that observed that a 5-min Apgar score of less than 7 carries a significantly higher risk of sepsis than infants with higher scores and that an Apgar score less than 5 at 1 min may be because of sepsis, especially with the presence of risk factors for infection [7].

Furthermore, low Apgar scores usually necessitate more prolonged and aggressive resuscitation, which is a known risk factor for sepsis [4].

In the current study, it was found that the mode of delivery was not associated significantly with increased frequency of sepsis. This is in agreement with other studies [8],[9].

However, this is not in agreement with a study that observed that babies born by vaginal delivery were more likely to have EOS than those delivered by cesarean section. This may be related to good sterilization and intrapartum chemoprophylaxis, which markedly decreased the risk of sepsis in neonates delivered by cesarean section [0].

In the current study, it was found that PROM more than 18 h, need for resuscitation, and maternal UTI were significant risk factors for neonatal sepsis, whereas chorioamnionitis was not on comparing the case and the control groups.

These results are in agreement with the studies of Kaufman and colleagues [11],[12], and not in agreement with the studies of López Sastre and colleagues [13],[14], who found that chorioamnionitis was also a significant risk factor for neonatal sepsis.

In the present study, clinical evaluation of neonates with sepsis showed that feeding intolerance (100%), respiratory distress (90%), temperature instability (84%), lethargy (66.7%), poor perfusion (83%), hypotension (56.7%), poor reflexes (64%), and jaundice (27%) were the most common clinical presentations. This is in agreement with a study that described them as the major clinical presentations of sepsis [9].

In this study, it was found that there was a significant difference in hematological parameters (Hb level, TLC, platelet count, I/T ratio, mature PMN, and immature PMN) between the case and the control group. These results were in agreement with those of some studies [15],[16],[17].

In the current study, there was a significant difference in the CRP level between the case and the control group. This is in agreement with the results some studies [18],[19],[20].

In the current study, blood cultures were positive in 23 (76.7%) cases. The sensitivity of blood cultures in neonatal sepsis is low and depends on the number and timing of cultures taken, blood volume, culture medium, technique, temperature and organism density [1].

Similar results have been found in the Betty and Inderpreet study [2], which found that culture-proven sepsis occurred in 41.6% of cases with sepsis.

In the study by Procianoy and Silveira [3], it was found that blood cultures were positive in only 18 of a total of 85 cases (21%).

In addition, a study reported that the actual burden of EOS as indicated by culture-proven cases is underestimated because blood cultures can be falsely negative in at least 50% of infants [4].

Furthermore, another study [5] reported that the administration of peripartum maternal antibiotic treatment makes the diagnostic value of neonatal blood cultures uncertain.

In the present study, Klebsiella pneumoniae was the most common organism isolated in the positive blood cultures, followed by S. aureus and E. coli (36.7, 16.7, and 13.3%, respectively), and the least common organisms were C. albicans and β-hemolytic streptococci (6.7 and 3.3%, respectively).

This is in agreement with the study of Dzwonek et al. [6], in which nearly half of the positive blood cultures grew K. pneumoniae.

However, in the study of de Benedetti et al. [3], the isolated pathogens included K. pneumoniae (47.5%), Pseudomonas aeruginosa (20%), E. coli (10%), C. albicans (10), S. aureus (7.5%), and Enterococcus spp. (5%).

This variation may be because of differences in the environment, the microbial etiology of sepsis, and supportive care practice in the centers [6].

In the current study, it was found that leptin levels were highly significantly higher in the patient group than the control group. Also, it was found that leptin levels decreased significantly in the patient group after antimicrobial therapy.

This is in agreement with the study of Orbak et al. [7], which found that serum leptin levels in newborns with septicemia were significantly higher than those of the control group and that leptin levels were significantly higher in patients before antimicrobial therapy than after antimicrobial therapy. Similar results have been found by a study by Saleh et al. [8] that included 14 full-term infants with clinical or proven septicemia and 14 full-term healthy infants in a control group. They showed a highly significant increase in serum leptin levels on comparing the studied cases before and after treatment separately and with the control group.

This is also in agreement with the studies of Bornstein and colleagues [29],[30], who found that leptin levels were significantly higher in adult septicemic patients.

This is not in agreement with the Koç et al.'s study [1], which found that there was no significant difference in serum leptin levels between septic and control infants; there was also no difference in serum leptin levels in septic neonates before and after therapy.

In the current study, it was also found that there was no correlation between serum leptin levels and birth weight.

