Nonketotic Hyperglycemia Research Articles

Hemibalismo-hemicoreia em estado hiperglicêmico não cetótico: distúrbio do movimento associado ao diabetes melito

Diabetes mellitus, especially when not under control, can lead to several neurological complications being the development of involuntary movements one of the rarest presentations. Nonketotic hyperglycemia in aged patients who present with ballismus-chorea movements and cerebral image alterations in computerized tomography (CT) and magnetic resonance constitute a syndrome of recent characterization and few cases in literature. We present a case of a 75 year-old male patient admitted with history of hemiballismus-hemichorea movements, hyperglycemia, glycated hemoglobin of 14.4% and CT with a hyperdense area in the topography of the right basal ganglia. After glycemic control, the neurological signs resolved completely and the initial hyperdense lesion disappeared.

Folic acid administration reduces neointimal thickening, augments neo-vasa vasorum formation and reduces oxidative stress in saphenous vein grafts from pigs used as a model of diabetes.

There is evidence that plasma homocysteine augments vein graft failure and that it augments both micro- and macro-angiopathy in patients with diabetes mellitus. It is therefore suggested that homocysteine may augment vein graft thickening, a major cause of vein graft failure, in diabetic patients, as well as impairing adaptive growth of a new vasa vasorum, possibly through overproduction of superoxide. In order to test these proposals, the effect of folic acid administration, which lowers plasma homocysteine, on vein graft thickening and microvessel density was studied in pigs used as a model of diabetes. Non-ketotic hyperglycaemia was induced in Landrace pigs by intravenous injection of streptozotocin, and folic acid was fed daily for 1 month. Vein grafts were excised and the thickness of the neointima and media and microvessel density were assessed by planimetry and superoxide formation. Plasma total homocysteine was significantly reduced by folic acid in both control and diabetic pigs, whereas glucose was unchanged. Compared with controls, diabetic pigs showed increased neointimal thickness and superoxide formation and decreased adventitial microvessel density. Folic acid reduced neointimal thickness and superoxide formation and augmented microvessel density in diabetic but not in control pigs. Folic acid administration reduces neointimal thickening, augments vasa vasorum neoformation and reduces oxidative stress in saphenous vein grafts from diabetic pigs. Folic acid may therefore be particularly effective in reducing vein graft failure in diabetic patients.

Crisis occipitales con alteraciones electroencefalográficas como manifestación inicial de diabetes mellitus

Focal motor seizures are common in nonketotic hyperglycemia but occipital seizures as the initial symptom of hyperglycemia are exceptional. Sporadic electroencephalographic description has rarely been reported. A 56-year-old man presented to the emergency department with a 4-day history of intermittent, 30-minute episodes of flashing lights (blue-yellow color), 3-4 times per day in his left lower temporal visual field. His past medical history was significant for hypercholesterolemia and hypertension. The results of the ophthalmology examination were normal. When asked, the patient reported polyuria, polydipsia and weight gain for the previous 4 months. His general state was good and no other neurological symptoms were present. Among the laboratory tests, non-ketonic hyperglycemia of 339 mg/dl and mild plasma hyperosmolarity of 302 mOsm/kg were found. The results of visual campimetry were normal. Brain magnetic resonance imaging showed minimal alterations unrelated to the visual symptoms. An electrographic seizure in the right occipital region associated with visual symptoms was recorded. The patient was treated with hydration and insulin and was completely asymptomatic after 48 hours.

Steroid-Induced Iatrogenic Disease After Treating for Pseudothrombocytopenia

Pseudothrombocytopenia, a spontaneous in vitro occurrence after the addition of anticoagulant to blood, causes clumping of platelets resulting in a spurious observation of low platelet counts (<10,000/μL) without any associated hemorrhagic manifestations. We describe a 46-year-old male patient who was diagnosed with immune thrombocytopenic purpura (ITP) based on a reported platelet count of 22,000/μL. He was prescribed high-dose glucocorticoid therapy, up to 60 mg of prednisolone daily for over a year. After repeated hospital admissions, he came under our care as an emergency admission for nonketotic hyperosmolar hyperglycemia. He was diabetic, osteopenic, and had been treated for tuberculosis, all likely consequences of prolonged glucocorticoid therapy. In the presence of persistent platelet counts below 10,000/μL, and without associated clinical hematological manifestations of ITP, a smear of citrated blood was examined and a platelet count of 215,000/μL was observed. This case highlights the possible consequences of misdiagnosis of pseudothrombocytopenia. Failure to recognize this phenomenon may lead to debilitating iatrogenic disease.

