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Query: UMLS:C0011849 (diabetes)
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Vaccinations protect to a high degree against infectious diseases, but may cause side effects. In the Netherlands since 1962 the adverse events following immunizations are registered and analysed by the National Institute of Health and Environment (RIVM). Since 1983 a permanent Committee of the Dutch Health Council reviews adverse events reported to the RIVM. With the so-called killed vaccines the side effects are mainly local (redness, swelling, pain) or general (fever, listlessness, irritability, sleep and eating problems). They are seen mainly after DPT-IPV vaccination against diphtheria, pertussis, tetanus and poliomyelitis. Some side effects occur rarely (collapse reactions, discoloured legs, persistent screaming and convulsions) and very rarely serious neurological events are reported. After MMR vaccination against measles, mumps and rubella, cases of arthritis, thrombocytopenia and ataxia are reported sporadically. Usually, they have a spontaneous recovery. During recent years a scala of diseases or symptoms have been associated with vaccination (presumed side effects). Careful and extensive investigations have shown that such hypotheses could not be supported. Examples are allergic diseases as asthma, diabetes mellitus, multiple sclerosis (after hepatitis B vaccination), autism and inflammatory bowel disease (after MMR vaccination) and sudden infant death syndrome. The total number of cases where at least a possible relation between side effects and vaccination is observed--apart from local reactions and moderate general symptoms--is very rare (about 0.25 per 1000 vaccinations) and does not balance the benefits from vaccination. There appears increasing doubt about the use and safety of vaccinations. More research is needed about the motives of people to choose for and against vaccination. The education about vaccination for parents and professionals who are involved with vaccination has to be improved. Internet can play an important role.
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PMID:[Childhood vaccinations anno 2004. II. The real and presumed side effects of vaccination]. 1503 89

Diabetes in childhood is the most common chronic disease and generally fits the type 1 category, even though other forms of non-autoimmune diabetes are now emerging in this age. At variance with adults, children and adolescents undergo physiological process, which may frequently require adjustments of clinical management of diabetes. Moreover, the hormonal and psychological changes during puberty may be crucial in conditioning management. Furthermore, common illnesses frequently affecting children may also destabilise metabolic control. Consequently, education in children is the cornerstone of treatment. This review focuses on the several and peculiar aspects of practical management of diabetes in paediatric age, which require professional figures such as paediatricians, nurses, dieticians, psychologists, social assistants originally trained in paediatric area, able to deal with the age-related medical, educational, nutritional and behavioural issues of diabetes.
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PMID:Management of diabetes in childhood: are children small adults? 1515 92

Hypoglycemia is a common side effect of intensive insulin therapy in patients with type 1 diabetes. Mild hypoglycemia is any episode that can be self-treated, while a severe episode requires external help for recovery. Acute hypoglycemia produces autonomic and neuroglycopenic symptoms, including cognitive impairment and mood changes, while sympathoadrenal stimulation can provoke acute hemodynamic changes with alterations in regional vascular perfusion and a risk of cardiac dysrhythmias. Neurological manifestations include coma, convulsions and focal abnormalities. Long-term morbidities associated with hypoglycemia include impaired awareness of hypoglycemia, counterregulatory hormonal deficiencies, hypoglycemia-associated autonomic failure, and, in rare cases, permanent cognitive impairment. Hypoglycemia affects all aspects of life for the person with type 1 diabetes, including employment, social interactions, driving, sport and leisure activities, and sleep. Appreciation of the potential morbidities of hypoglycemia should encourage physicians to utilize therapeutic regimens that decrease the risk of severe hypoglycemia.
Diabetes Res Clin Pract 2004 Sep
PMID:Morbidity of hypoglycemia in type 1 diabetes. 1531 71