These results are not in agreement with the studies of Christou et al. [32],[33],[34],[35], who found that birth weight was related strongly to leptin levels in cord blood.

In the current study, it was also found that there was no correlation between serum leptin levels and gestational age.

These results are not in agreement with the Tarquini et al.'s study [4], which found that gestational age was related strongly to leptin levels in cord blood.

In the current study, it was found that there were no correlations between serum leptin levels and all other hematological parameters (Hb level, TLC, platelets count, ANC, I/T ratio, and I/M ratio).

This is in agreement with other studies [27],[31] that found that there were no correlations between serum leptin levels and Hb level, TLC, platelets count, ANC, and I/M ratio and not in agreement with the Somech et al.'s study [6], which found that there were positive correlations between serum leptin and both TLC and ANC. Also, the Orbak et al.'s study [7] differed in that there was a positive correlation between serum leptin levels and the IT ratio.

In the current study, it was found that there was no correlation between serum leptin levels and CRP.

This is not in agreement with the results of the studies of Orbak and colleagues [27],[36],[37], who found that there was a positive correlation between serum leptin levels and CRP.

In the current study, it was also found that there was a positive correlation between leptin level and the sepsis score, which increased with increasing severity of sepsis.

This is not in agreement with the results of the Carlson et al.'s study [8], which showed that the severity of sepsis had no significant influence on serum leptin concentration. Also, the Quirós et al.'s study [9] found that increases in leptin levels were not associated with the severity of sepsis score.

Our study showed that serum leptin level was significantly higher in patients with a positive blood culture compared with those with a negative blood culture.

These results were not in agreement with the Díez et al.'s study [0], which found that patients with positive blood cultures showed lower serum leptin levels in septic adults.

In the current study, it was found that there was no significant difference in leptin levels between survivors and nonsurvivors in the case group.

These results were not in agreement with the Torpy et al.'s study [1], which found that leptin levels were lower in the non-survivors than in the survivors. Also, the Arnalich et al.'s study [0] showed that survivors of severe sepsis and septic shock had leptin concentrations that were 1.3-fold and 1.6-fold greater than those of non-survivors in each group.

Also, our results were not in agreement with the Quirós et al.'s study [9] study, which found that the increase in the leptin level was higher among nonsurvivor patients than in survivors.

Our study showed that the best cut-off value of serum leptin for the detection of sepsis is 2.856 ng/ml with a 76.1% sensitivity and a 71.4% specificity.


  Conclusion Top


From the results of the study, we conclude that serum leptin level increases significantly in neonates with sepsis and decreases significantly after antimicrobial therapy.

This suggests that leptin is not only an adipostatic hormone but also a stress-related hormone.

Also, it seems that serum leptin plays a role in neonatal sepsis.

Conflicts of interest

There are no conflicts of interest.[41]

 
  References Top

1.
Flanagan DE, Vaile JC, Petley GW, et al. Gender differences in the relationship between leptin, insulin resistance and the autonomic nervous system. Regul Pept 2007; 140:37–42.  Back to cited text no. 1
    
2.
Sarvikivi E, Lyytikäinen O, Soll DR, et al. Emergence of fluconazole resistance in a Candida parapsilosis strain that caused infections in a neonatalintensive care unit. J Clin Microbiol 2005; 43:2729–2735.  Back to cited text no. 2
    
3.
De Benedetti F, Auriti C, D'Urbano LE, et al. Low serum levels of mannose binding lectin are a risk factor for neonatal sepsis. Pediatr Res 2007; 61:325–328.  Back to cited text no. 3
    
4.
Gomella TL, Cunningham MD, Eyal FG, et al. Neonatal sepsis. Lange clinical manual of neonatology. 5th ed. NY, U.S.A: Lange Medical Books/McGraw-Hill; 2004. 434–442.  Back to cited text no. 4
    
5.
Gerdes JS. Diagnosis and management of bacterial infections in the neonate. Pediatr Clin North Am 2004; 51:939–959.  Back to cited text no. 5
    
6.
Guerina NG. Bacterial and fungal infections. In: Cloherty JP, Stark AR, editors. Manual of neonatal care. 4th ed. Philadelphia: Lippincott-Raven; 1997. 271–285.  Back to cited text no. 6
    
7.
Shah GS, Budhathoki S, Das BK, et al. Risk factors in early neonatal sepsis. Kathmandu Univ Med J (KUMJ) 2006; 4:187–191.  Back to cited text no. 7
    
