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Symptomatic hypoglycemia developed 5 to 45 months after transplantation in nine children who had renal transplants before 6 years of age. During hypoglycemia, serum glucose levels ranged from 14 to 39 mg/dl (0.8 to 2.1 mmol/L). Hypoglycemic episodes occurred between 1.7 and 7.5 years of age. Six patients had generalized seizures; the remaining three had diaphoresis with stupor or lethargy. None of the children had serious infections, diabetes, congenital defects of glucose metabolism, or a history of treatment with insulin or oral hypoglycemic agents. Six patients had hypoglycemic symptoms after a prolonged fast, and at least four had ketosis. Eight of the nine patients were receiving propranolol when hypoglycemia occurred. No differences in the daily prednisone dose, the number of transplant rejection episodes, or the frequency of treatment with medications other than propranolol were noted between hypoglycemic patients and 56 normoglycemic age-matched renal transplant recipients. All hypoglycemic patients were subsequently treated with frequent feedings and discontinuation of propranolol. No further hypoglycemic episodes have occurred in eight of nine patients. Symptomatic hypoglycemia should be recognized as a potentially devastating complication of pediatric renal transplantation.
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PMID:Hypoglycemia in pediatric renal allograft recipients. 305 55

The effects of pregnancy on acute metabolic complications of diabetes may have important consequences for both mother and fetus. The consequences of pregnancy for chronic complications of diabetes, including retinopathy, nephropathy, neuropathy, and hypertension, are not clear. Recent data are reviewed so that health care providers will be able to provide reasonable advice to insulin-dependent diabetic women contemplating pregnancy both for problems that may potentially arise during gestation and those that may affect long-term health and survival. Diabetic ketoacidosis is an uncommon problem that arises during gestation. Acute alterations in pH and electrolyte concentrations as well as hyperglycemia, however, may have important consequences for mother and fetus, including perinatal asphyxia and reduced fetal oxygen delivery. Hypoglycemia, on the other hand, may result in maternal coma or seizures and, when frequent, has been associated with infant respiratory distress syndrome. Background retinopathy often worsens during gestation, with regression common postpartum. Data suggest that progression of background disease is related to both glycemic control and the acute institution of intensive insulin therapy with those patients with poor control requiring more aggressive therapeutic intervention most adversely affected. The course of proliferative retinopathy is more variable, with both progression and regression reported. Preconception photocoagulation may prevent progression. Preconceptional ophthalmologic evaluation with frequent assessments during pregnancy is advised. Increases in 24-hour protein excretion are common during gestation in patients with preexisting renal disease and resolve in many patients postpartum. Serum creatinine and creatinine clearance increase during the first trimester and generally do not change during the remainder of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of pregnancy on complications of insulin-dependent diabetes mellitus. 313 6

Ketoacidosis is one of the common complications of Type I insulin-dependent diabetes mellitus. Several neurologic (cerebral) deficiencies have been associated with diabetic ketoacidosis, including cerebral edema with increased intracranial pressure resulting in coma; partial and generalized seizures; and cerebrovascular occlusive disease resulting in motor and/or sensory dysfunction. Intracerebral hematomas have not been reported. A child is described who had insulin-dependent diabetes mellitus with hyperglycemic ketoacidosis who developed multiple spontaneous intracerebral hematomas. Possible mechanisms are discussed.
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PMID:Spontaneous intracerebral hematomas in juvenile diabetic ketoacidosis. 315 Feb 80

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Convulsions may occur as a consequence of insulin-induced hypoglycaemia. We report three patients with insulin-dependent diabetes, who presented with generalized tonic-clonic seizures associated with nocturnal hypoglycaemia. None of the patients had experienced hypoglycaemia during waking hours and the convulsions were mistakenly diagnosed as idiopathic epilepsy. Recognition of the possible hypoglycaemia aetiology of these convulsions permitted appropriate alteration of the insulin regimens with no recurrence of convulsions. In one case, the seizure was associated with bilateral fractures of the neck of the humerus. Unrecognized hypoglycaemia should be considered as a possible cause of convulsions in insulin-dependent diabetic patients.
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PMID:Nocturnal convulsions and insulin-induced hypoglycaemia in diabetic patients. 342 71

Recognized risk factors for metrizamide myelography are seizure disorder, seizure-threshold-lowering drugs, dehydration, and possibly age. After observing serious neurologic complications in diabetic patients after routine metrizamide myelography, a retrospective study was conducted to determine if diabetes should be considered another independent and important risk factor. Forty-one diabetic patients who had lumbar metrizamide myelograms were compared with a control group of 110 nondiabetic patients. A significantly higher incidence was found of severe vomiting (15% vs. 3%, p less than 0.01) and neurologic complications (20% vs. 2%, p less than 0.001) in the diabetic population. Neurologic complications included one case each of seizure, severe encephalopathy, auditory and visual hallucinations, and prolonged somnolence and four cases of confusion-anxiety. Four of the diabetic patients had major transient elevations of blood pressure. These findings suggest that diabetics are a high-risk population for metrizamide myelography. The dose of metrizamide should be minimized, whenever possible. The new nonionic myelographic agents may prove to be safer in this population, but caution and careful follow-up should be exercised in the initial trials with these patients.
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PMID:Neurologic complications in diabetics after metrizamide lumbar myelography. 348