Chorea in the both lower limbs associated with nonketotic hyperglycemia.

Hemichorea-hemiballism (HC-HB) is a complication of non-ketotic hyperglycemia (NKH); in NKH patients, the frequency of occurrence of HC-HB is greater than that of bilateral chorea. We report the case of a hyperglycemic patient who showed chorea in both the lower limbs. Magnetic resonance imaging (MRI) of the brain revealed high signal intensity on T1-weighted images of the bilateral dorsolateral putamen. The abnormal involuntary movements disappeared after oral administration of haloperidol. Our case report that chorea associated with NKH is correlated with the topography of the basal ganglia.

PO25-TH-11 Hemichorea-hemiballism as the first presentation of non-ketotic hyperglycaemia

PO25-TH-11 Hemichorea-hemiballism as the first presentation of non-ketotic hyperglycaemia

Testing for monogenic diabetes among children and adolescents with antibody‐negative clinically defined Type 1 diabetes

Monogenic diabetes is frequently misdiagnosed as Type 1 diabetes. We aimed to screen for undiagnosed monogenic diabetes in a cohort of children who had a clinical diagnosis of Type 1 diabetes but were pancreatic autoantibody-negative. We studied 252 patients diagnosed clinically with Type 1 diabetes between 6 months and 17 years of age. Pancreatic autoantibodies [islet cell autoantibodies (ICA), glutamic acid decarboxylase antibodies (GADA) and/or insulinoma-associated antigen-2 antibodies (IA2A)] were absent in 25 cases (9.9%). The most frequent genes involved in monogenic diabetes [KCNJ11 and INS for neonatal diabetes and HNF1A and HNF4A for maturity-onset diabetes of the young (MODY)] were directly sequenced. Two of the 25 (8%) antibody-negative patients had de novo heterozygous mutations in INS; c.94G>A (G32S) and c.265C>T (R89C). The two patients presented with non-ketotic hyperglycaemia at 8 and 11 months of age. In contrast, the four antibody-positive patients who presented at a similar age (6-12 months) had a more severe metabolic derangement, manifested as ketosis in all four cases, with ketoacidosis in two. At ages 15 and 5 years, both INS mutation patients were prescribed a replacement dose of insulin with good glycaemic control [glycated haemoglobin (HbA(1c)) 7.0 and 7.2%]. No mutations were found in KCNJ11, HNF1A or HNF4A. The identification of patients with monogenic diabetes from children with clinically defined Type 1 diabetes may be helped by clinical criteria including the absence of pancreatic autoantibodies.

Forced eye closure-induced reflex seizure and non-ketotic hyperglycemia

We report an uncommon case of 53-year-old female patient with partial seizure induced by forced voluntary eye closure due to non-ketotic hyperglycemia. The initial laboratory tests showed an elevated blood glucose level of 550 mg/dL but no evidence of ketosis. Brain magnetic resonance imaging was normal. When the blood glucose levels decreased slowly to about 150 mg/dL in five days, the seizures ended completely. No anticonvulsants were used. Since seizures are generally refractory to antiepileptic medication, control of blood glucose is essential.

The relationship between serum level of leptin and oxidative stress in patients with hyperglycemia crisis

To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. A total of 96 patients with diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1 Uxkg(-1)xh(-1), with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)), the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF(2 alpha) were more markedly elevated than those in normal controls (all P<0.05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF(2 alpha) were significantly lower than those in patients on admission (all P<0.05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0.38, P<0.05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF(2 alpha) in patients after treatment (r(1)=-0.35, r(2)=-0.37, both P<0.05). In stepwise regression analysis, MDA and 8-iso-PGF(2 alpha) showed a significant association with leptin. The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.

Hemichorea—hemiballismus associated with nonketotic hyperglycemia: A possible role of inflammation

Three cases of hemichorea–hemiballismus (HC–HB) associated with nonketotic hyperglycemia were reported. Of them two patients presented as HC–HB and the remaining one as generalized chorea-ballismus (CB). Brain MRI showed characteristic T1-weighted high-intensity lesions in the contralateral or bilateral striatum without edema or mass effect. They all had a prior history of respiratory or urinary infection. Cerebrospinal fluid test in two patients showed an elevation of protein concentration with normal cell and an increased IgG content and elevated IgG index or 24 h IgG intrathecal synthesis rate. These results suggested that inflammation within the central nervous system may participate in the pathogenesis of chorea and ballismus induced by NKH.