8.
Mathai E, Christopher U, Mathai M, et al. Is C-reactive protein level useful in differentiating infected from uninfected neonates among those at risk ofinfection?. Indian Pediatr 2004; 41:895–900.  Back to cited text no. 8
    
9.
Mustafa S, Farooqui S, Waheed S, et al. Evaluation of c-reactive protein as early indicator of blood culture positivity in neonates. Pak J Med Sci 2005; 21:69–73.  Back to cited text no. 9
    
10.
Stoll BJ, Gordon T, Korones SB,et al. Early-onset sepsis in very low birth weight neonates: a report from the National Institute of Child Health andHuman Development Neonatal Research Network. J Pediatr 1996; 129:72–80.  Back to cited text no. 10
    
11.
Kaufman D, Fairchild KD. Clinical microbiology of bacterial and fungal sepsis in very-low-birth-weight infants. Clin Microbiol Rev 2004; 17:638–680.  Back to cited text no. 11
    
12.
Ottolini MC, Lundgren K, Mirkinson LJ, et al. Utility of complete blood count and blood culture screening to diagnose neonatal sepsis in the asymptomatic at risk newborn. Pediatr Infect Dis J 2003; 22:430–434.  Back to cited text no. 12
    
13.
López Sastre JB, Coto Cotallo GD, Fernández Colomer B. Neonatal invasive candidiasis: a prospective multicenter study of 118 cases. Am J Perinatol 2003; 20:153–163.  Back to cited text no. 13
    
14.
Ramasethu J. Thrombocytopenia in the newborn. Curr Hematol Rep 2004; 3:134–142.  Back to cited text no. 14
    
15.
Kuboyama RH, de Oliveira HB, Moretti-Branchini ML. Molecular epidemiology of systemic infection caused by Enterobacter cloacae in a high-risk neonatal intensivecare unit. Infect Control Hosp Epidemiol 2003; 24:490–494.  Back to cited text no. 15
    
16.
Garcia-Mayor RV, Andrade MA, Rios M, et al. Serum leptin levels in normal children: relationship to age, gender, body mass index, pituitary-gonadal hormones, and pubertal stage. J Clin Endocrinol Metab 1997; 82:2849–2855.  Back to cited text no. 16
    
17.
Nupponen I, Andersson S, Järvenpää AL, et al. Neutrophil CD11b expression and circulating interleukin-8as diagnostic markers for early-onset neonatal sepsis. Pediatrics 2001; 108:E12.  Back to cited text no. 17
    
18.
Stoll BJ. Infections of the neonatal infant. In: Kliegman RM, Jenson HB, Behrman RE, et al. editors. Nelson textbook of pediatrics. 18th ed. Philadelphia: Saunders; 2008. 794–810.  Back to cited text no. 18
    
19.
Marrekchi Z. Early-onset neonatal infection: experience from Yunisia. 19th Scientific Congress of the Egyptian Society for Neonatal and Preterm Care (ESNPC). Cairo University, Cairo (24th–25th March, 2007); 2007.  Back to cited text no. 19
    
20.
Joram N, Boscher C, Denizot S, et al. Umbilical cord blood procalcitonin and C reactive protein concentrations as markers for early diagnosis of very early onset neonatal infection. Arch Dis Child Fetal Neonatal Ed 2006; 91:F65–F66.  Back to cited text no. 20
    
21.
Kumar Y, Qunibi M, Neal TJ, et al. Time to positivity of neonatal blood cultures. Arch Dis Child Fetal Neonatal Ed 2001; 85:F182–F186.  Back to cited text no. 21
    
22.
Betty C, Inderpreet S. Early onset neonatal sepsis. Indian J Pediatr 2005; 72:23–26.  Back to cited text no. 22
    
23.
Procianoy RS, Silveira RC. The role of sample collection timing on interleukin-6 levels in early-onset neonatal sepsis. J Pediatr (Rio J) 2004; 80:407–410.  Back to cited text no. 23
    
24.
Luck S, Torny M, d'Agapeyeff K, Pitt A, Heath P, Breathnach A, et al. Horizontal transmission of Candida parapsilosis candidemia in a neonatal intensive care unit. J Clin Microbiol 2002; 40:2363–2369.  Back to cited text no. 24
    
25.
Hsu KK, Pelton SI, Shapiro DS. Detection of group B streptococcal bacteremia in simulated intrapartum antimicrobial prophylaxis. Diagn Microbiol Infect Dis 2003; 45:23–27.  Back to cited text no. 25
    
