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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Even in the absence of detectable ethanol or visible lipemia, a large plasma osmolal gap is the usual finding in cases of diabetic ketoacidosis. This gap decreases to an insignificant value within 20 h of treatment. Detailed biochemical analysis of six cases showed that, on average, the gap could be almost wholly accounted for by an increase in acetone, a decrease in the plasma water fraction, and smaller increments in amino acids and glycerol. Calculated plasma osmolality can seriously underestimate the true value in diabetic ketoacidosis, and so some previously observed anomalies may be explained.
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PMID:Excess osmolal gap in diabetic ketoacidosis explained. 158 30

We report here a case of diabetic ketoacidosis associated with hyperlipidemia and acute pancreatitis following alcohol abuse. A 23-year-old man was admitted to the hospital because of right upper abdominal and back pain developing into a state of unconsciousness and shock. He had been drinking 720 ml of whisky daily for 4 years. Laboratory data on admission revealed metabolic acidosis (pH 7.01, PaO2 84.6 mmHg, PaCO2 41.1 mmHg, HCO3- 16.3 mmol/l, BE-16.4 mmol/l), a high blood glucose level (640 mg/dl), strongly positive urinary ketone bodies, hypercholesteremia (913 mg/dl) and hypertriglyceridemia (8500 mg/dl). Furthermore, the levels of pancreatic enzyme including serum amylase (770 U/l) and elastase I (2721 ng/dl) were elevated. After successful treatment of the diabetic ketoacidosis with insulin and fluid supplementation, serum cholesterol, triglyceride and pancreatic enzyme levels decreased concomitantly with stabilization of the blood glucose level. From these findings, it is suggested that hyperlipidemia might have caused the acute pancreatitis which developed into diabetic ketoacidosis in this patient.
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PMID:[A case of non-insulin-dependent diabetes mellitus associated with diabetic ketoacidosis after the onset of hyperlipidemia and acute pancreatitis following alcohol abuse]. 193 46

Hyperlipemia in an acyanotic patient with diabetic ketoacidosis, alcoholism, and pancreatitis produced a falsely elevated concentration of methemoglobin (19 percent) and a lower-than-expected oxygen saturation measured with an automated spectrophotometer (IL-282 CO-Oximeter). In addition, there was a "normal" hemoglobin level despite a low hematocrit reading. In vitro studies showed that hyperlipemia corresponding to triglyceride levels of 500 mg/100 ml and greater produced erroneously high values for methemoglobin and total hemoglobin and "negative" values for carboxyhemoglobin. These abnormalities disappeared when the excessive lipids were removed by washing the erythrocytes in physiologic saline solution.
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PMID:Factitious methemoglobinemia caused by hyperlipemia. 673

A boy of 6 with diabetic ketoacidosis presented with a disturbance of lipid metabolism characterised by eruptive xanthomata, hepatomegaly, lipaemia retinalis, milky serum and hypertriglyceridemia with type V electrophoretic pattern. All the findings are typical diabetic hyperlipidaemia. The severity of the abnormalities are not solely due to delay in treatment because they are also caused by the unusual sensitivity of lipoprotein lipase to insulin deficiency. A histological and ultrastructural study of the xanthomata was performed.
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PMID:[Diabetic ketoacidosis with severe hypertriglyceridemia and eruptive xanthomata (author's transl)]. 678 45

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Confronted with a child deteriorating during treatment of diabetic ketoacidosis, Godfrey Nyamugunduru and Helen Roper describe how the child's management was complicated by gross hyperlipidaemia. At the point where the child's condition was deteriorating despite conventional management we invited two experts-Gilbert R Thompson and J I Mann-to suggest a course of action. The original authors then describe how they did manage the case, and our experts comment again.
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PMID:A difficult case. Childhood onset insulin dependent diabetes presenting with severe hyperlipidaemia. 900 85

A 19-year-old woman with diabetic lipemia and maturity-onset diabetes of the young (MODY) is reported. Though her insulin secretory activity was preserved, she fell into mild diabetic ketoacidosis (DKA) and showed type V hyperlipidemia. Post-heparin plasma activity of lipoprotein lipase (LPL) was decreased even 10 days after initiating insulin injection but not deficient. The abnormalities in lipid metabolism were improved by long-term insulin treatment. Though the contribution of the genetic background to the lipid abnormalities is not clear, the characteristics of MODY in this patient including insulin secretory capacity under stress conditions such as DKA might play a role in the development of diabetic lipemia.
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PMID:Diabetic lipemia with maturity-onset diabetes of the young. 926 Jul 68