This article deals with the use of oral contraceptives and IUDs by chronically ill adolescent females. Results of controlled studies of contraceptive choices and problems are reviewed for teenagers with cardiac disease, epilepsy, multiple sclerosis, migraine headaches, asthma, cystic fibrosis, inflammatory bowel disease, hepatitis, diabetes mellitus, thyroid disease, oligomenorrhea and amenorrhea. If oral contraceptives (OC) are prescribed for use in teens with cardiac disease, a contraceptive with 35ug or less of estrogen and the equivalent of 1 mg or less of norethindrone should be used. The low-dose progestin only pill can be prescribed, but should be used in conjunction with a back-up barrier method. Reports to date have failed to reveal increased seizure activity in epileptic pattients on OCs, and there is no significant evidence to date that OCs alter the course of multiple sclerosis. Although the evidence is inconclusive, the physician should use extreme caution in prescribing OCs for teens with prior migraines. Regarding asthmatic patients, no problems have been reported with IUD use except in regard to steroid therapy and its possible effect on reducing IUD effectiveness. No adverse effects 2ndary to the use of OCs in asthmatic patients have been reported. OCs should be avoided or used with extreme caution in the cystic fibrosis patient. Teens with active inflammatory bowel disease should be advised that OCs may be ineffective or dangerous; there are no reports available on the effects of the IUD on the disease. The pill is contraindicated during active liver disease or cirrhosis. The IUD is not highly recommended for contraception in diabetic teenagers, whereas a low-dose combined OC can be used with extreme caution. However, OCs should be avoided in the diabetic patient with nephropathy, vascular complications or retinopathy. There is at present no contraindication for contraceptive use by women with thyroid disease. Finally, patients with prolonged post pill amenorrhea and infertility are generally females with amenorrhea or oligomenorrhea before pill use.
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PMID:Contraceptive use in the chronically ill adolescent female: Part I. 351 58

A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.
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PMID:[Neonatal hypoglycemia caused by hyperinsulinism and subsequent epilepsy]. 357 76

A new clinical entity that is prevalent in young type I (insulin-dependent) diabetic patients, postexercise late-onset (PEL) hypoglycemia, is described. A prospective case-finding study suggested that PEL hypoglycemia occurred in 48 of approximately 300 diabetic type I patients who were diagnosed as diabetic before age 20 yr and who were monitored for up to 2 yr. Typically, hypoglycemia was nocturnal and occurred 6-15 h after the completion of unusually strenuous exercise or play. In more than half the cases the hypoglycemia resulted in loss of consciousness or seizures and necessitated treatment with subcutaneous glucagon or intravenous glucose and/or attendance by a health professional. The hypoglycemia was not limited to patients in good or excellent metabolic control and often occurred after a single bout of exercise in patients unaccustomed to exercise or in athletic patients who were making the transition from an untrained to a trained state. Surprisingly, 12 of the patients who experienced nocturnal PEL hypoglycemia were not using significant amounts of insulin that peaked at night. Type I diabetic patients should be made aware of the possibility of PEL hypoglycemia to enable them to make adjustments in their management plans in anticipation of unusually strenuous exercise, so that they may attempt to minimize or avoid late-onset hypoglycemia.
Diabetes Care
PMID:Postexercise late-onset hypoglycemia in insulin-dependent diabetic patients. 367 76

In a retrospective study the reports of 211 cases of cardiogenic cerebral embolism--diagnosed on the base of neurological and cardiological findings--were analyzed in view of signs and findings of prognostic value. There were 21 patients with TIA, 39 cases of RIND and 151 patients with cerebral infarction, 60 of which showed mild and 91 severe neurological symptoms. 38 patients died during the period of hospitalization. While sex of the patients as well as vascular risk factors (hypertension, diabetes mellitus, cigarette smoking) did not influence the clinical course of the disease, patients with TIA or RIND in general were younger (about 5 years) than those with severe stroke. Prognosis of cardiogenic cerebral embolism depended to a great degree on the underlying heart disease. Cerebral embolism after myocardial infarction showed a better remission of symptoms than embolism in atrial fibrillation. In the group of valvular diseases the course of embolic strokes in mitral lesions was worse than in aortal valve disease. Prognosis was worst in endocarditis, both in view of neurological deficit and of mortality. Mostly, the cardiogenic emboli lead to infarctions of the middle cerebral artery territory (78 per cent) with a predilection for the left hemisphere. In media-syndromes the clinical course was significantly worse in patients with additional homonymous visual defect compared to incomplete infarctions. Initial disturbance of conscience reduced prognosis quoad vitam et restitutionem significantly. Of the neuroradiological findings, the detection of arterial occlusion or circulatory disturbance in angiography as well as the finding of an ischemic lesion in computed axial tomography (CAT) was correlated with a severe course of the embolic stroke. While 7 patients with hemorrhagic infarction in CAT-Scan showed no differences in the clinical course, the 14 patients with pathological cerebral spinal fluid findings in embolism had an unfavourable prognosis. The development of epileptic seizures did not influence the further course of the infarction to a significant extent. Results are compared with the current world literature.
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PMID:[Prognosis of cardiogenic cerebral embolism]. 374 66


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