Proinflammatory cytokines in response to insulin-induced hypoglycemic stress in healthy subjects

Hyperglycemic crises of diabetic ketoacidosis and nonketotic hyperglycemia are associated with elevation of counterregulatory hormones and proinflammatory cytokines, markers of lipid peroxidation, and oxidative stress. To investigate if other conditions besides hyperglycemia could evoke such a prompt increase in cytokine levels, lipid peroxidation, and oxidative stress markers, we induced hypoglycemic stress by standard insulin tolerance test and measured proinflammatory cytokines, markers of lipid peroxidation, reactive oxygen species (ROS), and counterregulatory hormones. Insulin tolerance test was performed in 13 healthy male subjects with no history of infection, cardiovascular risk factors, or abnormal glucose. At baseline and at 30, 45, 60, 120, and 240 minutes after insulin injection, the following parameters were measured: glucose, cortisol, corticotropin, epinephrine (EP), norepinephrine (NE), growth hormone, tumor necrosis factor (TNF)– α, interleukin (IL) 1 β, IL-6, IL-8, free fatty acids, white blood cells, lipid peroxidation markers by thiobarbituric acid assay, and ROS by dichlorofluorescein method. The peak value of white blood cell count at 120 minutes was significantly associated with the peak values of NE at 30 minutes and cortisol at 60 minutes. By comparing the area under the curve of measured parameters, EP emerged as significant predictor of TNF- α ( P = .05) and IL-8 ( P = .027). Cortisol emerged as predictor of IL-1 β significantly ( P = .05). Corticotropin predicted area under the curve of IL-6 with borderline significance ( P = .06). In the present study, insulin-induced hypoglycemia in nondiabetic male subjects is associated with increased proinflammatory cytokines (TNF- α, IL-1 β, IL-6, and IL-8), markers of lipid peroxidation, ROS, and leukocytosis. Elevations of NE, EP, corticotropin, and cortisol in hypoglycaemia are associated with the elevation of the proinflammatory cytokines and leukocytosis.

A Case of Hemichorea-hemiballism Caused by Non-ketotic Hyperglycemia without Striatal Hyperintensity on T1-weighted MRI

A Case of Hemichorea-hemiballism Caused by Non-ketotic Hyperglycemia without Striatal Hyperintensity on T1-weighted MRI

Atypical onset of diabetes in a teenage girl: a case report

BackgroundChorea, hemichorea-hemiballismus and severe partial seizures may be the presenting feature of nonketotic hyperglycemia in older adults with type 2 diabetes, but cases in children with type 1 diabetes are rare, since the most easily recognized symptoms of type 1 diabetes in children are secondary to hyperglycemia, glycosuria, and ketoacidosis.Case presentationA previously healthy 15-year-old girl presents with sudden onset of right-sided chorea. Brain CT did not detect any abnormal density areas. A T1-weighted image of brain MRI was normal. Investigations revealed hyperglycemia with absent ketones and normal serum osmolality. Achievement of normoglycemia with insulin therapy determined the involuntary movements to regress completely within a day. The direct effect of hyperglycemia could be the pathogenesis of the chorea in our patient. Severe hyperglycemia without ketosis at the clinical onset of insulin-dependent diabetes mellitus (type 1) has been reported in children and adolescents, but nonketotic hyperglycemia is an unusual cause of chorea-ballismus in children, and chorea-ballismus is also a rare manifestation of primary diabetes mellitus.ConclusionThe importance of clinical evaluation, laboratory testing and neuroimaging for the differential diagnostics of chorea is emphasized.

Biballism due to non-ketotic hyperglycaemia

We describe the case of a 70-year-old woman, with type 1 diabetes mellitus, who suddenly developed a movement disorder on the left side of her body that rapidly extended to the right side, evoking biballism. There was no facial involvement and no vascular lesions on cerebral MRI but non-ketotic hyperglycaemia was present. A combination of a reduction in glucose levels and the use of neuroleptic drugs resulted in the disappearance of the abnormal movements. In this report, we discuss the association between non-ketotic hyperglycaemia and ballism along with a review of the literature.