Psychological aspects and patients' acceptance of type 1 diabetes (DM1) may exercise some influence in their glycemic control. In this project the influence of psychological aspects were evaluated on glycemic control of DM1 patients. A retrospective study of participants from Diabetes Weekend (DW), an educational project in DM1 was carried out in Minas Gerais. In a sample of 150 subjects (66M/84F, 21.6+/-13.5 years and duration of DM of 8.5+/-7.9 years) we analyzed: type of insulin, insulin delivery, insulin dose per day and insulin dose per day in DW, psychological profile, capillary glycemia and previous history of convulsion crisis, severe hypoglycemia or diabetic ketoacidosis (CAD). Glucose was monitored 4 times a day by a digital glucose monitor. 20.9% of the patients with DM1 felt very well (G1); 39.5% well (G2), 25.6% with difficult glycemic control (G3), 9.3% trying to accept (G4) and 4.7% reported to be very bad about their DM1. The average capillary glycemia (ACG, in mg/dl) was significantly lower in G1 than in the others (169.8; G2: 182.3; G3: 199.3; G4: 200.7). There were no significant association of this psychological aspects and previous history of CAD, hypoglycemia or convulsion crisis. DM1 duration over 5 years was associated to lower acceptance of the disease (p= 0.017) and age of patients (p= 0.000). 13.9% of patients reported to be ashamed of their disease; the ACG was significantly higher in this group as compared to others (246.2 vs. 178.1; p= 0.007). In 91 patients (60.4%) who mention to have apprehension of feeling sick in public the ACG was significantly higher (200.4 vs. 184.5; p= 0.014). The systematic glucose monitoring showed positive association between psychological aspects and worse glycemic control. The psychological and multidisciplinary approach of DM1 patients is very important to try to improve the metabolic control, to prevent future complications, which results in better quality of life for these patients.
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PMID:[Psychological aspects and blood glucose control of a type 1 diabetes mellitus group from Minas Gerais]. 1564 Aug 81

Caffeine is a mild central nervous stimulant that occurs naturally in coffee beans, cocoa beans and tea leaves. In large doses, it can be profoundly toxic, resulting in arrhythmia, tachycardia, vomiting, convulsions, coma and death. The average cup of coffee or tea in the United States is reported to contain between 40 and 150 mg caffeine although specialty coffees may contain much higher doses. Over-the-counter supplements that are used to combat fatigue typically contain 100-200 mg caffeine per tablet and doses of 32-200mg are included in a variety of prescription drug mixtures. Fatal caffeine overdoses in adults are relatively rare and require the ingestion of a large quantity of the drug, typically in excess of 5 g. Over a period of approximately 12 months our office reported two cases of fatal caffeine intoxication. In the first case, the femoral blood of a 39-year-old female with a history of intravenous drug use contained 192 mg/L caffeine. In the second case, femoral blood from a 29-year-old male with a history of obesity and diabetes contained 567 mg/L caffeine. In both cases, the cause of death was ruled as caffeine intoxication and the manner of death was accidental.
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PMID:Fatal caffeine overdose: two case reports. 1593 84

A 20-year-old male was admitted to emergency room with convulsion. He had insulin-dependent diabetes mellitus for 8 years. He had suffered nocturnal hypoglycemia after strenuous exercise without additional calories. After recovery, the patient complained of bilateral anterior shoulder dislocation. Patient's history revealed another episode of bilateral shoulder dislocations after an hypoglycemic convulsion 3 years ago.
Diabetes Res Clin Pract 2006 Mar
PMID:Recurrent bilateral dislocation of the shoulders due to nocturnal hypoglycemia: a case report. 1612 71

The World Health Organization defines sexual health as "a state of physical, emotional, mental and sexual well-being related to sexuality." This broad definition goes beyond simply inquiring about sexual dysfunction and ideally fits the model of patient-centered primary care. As we observe that sexual health and physical health are often closely related, discussions about sexual activity can be very revealing. Sexual intimacy appears positively related to loving relationship satisfaction and stability. Sexual problems have a clear negative impact on both the quality of life and emotional state regardless of age. Learning about specific sexual dysfunctions among men can reveal a variety of as-yet-undiagnosed comorbid pathologic conditions such as: (i) depression and other emotional illnesses; (ii) psychosocial stress; (iii) actual cardiovascular disease as well as related risk factors such as hypertension, diabetes, and/or hyperlipidemia; (iv) hyperprolactinemia; and (v) low serum testosterone. Specific sexual dysfunctions among women can reveal pathologic conditions such as: (i) depression and other adverse imitational and psychosocial conditions; (ii) low serum estrogen or testosterone; and/or (iii) vaginal or pelvic disorders. A discussion about sexual health can be accomplished efficiently in a primary care office with the inquiring clinician having the option to deal with any sexual problems and dysfunctions directly, or to refer the patient to an appropriate specialized care source.
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PMID:Sexual health inquiry and support is a primary care priority. 1640 13

