## 1 Introduction  
Hypothermia, defined as a core body temperature of 35 \({}^{\circ}\)C or lower, results from a critical imbalance between heat production and heat loss, disrupting normal physiological function [1; 2; 3; 4; 5]. It is categorized by severity: mild hypothermia ranges from 35 \({}^{\circ}\)C to 32 \({}^{\circ}\)C, moderate from 32 \({}^{\circ}\)C to 28 \({}^{\circ}\)C, and severe hypothermia occurs when the core temperature drops below 28 \({}^{\circ}\)C [6; 7; 8; 9]. Hypothermia can be classified into two main types based on its cause: primary hypothermia, which results from direct exposure to cold environments, and secondary hypothermia, which arises due to systemic conditions impairing thermoregulation, such as alcohol intoxication, trauma, or metabolic diseases [9].  
In primary hypothermia, the core body temperature drops primarily due to environmental exposure, and metabolic changes may not be pronounced or specific. Conversely, secondary hypothermia often involves additional physiological stressors, leading to more complex biochemical alterations. For instance, secondary hypothermia is frequently associated with underlying conditions that can disrupt normal protein synthesis, immune function, and enzyme activity [10; 11; 12; 13]. These factors may manifest as altered total protein (TP), globulins, and amylase (AMY) levels, which are influenced by the body's metabolic state rather than hypothermia itself. Low TP levels could suggest malnutrition or hepatic insufficiency, while changes in globulin levels may indicate chronic inflammatory or immune responses. Elevated AMY might be associated with pancreatic injury or other systemic conditions contributing to secondary hypothermia [2; 3; 14; 15]. However, it is important to recognize that these biomarkers alone are non-specific and can be influenced by a range of factors unrelated to hypothermia.  
Postmortem biochemical analysis, while valuable, has limitations in distinguishing primary from secondary hypothermia. Total protein, globulins, and AMY levels can remain within normal ranges or show only minor deviations depending on the underlying condition and time elapsed since death [16; 17; 18]. Forensic investigations must therefore rely on an integrated approach, combining clinical history, environmental factors, autopsy findings, and toxicology reports to accurately determine the cause of death [19]. In particular, autopsy findings, such as the presence of cold-induced tissue damage, frostbite, or specific organ injuries, should be considered alongside biochemical data to form a complete picture of the hypothermic process [20; 21; 22].  
In forensic and clinical contexts, postmortem serum markers like amylase and gamma-glutamyl transferase (GGT) have garnered attention for their potential to indicate specific causes of death. Elevated AMY and lipase levels, typically associated with pancreatic and hepatobilary conditions, may also signal broader systemic failure in cases of trauma or intoxication [23; 24]. GGT has been proposed as a marker for chronic alcohol abuse, which could contribute to secondary hypothermia through impaired thermoregulation and systemic compromise, though its utility in postmortem settings remains debated [25]. However, the postmortem persistence of these markers and their reliability in distinguishing between different causes of death, including hypothermia, requires further investigation.  
The objective of this study was to identify biochemical markers that may assist in distinguishing between primary and secondary hypothermia, particularly in cases complicated by acute alcohol and benzodiazepine ingestion. This study seeks to explore the utility of total protein, globulins, and amylase, among other markers, in creating an accurate classification of hypothermia-related deaths.