Diabetic ketoacidosis results from insulin deficiency and insulin resistance and is marked by hyperglycaemia, ketoacidosis, dehydration and electrolyte losses. Management includes correction of shock, dehydration, electrolyte deficits, hyperglycaemia, acidosis and sepsis (if present). Warning signs include severe dehydration, shock, pH < 7.0, hypokalaemia, hypernatraemia, hyperosmolality, hyperlipidaemia, deterioration in consciousness and diabetic ketoacidosis in very young patients. The principles of treatment include (i) admission to a unit with paediatric experience, (ii) treatment of shock, (iii) rehydration over 24-36 h, or longer if the osmolality is >360 mmoll(-1), (iv) normal saline for rehydration unless the patient is hypernatraemic, (v) avoidance of bicarbonate unless acidosis is interfering with myocardial contractility, (vi) insulin infusion to achieve a fall in blood glucose levels of 5 mmol h(-1), (vi) potassium, (vii) use of 5% glucose when the blood glucose level falls <12mmoll(-1), (ix) treatment of any complications and (x) change to subcutaneous insulin when diabetic ketoacidosis is controlled.
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PMID:Practical management of diabetic ketoacidosis in childhood and adolescence. 982 96

As a result of superior efficacy and overall tolerability, atypical antipsychotic drugs have become the treatment of choice for schizophrenia and related disorders, despite their side effects. Weight gain is a common and potentially serious complication of some antipsychotic drug therapy, and may be accompanied by hyperlipidemia, hypertension and hyperglycemia and, in some extreme cases, diabetic ketoacidosis. The molecular mechanism(s) responsible for antipsychotic drug-induced weight gain are unknown, but have been hypothesized to be because of interactions of antipsychotic drugs with several neurotransmitter receptors, including 5-HT(2A) and 5-HT(2C) serotonin receptors, H(1)-histamine receptors, alpha(1)- and alpha(2)-adrenergic receptors, and m3-muscarinic receptors. To determine the receptor(s) likely to be responsible for antipsychotic-drug-induced weight gain, we screened 17 typical and atypical antipsychotic drugs for binding to 12 neurotransmitter receptors. H(1)-histamine receptor affinities for this group of typical and atypical antipsychotic drugs were significantly correlated with weight gain (Spearman rho=-0.72; p<0.01), as were affinities for alpha(1A) adrenergic (rho=-0.54; p<0.05), 5-HT(2C) (rho=-0.49; p<0.05) and 5-HT(6) receptors (rho=-0.54; p<0.05), whereas eight other receptors' affinities were not. A principal components analysis showed that affinities at the H(1), alpha(2A), alpha(2B), 5-HT(2A), 5-HT(2C), and 5-HT(6) receptors were most highly correlated with the first principal component, and affinities for the D(2), 5-HT(1A), and 5-HT(7) receptors were most highly correlated with the second principal component. A discriminant functions analysis showed that affinities for the H(1) and alpha(1A) receptors were most highly correlated with the discriminant function axis. The discriminant function analysis, as well as the affinity for the H(1)-histamine receptor alone, correctly classified 15 of the 17 drugs into two groups; those that induce weight gain and those that do not. Because centrally acting H(1)-histamine receptor antagonists are known to induce weight gain with chronic use, and because H(1)-histamine receptor affinities are positively correlated with weight gain among typical and atypical antipsychotic drugs, it is recommended that the next generation of atypical antipsychotic drugs be screened to avoid H(1)-histamine receptors.
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PMID:H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs. 1294 44

Recently there has been increased concern over the side effects of the atypical antipsychotic drugs, including diabetes, hyperlipidemia and obesity. The relationship between diabetes and antipsychotic drugs requires a careful analysis. Patients with schizophrenia are known to suffer from diabetes more often than the general population. In addition, a number of case reports indicate that the conventional antipsychotic as well as atypical antipsychotic drugs produce diabetes. Clozapine and olanzapine, in particular, have been implicated producing diabetes as well as diabetic ketoacidosis. Epidemiological surveys have supplemented the case reports, finding increased incidence of diabetes in patients treated with atypical antipsychotic agents, but these surveys have not yielded consistent results regarding the differential effects of the various atypical antipsychotic drugs. The mechanism by which antipsychotic agents produce diabetes is not elucidated. Weight gain and consequent alteration in triglycerides and cholesterol have been known to occur frequently with olanzapine and clozapine. The ensuing metabolic syndrome itself may cause insulin resistance and diabetes. In the absence of definitive scientific data on the differential effects of antipsychotic drugs in inducing diabetes, clinical prudence and careful monitoring of all patients on atypical antipsychotic drugs is necessary. Aripiprazole and ziprasidone have not been shown to increase weight or produce diabetes, but more information on the diabetogenic effects of ziprasidone and aripiprazole is needed. In order to assess the differential effects of atypical antipsychotic drugs in producing diabetes and the mechanisms by which they produce this reaction, further research is necessary.
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PMID:Side effects of atypical antipsychotic drugs. 1528 97


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