A 45-yr old diabetic patient, who had received a diagnosis of grand mal epilepsy, for two episodes of nocturnal tonic-clonic convulsions, underwent continuous glucose monitoring (CGM). During CGM, the patient had an episode of tonic-clonic convulsion, and at the same time a prolonged nocturnal hypoglycemia (<2.2 mmol/l) was observed. CGM revealed that tonic-clonic convulsions, which had been interpreted as a manifestation of epilepsy, were in fact a symptom of severe hypoglycemia. In order to assess the pathogenesis of hypoglycemia, the patient underwent a 75-g oral glucose tolerance test, that was interrupted shortly afterwards for hypoglycemic symptoms (i.e., reactive hypoglycemia). To our knowledge, this is the first case ever reported of reactive hypoglycemia associated with Type 2 diabetes.
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PMID:Seizures as the only clinical manifestation of reactive hypoglycemia: a case report. 1641 98

Clinical studies conducted since the 1970s by the pediatric diabetology group of the Free University of Brussels have demonstrated that screening for subclinical retinopathy, neuropathy and nephropathy should be started at puberty and at least 3 years after the diabetes diagnosis. The goal is to detect early abnormalities responsible for subclinical disorders that can be reversed by improved metabolic control, thus preventing the occurrence of irreversible potentially incapacitating lesions. A 1974 retinal fluorescein angiography study showed that the development of microaneurysms, which are irreversible lesions, could be preceded by fluorescein leakage due to disruption of the blood-retinal barrier. Risk factors for early retinopathy include: duration of diabetes, age at diagnosis (with younger children having longer times to retinopathy), puberty and sex (with onset one year earlier in girls than in boys), long-term bad metabolic control over several years, high cholesterol levels and excessive body mass index (BMI). On the other hand, rapid improvement of diabetic control may worsen diabetic retinopathy (1985). Minimal EEG abnormalities were found in relationship to frequent and severe hypoglycemic comas and/or convulsions and retinopathy (1979). Desynchronization of action potentials in distal nerve fibers preceded conduction velocity slowing (1981). A single high glycated hemoglobin value was associated with peroneal motor nerve conduction slowing (1985), which was not observed in the femoral nerve (1987). Sympathetic skin response (1996) and statistical analysis of heart rate variability (2001) could have some interest for the diagnosis of early diabetic autonomic neuropathy. Early microproteinuria is of mixed origin, being both glomerular (microalbumin) and tubular (Beta2-microglobulin). Exercise testing to exhaustion did not provide additional information than the basal excretion (1976). Microtransferrinuria (1984) and urinary acid glycosaminoglycans output (2001) could also be predictive markers of glomerular dysfunction. Physical training reduced exercise-related proteinuria by half (1988). High levels of serum lipoprotein (a) were not associated with the presence of subclinical complications (1996). On the other hand, ultra sensitive C-reactive protein could be an interesting indicator for the risk of developing early complications (2002). Poor metabolic control was associated with higher levels of triglycerides, total cholesterol, LDL cholesterol and apolipoprotein B (1990). Decreased gluthatione peroxidase, gluthatione reductase and of vitamin C levels, denoting moderate oxidative stress, were found (1996), although there was no evidence of increased LDL cholesterol peroxidation (1998). Erythrocytes exhibited increased glycolytic activity and neutrophils decreased migration in relationship with metabolic control (1992). The degree of metabolic control influenced serum triiodothyronine levels (1985), magnesium concentrations (1999) and infection by Helicobacter Pylori (1997). Insulin therapy could activate the complement pathway if intermediate and long-acting insulin preparations without protamine sulphate are used (1992) and provoke higher BMI in adolescents on 4 insulin injections (1988). Well-being was inversely related to glycated hemoglobin levels (1997).
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PMID:Screening for subclinical complications in young type 1 diabetic patients: experience acquired in Brussels. 1643 30

