Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
 ...
PMID:Hyperglycemic crises and their complications in children. 1731 23

The authors seek to find new connections between recent results of biology and older theories. This paper aims to assemble the jigsaw puzzle. The theoretical background of the hypothesis was described in the previous issue of the journal (Sikter et al. 2017a). Human stress response often coexists with persistent hypocapnia or hypercapnia - developing via psychosomatic pathomechanism - which can lead to mental and psychosomatic illnesses. Chronic hypocapnia mainly generates hyperarousal disorders which may be reversible for an extended time, however, vicious cycles may start when hypoxia and/or severe somatic diseases are simultaneously present (commonly in the elderly), which conditions often end with death without medical help. Chronic hypercapnia devastates the organism initially without symptoms, partly due to neurohumoral contraregulation, consequential dysregulation and metabolic remodeling. Psychosomatic disorders (e.g., diseases of civilization that evolve in people with disadvantaged psychosocial situations) develop over years and decades, causing irreversible changes. Hypercapnia usually occurs in clinical pictures of chronic obstructive pulmonary disease, obesity hypoventilation syndrome, obstructive sleep apnea, and its unobstructed version (sleep-related hypoventilation), generating various organic disorders (hypertension, type 2 diabetes, cardiovascular disorders, immunological diseases, depression, etc.). Because of the above, chronic hypocapnia and hypercapnia cannot be regarded as harmless accompanying phenomena. That is why we have to strive for restoring eucapnia and normalizing the induced ionic changes, which does not appear to be a hopeless task.
 ...
PMID:New aspects in the pathomechanism of diseases of civilization, particularly psychosomatic disorders. Part 2. Chronic hypocapnia and hypercapnia in the medical practice. 2930 7