Postmortem measurement of C-reactive protein and interpretation of results in ketoacidosis

Lindroos-Jokinen, Katarina; Keltanen, Terhi; Vanhala, Teija; Valonen, Tiina; Sajantila, Antti

doi:10.1016/j.legalmed.2012.01.009

Cited by 15 publications

(6 citation statements)

References 23 publications

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“…In the realm of forensic pathology, C-reactive protein levels in diabetic and alcoholic ketoacidosis have been investigated by Lindroos-Jokinen et al ( 85 ). These authors observed that C-reactive protein levels could successfully be measured in postmortem material up to 18 days after death.…”

Section: C-reactive Proteinmentioning

confidence: 99%

Postmortem diagnosis of diabetes mellitus and its complications

Palmière¹

2015

Croat Med J

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Diabetes mellitus has become a major cause of death worldwide and diabetic ketoacidosis is the most common cause of death in children and adolescents with type 1 diabetes. Acute complications of diabetes mellitus as causes of death may be difficult to diagnose due to missing characteristic macroscopic and microscopic findings. Biochemical analyses, including vitreous glucose, blood (or alternative specimen) beta-hydroxybutyrate, and blood glycated hemoglobin determination, may complement postmortem investigations and provide useful information for determining the cause of death even in corpses with advanced decompositional changes. In this article, we performed a review of the literature pertaining to the diagnostic performance of classical and novel biochemical parameters that may be used in the forensic casework to identify disorders in glucose metabolism. We also present a review focusing on the usefulness of traditional and alternative specimens that can be sampled and subsequently analyzed to diagnose acute complications of diabetes mellitus as causes of death.

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Section: C-reactive Proteinmentioning

confidence: 99%

Postmortem diagnosis of diabetes mellitus and its complications

Palmière¹

2015

Croat Med J

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“…It appears that DKA is an inflammatory state associated with an immune and systemic inflammatory response that results in disruption in the integrity of these tight junctions. For example, patients who present with severe and fatal DKA have a non‐infectious systemic inflammatory response with elevated levels of proinflammatory cytokines , raised C‐reactive protein , complement activation , generation of reactive oxygen species and reduced levels of antioxidants . This neuroinflammatory response is also strongly expressed in the choroid plexus epithelium .…”

Section: Neuropathology In Dkamentioning

confidence: 99%

Cerebral edema in children with diabetic ketoacidosis: vasogenic rather than cellular?

Tasker

Acerini

2014

Pediatr Diabetes

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Cerebral edema (CE) is accumulation of water in the intracellular or extracellular spaces of the brain. Vasogenic edema occurs when there is breakdown of the tight endothelial junctions of the blood-brain barrier (BBB), leading to extravasation of intravascular protein and fluid into the interstitial space of the brain. In cellular edema the BBB remains intact and there is swelling of astrocytes with corresponding reduction in extracellular space. In this review we bring together clinical evidence from neuropathology and cerebral magnetic resonance (MR) studies in pediatric patients presenting in diabetic ketoacidosis (DKA), and use applied physiology to understand whether CE complicating DKA is vasogenic, rather than cellular in origin. Because the first-line of defense against CE is the interface between the intravascular compartment and the extracellular space in the brain much of the focus in this review is the BBB. The principal pathologic finding in fatal cases is perivascular with BBB disruption and albumin extravasation, suggesting increased vascular permeability. DKA induces an inflammatory response and the mechanism of BBB transcellular permeability may be an immunologic cascade that disrupts tight junctions. The principal MR finding in subclinical cases of CE is vasogenic rather than cellular edema. We propose that the following physiology be considered when treating cases: bolus dose of intravenous mannitol may result in fall in serum sodium concentration, and therefore clinical worsening. Failure to respond to mannitol should prompt the use of 3% hypertonic saline (HS). Bolus dose of intravenous 3% HS is expected to effect vasogenic edema provided that the reflection coefficient is close to 1. Failure to respond to 3% HS should prompt the use of mannitol.

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“…This change in immunity due to alcohol persists for a considerable period after alcohol withdrawal1920). Several studies have reported postmortem increased CRP levels due to AKA rather than inflammation521). The accumulative oxidative stress of acetoacetate and β-hydroxybutyrate, which are the causative agents in ketoacidosis, is believed to result in inflammatory status and an increase in postmortem CRP22).…”

Section: Discussionmentioning

confidence: 99%

Delta Neutrophil Index is Useful to Predict Poor Outcomes in Male Patients with Alcoholic Ketoacidosis

Kim

Shin

Kim

et al. 2019

Electrolyte Blood Press

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Background Alcoholic ketoacidosis (AKA) is known as a benign disease, but the related mortality reported in Korea is high. Acidosis and alcohol change the immunity profile, and these changes can be identified early using the delta neutrophil index (DNI). We aimed to evaluate the use of DNI and other standard laboratory parameters as predictors of prognosis in AKA patients. Methods One hundred eighteen males with AKA were evaluated at the Wonju Severance Christian hospital between 2009 and 2014. We performed a retrospective analysis of demographic, clinical, and laboratory parameters data. Receiver operating characteristic curves (ROC) and multivariate Cox regression was used to identify renal survival and mortality. Results Survival patients had lower initial DNI levels than non-survival patients (4.8±6.4 vs 11.4±12.5, p<0.001). In multivariate-adjusted Cox regression analysis, higher initial increased DNI (HR 1.044, 95% CI 1.003–1.086, p=0.035), and lower initial pH (HR 0.044, 95% CI 0.004–0.452, p=0.008) were risk factors for dialysis during hospitalization. Further, higher initial DNI level (HR 1.037; 95% CI 1.006-1.069; p=0.018), lower initial pH (HR 0.049; 95% CI 0.008–0.312; p=0.001) and lower initial glomerular filtration rate (GFR) (HR 0.981; 95% CI 0.964–0.999; p=0.033) were predictors of mortality. A DNI value of 4.5% was selected as the cut-off value for poor prognosis and Kaplan-Meier plots showed that AKA patients with an initial level DNI ≥4.5% had lower cumulative survival rates than AKA patients with an initial DNI <4.5%. Conclusion Increased initial serum DNI levels may help to predict renal survival and prognosis in male AKA patients.

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Postmortem measurement of C-reactive protein and interpretation of results in ketoacidosis

Cited by 15 publications

References 23 publications

Postmortem diagnosis of diabetes mellitus and its complications

Postmortem diagnosis of diabetes mellitus and its complications

Cerebral edema in children with diabetic ketoacidosis: vasogenic rather than cellular?

Delta Neutrophil Index is Useful to Predict Poor Outcomes in Male Patients with Alcoholic Ketoacidosis

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