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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.
Diabetes 1998 Dec
PMID:Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment. 983 23

We treated two cases of diabetes mellitus who developed acute pulmonary edema following accidental aspiration of sweetened water for emergency treatment, when they had fallen into hypoglycemic coma following an overdose of injectable insulin. Although they showed hypoxemia and radiological examinations revealed pulmonary edema, they improved by giving only oxygen and antibiotics in a few days. The osmotic pressure of the sweetened water in each case was approximately 2,600 mOsm and 1,900 mOsm. We suppose that the pathogenesis of the pulmonary edema was due to the sweetened water causing water within the pulmonary vessels to permeate into the alveoli.
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PMID:Acute pulmonary edema caused by accidental aspiration of sweetened water in two cases of diabetes mellitus. 986 63

A 77-year-old man with type II diabetes taking a stable dose of subcutaneous, twice daily human insulin developed symmetrical, inflammatory, rheumatoid factor positive polyarthritis. Within 2 weeks of starting therapy with prednisone 5 mg daily and hydroxychloroquine 400 mg daily he had 2 episodes of severe hypoglycemic coma requiring emergency care. His blood glucose became controlled again when his insulin was decreased by 37%. There are no reported cases of hypoglycemia in diabetic or nondiabetic patients treated with hydroxychloroquine. Hydroxychloroquine has been reported to reduce insulin requirements in refractory type II diabetes by an average of 30%. When hydroxychloroquine is initiated for the treatment of polyarthritis in a type II diabetic requiring insulin or sulfonylurea treatment, blood glucose levels should be monitored closely and the insulin dose may need to be reduced.
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PMID:Hypoglycemia induced by hydroxychloroquine in a type II diabetic treated for polyarthritis. 991 62

The treatment of patients with type 1 diabetes mellitus has to focus on short-term and long-term risks of the disease which means to avoid hyperglycemic or hypoglycemic coma as well as late complications. As we know from the DCCT study metabolic control substantially lowers the risk for retinopathy, nephropathy and neuropathy. We also know, that keeping the blood glucose in a nearly normal range inevitably is connected with a marked increase of severe hypoglycemia, an event which occurs more frequently when normoglycemia has been reached and the further slow decline of blood glucose is not recognized by the patient (autonomous neuropathy, hypoglycemia unawareness of other origin, long duration of diabetes etc.). Furthermore, counterregulatory hormones as glucagon and epinephrine may be lacking due to diminished or even lost alpha cells within the islets and as recently observed due to fibrosis of the adrenal medulla in long-term diabetes. The consequences of severe hypoglycemia are manifold: in the actual situation of unconsciousness the risk of heavy injuries and as long-term consequences irreversible brain damage may occur. Finally, the effort of the patient to reach normoglycemia includes the burden of an intensive blood glucose self-control day by day. This broad scenario of all the achievements and of all the problems connected with an intensified insulin treatment has to be regarded when the indication for an islet transplant will be discussed. From our point of view as clinicians it seems adequate not to give definite recommendations but to express our considerations for islet transplantation in patients with type 1 diabetes mellitus with the following list (table 1). It must be clearly stated, that at present transplantation of isolated islets by no means can serve as a treatment for a larger number of patients and this may hold through also for the foreseeable future. In this context, also the many contraindications should be summarized (table 2). Consequently we have to deal with several questions and problems which can be subdivided into those regarding the possible benefit for the patients from an islet graft (full success = insulin independence, partial success = lower exogenous insulin requirement due to additional endogenous insulin, measured by C-peptide levels, more stable glucose metabolism) and those regarding possible side effects (primary risk of implantation, threat for rejection of the primarily transplanted kidney). Furthermore, one may ask for risks when islets are transplanted alone (ITA). We therefore will address the following areas: 1. Simultaneous islet and kidney transplants 2. Islet transplants after kidney transplantation alone (IAK) 3. Islet transplantation after pancreas transplantation failure (P-failure) 4. Defect hypoglycemia counterregulation--life threatening hypoglycemia unawareness as indication for islet transplantation? 5. Autonomous cardiac neuropathy as indication for islet transplantation? 6. Significant clinical problems with exogenous insulin therapy as indication for islet transplantation?
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PMID:Indications for clinical islet transplantation today and in the forseeable future--the diabetologist's point of view. 993 Sep 51

The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.
Diabetes Res Clin Pract 2000 Feb
PMID:Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma. 1067 Sep 9

Localized fibrous tumor of the pleura is a rare, slowly growing, benign tumor which originates from the submesothelial stem cells of the pleura visceralis. Most of these tumors clinically behave asymptomatically, although tumor-associated hypoglycemia occurs in a few cases and can lead to hypoglycemic coma. Laboratory investigations show significant elevation of paraneoplastic IGF-II with a 2-3 times higher effect on the blood glucose level than insulin. Further, one finds reduced synthesis of IGFBP-3, which inhibits the action of IGF-II by inducing a complex with the paraneoplastic protein. As treatment, surgical resection of the tumor is recommended. We report on the case of a 72-year-old man with diabetes mellitus type II, who complained of recurrent hypoglycemic episodes. Diagnostic evaluation showed a fibrous tumor attached to the right diaphragm. After surgical treatment the hypoglycemic episodes disappeared.
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PMID:[Paraneoplastic hypoglycemia in localized fibrous tumors of the pleura]. 1119 68

