Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We demonstrated the existence in the retina of an argyrophilic perivascular membrane comparable in all respects to that which exists throughout the vascular system. We compared our findings by light microscopy with those previously reported. We identified, by electron microscopy, the normal general location of the network between the basal laminae of the glial and vessel cells and demonstrated its selective staining with silver methenamine. These perivascular fibers, intercapillary strands, and bridges develop in relation to the process of retinal vascularization and the potential for forming these fibers is reactivated in senility and disease, as in diabetes. We summarized the evidence by concluding that these fibers are most likely composed of reticulin; it appears provable that in the past there may have been some confusion with neural fibers.
 ...
PMID:Perivascular and intervascular reticular fibers of the retina. 5 89

This brief review of abdominal emergencies is by no means encyclopedic. Indeed, it simply reflects the multiplicity of problems that can occur and suggests the need for a high index of suspicion and an optimistic attitude toward their solution. In addition, the surgeon must keep in mind the fact that cancer patients may also suffer acute abdominal distress from extra-abdominal causes such as pneumonia, myocardial infarction, diabetes mellitus, and hematologic abnormalities such as porphyria or sickle cell anemia. Inflammatory bowel disease, pelvic inflammatory disease, acute hepatitis or other similar problems more commonly seen in general hospital populations may also develop. Consultations for an acute condition of the abdomen in patients receiving marrow-suppressing chemotherapy are challenging problems and repeated examination every few hours is required to detect subtle changes. Hypovolemia, sepsis, confusion and unexplained metabolic acidosis may be the only criteria for surgical exploration. An unnecessary operation in a leukopenic and thrombocytopenic patient is indeed risky, but failure to drain an occult abscess or resect a perforated segment of bowel is always lethal. An additional consideration is the likelihood of response to further treatment of the underlying disease. Unless further effective therapy is unavailable, pessimism is unwarranted.
 ...
PMID:Abdominal emergencies. 31 58

Neonatal small left colon syndrome is a cause of functional colon obstruction in newborn infants, with a high association of maternal diabetes. There has been much confusion regarding its relationship to meconium plug syndrome and aganglionosis. Six cases of aganglionosis (2 in infants of diabetic mothers) were encountered in which the radiographic findings were identical to small left colon syndrome, indicating the need for caution in dismissing aganglionosis solely on the basis of a small left colon seen radiographically in a newborn infant with colon obstruction. Small left colon and meconium plug syndrome are overlapping entities in the total spectrum of functional intestinal obstruction in newborn infants.
 ...
PMID:Neonatal small left colon syndrome: its relationship to aganglionosis and meconium plug syndrome. 91 57

Addison's disease, when caused by idiopathic atrophy of the adrenal cortex, is frequently associated with other endocrine abnormalities. Primary hypothyroidism and hypogonadism have been reported in association with adrenal insufficiency; understandably, such cases may lead to diagnostic confusion with respect to possible pituitary disease. This case study concerns a woman who exhibited, in sequence and over a period of 17 years, hypogonadism, hypoadrenalism, diabetes mellitus and, finally, hypothyroidism. Originally misdiagnosed as having Sheehan's syndrome, she eventually became hyperpigmented. The true nature of her illness was then revealed to be primary insufficiency of multiple endocrine glands, with the demonstration of elevated levels of several pituitary hormones. Because multiple endocrine insufficiencies may coexist or develop with time, we suggest that a patient with a single documented endocrine deficiency be investigated initially and serially for additional glandular deficiencies.
 ...
PMID:The syndrome of multiple endocrine gland insufficiency. 93 64

Stress is a potential contributor to chronic hyperglycemia in diabetes. Stress has long been shown to have major effects on metabolic activity. Energy mobilization is a primary result of the fight or flight response. Stress stimulates the release of various hormones, which can result in elevated blood glucose levels. Although this is of adaptive importance in a healthy organism, in diabetes, as a result of the relative or absolute lack of insulin, stress-induced increases in glucose cannot be metabolized properly. Furthermore, regulation of these stress hormones may be abnormal in diabetes. However, evidence characterizing the effects of stress in type I diabetes is contradictory. Although some retrospective human studies have suggested that stress can precipitate type I diabetes, animal studies have shown that stressors of various kinds can precipitate--or prevent--various experimental models of the disease. Human studies have shown that stress can stimulate hyperglycemia, hypoglycemia, or have no affect at all on glycemic status in established diabetes. Much of this confusion may be attributable to the presence of autonomic neuropathy, common in type I diabetes. In contrast, more consistent evidence supports the role of stress in type II diabetes. Although human studies on the role of stress in the onset and course of type II diabetes are few, a large body of animal study supports the notion that stress reliably produces hyperglycemia in this form of the disease. Furthermore, there is mounting evidence of autonomic contributions to the pathophysiology of this condition in both animals and humans.
Diabetes Care 1992 Oct
PMID:Stress and diabetes mellitus. 142 10

