Adrenergic Symptoms Research Articles

Altered recognition of hypoglycaemic symptoms in type I diabetes during intensified control with continuous subcutaneous insulin infusion.

The effect of intensified metabolic control obtained with continuous subcutaneous insulin infusion (CSII) on the frequency and symptoms of hypoglycaemia was studied in type I diabetic patients. The reproducibility of the questionnaire used to evaluate the hypoglycaemic symptoms was verified in a control group receiving unchanged conventional insulin therapy for 2 months. Metabolic control was significantly improved during CSII (HbA1c 6.8 +/- 0.4% versus 8.7 +/- 0.7%, normal range up to 5.4%) in all patients while no change was seen in the control group. The results of frequent self glucose monitoring showed that the incidence of low glucose levels (below 3.5 mmol/l) increased about threefold in the CSII group. Awareness of hypoglycaemia was clearly changed during CSII with less pronounced adrenergic symptoms while no alterations were found in the group with unchanged metabolic control. These results emphasize the importance of regular self glucose monitoring during CSII and of informing the patients that their hypoglycaemic symptoms may change during intensified control.

Effect of adrenergic agents on postgastrectomy hypoglycemia.

Reactive hypoglycemia was documented in ten postgastrectomy patients by a control oral glucose tolerance test (OGTT). Nine patients experienced nausea, flushing, and fatigue during the first hour of the test. Neuroglycopenic or adrenergic symptoms of hypoglycemia occurred in eight patients two to five hours after oral glucose. The oral administration of phenylephrine elixir, 15 mg., thirty minutes before a repeat OGTT, significantly raised thelowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 45.2 +/- 3.8 mg./dl. (p less than 0.05) but did not affect the occurrence of either the early or the late symptoms. In contrast, propranolol, 10 mg., raised the lowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 57 +/- 5.2 mg./dl. (p less than 0.02) and prevented the occurrence of early and late symptoms. Neither peak nor total plasma insulin levels were affected by either drug. The rate of glucose utilization, as determined by intravenous glucose tolerance tests, did not significantly change after the oral administration of either drug. It is concluded that propranolol ameliorated the symptoms and chemical hypoglycemia after oral glucose and merits more detailed study as a long-term therapy for this disorder.

Reactive hypoglycemia

The hypoglycemoses include a large category of distinctly unique entities. Guidelines for a clinical, physiological approach to these disorders is presented. Within this diagnostic spectrum of hypoglycemia lies the reactive hypoglycemic disorders that are characterized by their postprandial onset, adrenergic mediated symptoms, and relatively benign causes. The spectrum of reactive hypoglycemia includes early alimentary-reactive hypoglycemia, late diabetic-reactive hypoglycemia, hormonal deficiency states, and idiopathic hypoglycemia. A new postprandial hypoglycemic disorder, fructose 1–6 diphosphatase, can be added to this list. The frequent sampling of blood-glucose values in the postprandial state will frequently lead to the finding of a biochemically low blood-glucose value of below 50 ml 100 ml , and these individuals show no hypothalamic-pituitary-adrenal stress to the low blood sugar and do not manifest adrenergic symptoms. Their low blood-glucose value simply reflects the transition in intermediary metabolism between the fed and fasting state and provides a biochemical marker of this event. We refer to this asymptomatic biochemical event as transitional low blood-glucose state. It has no clinical implication and may frequently be confused with the bona fide reactive hypoglycemic disorders. Using a symptomatic, counter-regulatory model to define hypoglycemia as a bona fide disorder, findings are presented in patients with the varying types of reactive hypoglycemia, and their results are compared to normal controls and to a weight-matched and disease patient controls. Abnormalities in insulin secretion are discussed as relating to the pathophysiology causal in the hypoglycemia. An approach to therapy is presented based upon the classification of the patient as to the type of hypoglycemia and their abnormalities in insulin secretion.

The Heart and Hyperthyroidism: Use of Beta-Adrenergic Blocking Drugs

Many of the manifestations of hyperthyroidism are secondary to increased adrenergic activity. In recent years the beta adrenergic blocking drugs, as represented by d,1-propranolol, have become the agents of choice for ameliorating the adrenergic signs and symptoms of hyperthyroidism. Propranolol improves the tachycardia, tremor, restlessness, anxiety, and myopathy.

Systemic manifestations of neurogenic tumors

Summary 1. Patients with neurogenic tumors (neuroblastoma, ganglioneuroblastoma, and ganglioneuroma) may secrete catecholamines and/or their degradation products in the urine. These patients may also exhibit symptoms and signs presumably ascribable to effects of the catecholamines. It is not known how many patients with these tumors elaborate catecholamines or how often these symptoms and signs are present. 2. The occurrence of adrenergic symptoms and signs and increased secretion of catecholamines is of practical importance in the diagnosis and management of this group of common and highly malignant tumors. 3. Increased elaboration of catecholamines may be detected either by measuring epinephrine or norepinephrine in the urine or their degradation products. VMA which is an important degradation product is measured with greater ease than its precursors. Excessive quantities in the urine are indicative that the tumor is elaborating catecholamines. 4. Hypertension, diarrhea, excessive sweating, flushing, pallor, rash, polyuria, and polydipsia are findings most characteristically associated with these tumors. 5. Considerable variation exists in thesymptomatology of patients with these tumors, possibly because of variability in the predominant metabolite of the catecholamine secreted by the tumor.