26.
Dzwonek AB, Neth OW, Thiébaut R, et al. The role of mannose-binding lectin in susceptibility to infection in preterm neonates. Pediatr Res 2008; 63:680–685.  Back to cited text no. 26
    
27.
Orbak Z, Ertekin V, Akçay F, et al. Serum leptin levels in neonatal bacterial septicemia. J Pediatr Endocrinol Metab 2003; 16:727–731.  Back to cited text no. 27
    
28.
Saleh M, Sherif L, Elwakkad A, et al. Leptin: does it have a role in neonatal sepsis?. J Appl Sci Res 2008; 4:353–359.  Back to cited text no. 28
    
29.
Bornstein SR, Licinio J, Tauchnitz R, et al. Plasma leptin levels are increased in survivors of acute sepsis: associated loss of diurnal rhythm, in cortisol andleptin secretion. J Clin Endocrinol Metab 1998; 83:280–283.  Back to cited text no. 29
    
30.
Arnalich F, López J, Codoceo R, et al. Relationship of plasma leptin to plasma cytokines and human survivalin sepsis and septic shock. J Infect Dis 1999; 180:908–911.  Back to cited text no. 30
    
31.
Koç E, Ustündağ G, Aliefendioğlu D, et al. Serum leptin levels and their relationship to tumor necrosis factor-alpha and interleukin-6 in neonatal sepsis. J Pediatr Endocrinol Metab 2003; 16:1283–1287.  Back to cited text no. 31
    
32.
Christou H, Connors JM, Ziotopoulou M, et al. Cord blood leptin and insulin-like growth factor levels are independent predictors of fetal growth. J Clin Endocrinol Metab 2001; 86:935–938.  Back to cited text no. 32
    
33.
Yang SW, Kim SY. The relationship of the levels of leptin, insulin-like growth factor-I and insulin in cord blood with birth size, ponderal index, and gender difference. J Pediatr Endocrinol Metab 2000; 13:289–296.  Back to cited text no. 33
    
34.
Tarquini B, Tarquini R, Perfetto F, et al. Genetic and environmental influences on human cord blood leptin concentration. Pediatrics 1999; 103:998–1006.  Back to cited text no. 34
    
35.
Matsuda J, Yokota I, Iida M, et al. Serum leptin concentration in cord blood: relationship to birth weight and gender. J Clin Endocrinol Metab 1997; 82:1642–1644.  Back to cited text no. 35
    
36.
Somech R, Reif S, Golander A, et al. Leptin and C-reactive protein levels correlate during minor infection in children. Isr Med Assoc J 2007; 9:76–78.  Back to cited text no. 36
    
37.
Maruna P, Gürlich R, Frasko R, et al. Serum leptin levels in septic men correlate well with C-reactive protein (CRP) and TNF-alpha but not with BMI. Physiol Res 2001; 50:589–594.  Back to cited text no. 37
    
38.
Carlson GL, Saeed M, Little RA,et al. Serum leptin concentrations and their relation to metabolic abnormalities in human sepsis. Am J Physiol 1999; 276:E658–E662.  Back to cited text no. 38
    
39.
Quirós AB, Flores JC, Arranz E, Garrote JA, Asensio J, Pérez A. Influence of leptin levels and body weight in survival of children with sepsis. Acta Paediatr 2007; 91:626–631.  Back to cited text no. 39
    
40.
Díez ML, Santolaria F, Tejera A, et al. Serum leptin levels in community acquired pneumonia (CAP) are related to nutritional status and not to acutephase reaction. Cytokine 2008; 42:156–160.  Back to cited text no. 40
    
41.
Torpy DJ, Bornstein SR, Chrousos GP. Leptin and interleukin-6 in sepsis. Horm Metab Res 1998; 30:726–729.  Back to cited text no. 41
    


    Figures

  [Figure 5], [Figure 4], [Figure 3], [Figure 2], [Figure 1]
 
 
    Tables

  [Table 3], [Table 2], [Table 1]


This article has been cited by
1 Mean platelet volume and serum uric acid in neonatal sepsis: A case-control study
Mohsen M. Shalaby,Yasser M. Ismail,Ahmad A. Sobeih,Neveen T. Abed,Omima M. Abdel Haie,Ola G. Behairy,Eman R. Abd Almonaem,Eman G. Behiry,Mahmoud A. Abd-El-Aziz
Annals of Medicine and Surgery. 2017;
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and Me...
Results
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed787    
    Printed0    
    Emailed0    
    PDF Downloaded126    
    Comments [Add]    
    Cited by others 1    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]