Life style has to be adapted to insulin regimens in conventionally intensified insulin therapy. Functional insulin therapy (FIT) allows for flexible adjustments to changing insulin requirements. FIT is based on separating the substitution of basal, meal dependent and correction insulin by the patient. The patient has to acquire special knowledge. We here report longitudinal data of 183 patients out of 221 patients who have been educated by FIT outpatient programs in the years 1990 to 1996. The 3 month FIT education program consisted of sixteen hours in total. Five and a half hours were held in a whole day preparation seminar and the other seven hours in evening sessions each of 90 minutes duration. Prior to FIT education patients were treated by intensified conventional insulin therapy. Mean glycosylated hemoglobin prior to FIT education was 7.0% (normal range 3.7-5.6%). After FIT education glycosylated hemoglobin remained unchanged. However, the percentage of patients experiencing severe hypoglycemic episodes (stupor and coma) in a one year course was significantly reduced from 26% prior to FIT education to 14% after FIT education--hypoglycemic coma was reduced from 13% to 7% respectively. Thus, we can report that FIT reduces the risk of severe hypoglycemia. We believe that our data should stimulate the broad supply of FIT education programs available to diabetes patients in Switzerland.
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PMID:[Reduction of severe hypoglycemia by functional insulin therapy of type I diabetes mellitus]. 1184 13

A 56-year-old woman with diabetic triopathy, rheumatoid arthritis and chronic renal failure was admitted for severe hypoglycemic coma. Arthralgia had been deteriorating for 6 months. Therefore, 5 mg of prednisolone was administered. Postprandial blood glucose (PPG), however, elevated from 260 to 290 mg/dl, although fasting blood glucose (FBG) levels ranged from 80 to 110 mg/dl. Three months after, 270 mg of nateglinide was given in addition to acarbose. After 2 days, hypoglycemia occurred at 02:00 h. Nateglinide was then decreased to 180 mg (before breakfast and lunch). After 5 days, hypoglycemia re-occurred at 01:00 h. Nateglinide was subsequently decreased to 90 mg before breakfast. The PPG levels ranged from 130 to 150 mg/dl. Hypoglycemia did not occur during the next 2 months. On admission, FBG; 59 mg/dl, fasting immunoreactive insulin; 34 microU/ml, indicated hyperinsulinemic hypoglycemia. We administered 20 g of glucose intravenously, however, hypoglycemia recurred 4 times and 20 g of glucose was then administered. Although the plasma nateglinide level decreased, the nateglinide metabolite, N-[trans-4-(1-hydroxy-1methylethyl)-cyclohexanecarbonyl]-D-phenylalanine levels still had not decreased 29 h after nateglinide administration. Therefore, chronic renal failure appeared to alter the pharmacokinetic parameters of the nateglinide metabolite, which had accumulated by chronic renal failure. The nateglinide metabolite caused severe hypoglycemia in this case.
Diabetes Res Clin Pract 2003 Mar
PMID:Hypoglycemia due to nateglinide administration in diabetic patient with chronic renal failure. 1259 15

The pharmacology, clinical efficacy, adverse effects, drug interactions, and place in therapy of bitter melon are described. Bitter melon (Momordica charantia) is an alternative therapy that has primarily been used for lowering blood glucose levels in patients with diabetes mellitus. Components of bitter melon extract appear to have structural similarities to animal insulin. Antiviral and antineoplastic activities have also been reported in vitro. Four clinical trials found bitter melon juice, fruit, and dried powder to have a moderate hypoglycemic effect. These studies were small and were not randomized or double-blind, however. Reported adverse effects of bitter melon include hypoglycemic coma and convulsions in children, reduced fertility in mice, a favism-like syndrome, increases in gamma-glutamyltransferase and alkaline phosphatase levels in animals, and headaches. Bitter melon may have additive effects when taken with other glucose-lowering agents. Adequately powered, randomized, placebo-controlled trials are needed to properly assess safety and efficacy before bitter melon can be routinely recommended. Bitter melon may have hypoglycemic effects, but data are not sufficient to recommend its use in the absence of careful supervision and monitoring.
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PMID:Bitter melon (Momordica charantia): a review of efficacy and safety. 1262 17

A 46-year-old woman with a nine-year history of diabetes mellitus (DM) without treatment had an acute onset of right hemiballism. For the treatment of hyperglycemia (random blood sugar 588 mg/dl) conventional insulin therapy was started, and HbA1c rapidly decreased from 16.3% to 8.8% over the first two months. During this period, there were no hypoglycemic symptoms or episodes, though amnesia appeared just after the insulin therapy was started. T1-weighted MRI showed hyperintensity in the left basal ganglia, which has been reported in many cases of chorea or ballism associated with DM. In addition, there were unique changes in the left temporal lobe, including transient contrast enhancement along the cortex followed by transient hyperintensity in the cortical-subcortical area on T2 weighted and FLAIR images, and then hyperintensity along the cortex on T1 weighted images and atrophy. These findings were thought to indicate a consecutive process, i.e., capillary hyperlucency followed mainly by vasogenic edema and then laminar necrosis. Similar MR findings were reported in hypoglycemic coma. MRA also revealed a transient vasospasm in the left MCA M1-M2 portions in this patient. These signal changes may have been related to the prolonged hyperglycemic state as well as blood sugar control that was too rapid.
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PMID:[Abnormal MR findings in the temporal lobe and basal ganglia along with vasospasm in a case of hemiballism associated with diabetes mellitus]. 1450 51


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