Non Ketotic Hyperosmolar Hyperglycemia presenting as Epilepsia Partialis Continua. (An unusual presentation of a common disorder)

We report a patient with epilepsia partialis continua (EPC) associated with non ketotic hyperosmolar hyperglycemia. EPC is uncommon presenting clinical finding during nonketotic hyperglycemia. This case was reported in Medical Intensive Care Unit (MICU) in Hamad Medical Corporation, Doha, Qatar.

Magnetic Resonance Imaging Changes Associated With Transient Homonymous Hemianopia in Patients With Nonketotic Hyperglycemia

Magnetic Resonance Imaging Changes Associated With Transient Homonymous Hemianopia in Patients With Nonketotic Hyperglycemia

Magnetic Resonance Imaging Changes Associated With Transient Homonymous Hemianopia in Patients With Nonketotic Hyperglycemia—Reply

Magnetic Resonance Imaging Changes Associated With Transient Homonymous Hemianopia in Patients With Nonketotic Hyperglycemia—Reply

Pathophysiology and Management of Fluid and Electrolyte Disturbances in Patients on Chronic Dialysis with Severe Hyperglycemia

The mechanisms of fluid and solute abnormalities that should be considered in any patient with severe hyperglycemia include changes in the total amount of extracellular solute, osmotic diuresis, intake of water driven by thirst, and influences from associated conditions. The absence of osmotic diuresis distinguishes dialysis-associated hyperglycemia (DH) from hyperglycemia with preserved renal function (HPRF). Mainly because of this absence, comparable degrees of hyperglycemia tend to produce less hypertonicity and less severe intracellular volume contraction in DH than in HPRF, while extracellular volume is expanded in DH but contracted in HPRF. Ketoacidosis can develop in both DH and HPRF. Among DH patients, hyperkalemia appears to be more frequent when ketoacidosis is present than when nonketotic hyperglycemia is present. Among HPRF patients, the frequency of hyperkalemia appears to be similar whether ketoacidosis or nonketotic hyperglycemia is present. Usually patients with severe DH have no symptoms or may exhibit a thirst. Infrequent clinical manifestations of DH include coma and seizures from hypertonicity or ketoacidosis and pulmonary edema from extracellular expansion. Insulin infusion is usually the only treatment required to correct the biochemical abnormalities and reverse the clinical manifestations of DH. Monitoring of the clinical manifestations and biochemical parameters during treatment of DH with insulin is needed to determine whether additional measures, such as administration of saline, free water, or potassium salts, as well as emergency hemodialysis (HD) are needed. Emergency HD carries the risk of excessively rapid decline in tonicity; its benefits in the treatment of DH have not been established.

Hemibalismo secundario a descompensación hiperglucémica hiperosmolar

Non-ketotic hyperglycemia has occasionally been associated with various neurological abnormalities including movement disorders. Hyperglycemic hyperosmolar syndrome (HHS) is the second most common cause of hemiballism-hemichorea, which is due to a contralateral putaminal lesion. We describe a 95-year-old woman with HHS who developed hemichorea-hemiballism syndrome due to a putaminal lesion.

CT and MRI findings of chorea associated with nonketotic hyperglycemia

Objective To explore the imaging diagnosis of chorea associated with nonketotic hyperglycemia by describing its CT and MR findings and correlating those findings with the clinical manifestations. Methods The imaging findings and clinical data from 6 patients with chorea associated with nonketotic hyperglycemia were retrospectively analyzed. All 6 patients had unenhanced CT scans, 1 also had MR imaging examination. Three of 6 patients had follow-up CT scans and 1 of 3 patients had follow-up MRimaging studies. Results CT studies of all 6 patients showed unilateral or bilateral hyperdense striatum.The putamen was involved in all 6 patients, the caudate nucleus or lateral portion of the globus pallidus were involved in 5 of all 6 patients. All 3 follow-up CT studies depicted a decreased or resolved hyperdensity of the abnormal striatum. T1-weighted MR images in 1 patient showed the hyperintense lesions of bilateral lentiform nuclei, T2-weighted MR images of the patient showed the hypointense lesions of the corresponding lentiform nuclei, and its follow-up MR images depicted invariable signal intensity of T1-weighted and T2-weighted images. In all patients, the chorea resolved within 2 to 6 days after treatment of the hyperglycemia. Conclusion The characteristic imaging findings of chorea associated with nonketotic hyperglycemia can suggest an accurate diagnosis. Key words: Choreatic disorders; Hyperglycemia; Tomography, X-ray computed; Magneticresonance imaging