This chapter describes a physiological and profound effect of amylin to inhibit meal-related glucagon secretion. Glucagon is processed from a large precursor, proglucagon, in a tissue-specific manner in pancreatic alpha-cells. In addition to amino acid nutrient stimuli, glucagon is also secreted in response to stressful stimuli, such as hypoglycemia and hypovolemia. Glucagon primarily acts on liver to initiate glycogenolysis and gluconeogenesis, resulting in a rapid increase in endogenous production of glucose. With longer stimulation, glucagon action at the liver results in a glucose-sparing activation of free fatty acid oxidation and production of ketones. During hypoglycemia, glucagon secretion is clearly a protective feed-back, defending the organism against damaging effects of low glucose in brain and nerves (neuroglycopenia). Amino acid-stimulated glucagon secretion during meals has a different purpose: amino acids stimulate insulin secretion, which mobilizes amino acid transporters and effects their storage in peripheral tissues. At the same time, insulin obligatorily recruits GLUT4 glucose transporters in muscle and fat. The hypoglycemic potential of such GLUT4 mobilization is averted only by the simultaneous liberation of endogenous glucose in response to feedforward (anticipatory) glucagon secretion. The effect of amylin and its agonists to inhibit amino acid-stimulated glucagon secretion is both potent (EC50 = 18 pM) and profound (approximately 70% inhibition). This glucagonostatic action appears to be extrinsic to the pancreatic islet, occurring in intact animals and in patients, but not in isolated islets or isolated perfused pancreas preparations. On the other hand, the effect of hypoglycemia to stimulate glucagon secretion, which is intrinsic to the islet and occurs in isolated preparations, is not affected by amylin or its agonists. The physiological interpretation of these actions fits with the general concept, illustrated in Fig. 1, that amylin and insulin secreted in response to meals shut down endogenous production as a source of glucose, in favor of that derived from the meal. Amylin and insulin secreted in response to nutrients already absorbed act as a feedback switch for glucose sourcing. The insulinotropic (incretin) gut peptides, GLP-1 and GIP, secreted in response to yet-to-be-absorbed intraluminal nutrients, amplify beta-cell secretion and thereby activate the glucose sourcing switch in a feedforward manner. Hypoglycemia-stimulated glucagon secretion and nutrient (amino acid)-stimulated glucagon secretion are two clearly different processes, differently affected by amylin. The balance of glucose fluxes is disturbed in diabetic states, partly as a result of inappropriate glucagon secretion. Although glucose production due to glucagon secreted in response to hypoglycemia is normal or even reduced in diabetic patients, the secretion of glucagon (and production of endogenous glucose) in response to protein meals is typically exaggerated. Absence of appropriate beta-cell suppression of alpha-cell secretion has been invoked as a mechanism that explains exaggerated glucagon responses, especially prevalent in patients with deficient beta-cell secretion (type 1 diabetes and insulinopenic type 2 diabetes). A proposed benefit of insulin replacement therapy is the reduction of absolute or relative hyperglucagonemia. High glucagon is said to be necessary for ketosis in severe forms of diabetes. A further benefit of reversing hyperglucagonemia is reduction of the excessive endogenous glucose production that contributes to fasting and postprandial hyperglycemia in diabetes. The idea that amylin is a part of the beta-cell drive that normally limits glucagon secretion after meals fits with the observation that glucagon secretion is exaggerated in amylin-deficient states (diabetes characterized by beta-cell failure). This proposal is further supported by the observation that postprandial glucagon suppression is restored following amylin replacement therapy in such states. These observations argue for a therapeutic case for amylin replacement in patients in whom excess glucagon action contributes to fasting and postprandial hyperglycemia and ketosis. The selectivity of amylin's glucagonostatic effect (wherein it is restricted to meal-related glucagon secretion, while preserving glucagon secretion and glucagon action during hypoglycemia) may confer additional benefits; the patient population amenable to amylin replacement therapy is likely to also be receiving insulin replacement therapy, and is thereby susceptible to insulin-induced hypoglycemia. Most explorations of the biology of amylin have used the endogenous hormone in the cognate species (typically rat amylin in rat studies). Clinical studies have typically employed the amylinomimetic agent pramlintide. Studies of amylinomimetic effects on glucagon secretion include effects of rat amylin in anesthetized non-diabetic rats (Jodka et al., 2000; Parkes et al., 1999; Young et al., 1995), effects of rat amylin in isolated perfused rat pancreas (Silvestre et al., 1999), effects of pramlintide in anesthetized non-diabetic rats (Gedulin et al., 1997b,c,d, 1998), effects of pramlintide in patients with type l diabetes (Fineman et al., 1997a,b,c,d, 1998a; Holst, 1997; Nyholm et al., 1996, 1997a,b,c; Orskov et al., 1999; Thompson and Kolterman, 1997), and effects in patients with type 2 diabetes (Fineman et al., 1998b). In addition, effects of amylin antagonists have been observed in isolated preparations (Silvestre et al., 1996), and effects of antagonists or neutralizing antibody have been determined in whole-animal preparations (Gedulin et al., 1997a,e,f).
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PMID:Inhibition of glucagon secretion. 1649 45


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