Clinical diabetic nephropathy in man is the consequence of the development of a specific constellation of glomerular, tubular, vascular, and interstitial structural abnormalities accompanied by highly characteristic immunohistochemical alterations that, together, are unique to diabetes. Because changes resembling the specific pathology of diabetes do not develop in patients with conditions that lead to long-standing glomerular hyperfunction (such as unilateral nephrectomy), it is unlikely that glomerular hemodynamic abnormalities per se can be the cause of diabetic nephropathy. Whether hemodynamic abnormalities represent a risk factor that, in the presence of the diabetic state, can accelerate the rate of development of the basic lesions of diabetic nephropathy is currently unclear. However, there is considerable evidence that when the renal lesions of diabetes are far advanced, factors such as systemic hypertension can determine the rate of renal functional deterioration in diabetes as in other disorders. Although the diabetic rat may be a useful model for the study of aspects of the pathogenesis of diabetic nephropathy, much confusion has resulted from the inclusion of focal segmental glomerular sclerosis as a diabetic lesion. Similarly, the acceptance of all increases in urinary protein excretions in this model as resulting from or reflecting of diabetic nephropathology can be misleading. It is concluded that treatment aimed at manipulating renal hemodynamics in diabetic patients without evidence of renal disease should remain in the realm of clinical research.
 ...
PMID:An overview of renal pathology in insulin-dependent diabetes mellitus in relationship to altered glomerular hemodynamics. 146 81

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely caused by confusion in the definition and measurement of this disorder. We have reviewed various clinical manifestations associated with somatic and autonomic neuropathy, and we herein discuss current views related to the management of the various abnormalities. Although unproven, the best evidence suggests that near-normal control of blood glucose in the early years after diabetes onset may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose also may lead to reversibility of early diabetic neuropathy, but again, this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, refinements must be made in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.
Diabetes Care 1992 Dec
PMID:Diabetic neuropathies. 146 46

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
 ...
PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

The effective clinical management of diabetes requires accurate means to measure and monitor prevailing blood glucose concentrations. This can be accomplished with regular home glucose monitoring and periodic measurement of indicators that reflect ambient glycaemia during defined temporal intervals. The amount of glycated haemoglobin provides an index of integrated long-term glycaemia, whereas the amount of glycated albumin provides an index of short to intermediate term integrated glycaemic control. However, there is confusion regarding the various methods for estimation of glycated serum or plasma proteins, in part because the different methods use different reaction principles, measure different substances, and express results in different units. This article reviews the principles underlying different assays for measurement of glycated albumin and glycated serum proteins, compares their ranges of values, and discusses their clinical relevance assessed by studies published in the recent medical literature. The methods evaluated include commercially available assays for measuring glycated albumin with monoclonal antibodies and with affinity chromatography (including HPLC), and the fructosamine assay for glycated serum proteins.
 ...
PMID:Perspective: measurement of circulating glycated proteins to monitor intermediate-term changes in glycaemic control. 148 60

Insulin resistance and beta-cell failure account for the complex clinical presentation of non-insulin-dependent diabetes mellitus (NIDDM). Insulin resistance primarily involves defective regulation of hepatic glucose production and the peripheral utilization of glucose. Considerable progress has been made in understanding the basic molecular biology, biochemistry, and physiology of these processes. Similarly, the mechanisms involved in insulin synthesis, processing, storage, and secretion are being elucidated. The relative contributions of insulin resistance and beta-cell failure are difficult to evaluate when the disease is fully established and clinically apparent but may be more obvious early, i.e., in people with impaired glucose tolerance or individuals at risk for developing the disease. The latter can be identified because there is a strong genetic determinant for NIDDM; the offspring of two diabetic parents have a markedly increased incidence of the disease. In addition to genetic factors, environmental components contribute to the multifactorial etiology of NIDDM. Efforts to establish the importance of these different factors will be assisted if a metabolic staging of NIDDM can be agreed on. This staging, which should correlate the pathophysiological events responsible for the transition from normal glucose tolerance to frank NIDDM with clinical status, would be based on what is known about insulin resistance and beta-cell function. Staging will also provide for a classification of the number of causes that lead to NIDDM, if indeed, there is more than one cause of the general phenotype. Strategies for defining the gene or genes responsible for NIDDM can be subsequently devised based on the temporal sequence of appearance of pathophysiological defects and what is known about the molecular biology of insulin action. Understanding the defective metabolic code that results in NIDDM will require the concerted efforts of investigators from various disciplines. This is used throughout the text to avoid confusion with those people who have impaired glucose tolerance but not NIDDM.
Diabetes Care 1992 Mar
PMID:Molecular physiology and genetics of NIDDM. Importance of metabolic staging. 155 7


1 2 3 4 5 6 7 8 9 10 Next >>