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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small vessel disease has been described in various cardiac conditions including diabetes mellitus, amyloidosis, and connective tissue disease. Less well understood is the incidence and morphological features of small vessel disease in patients with myocardial disease of unknown etiology. This study examines the incidence, clinical presentation, and pathological changes of small vessel disease in patients with normal epicardial coronary arteries undergoing endomyocardial biopsy. Biopsy specimens in 110 consecutive patients were analyzed by light and electron microscopy. Small vessel abnormalities were present in 16 patients (14.6 percent) of whom five patients had associated hypertension and 11 patients had idiopathic small vessel disease. There were six males and 10 females with a mean age of 53 (26 to 76) years. Clinical presentations were arrhythmias, heart failure, or chest pain. The left ventricular ejection fraction was reduced (less than 50 percent) in 12 of these 16 patients. The morphological features of small vessel disease included marked thickening of the arterial wall owing to subendothelial deposits of heterogeneous electron dense materials consisting of microfibrils, collagen and elastic fibers, cellular debris, and other amorphous substances. Subendothelial deposits comprised a mean 60 percent (40 to 76 percent) of the arterial wall thickness.
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PMID:Morphological changes in small vessels on endomyocardial biopsy. 371 82

We developed a true-or-false questionnaire with several hundred questions about symptoms encountered in peripheral neuropathy, to be scored by optical reader and computer. Responses were grouped into scales called "Neuropathy," "Weakness," "Sensory," "Autonomic," and subsets of these. Profiles in health were estimated for each scale based on responses from 300 healthy subjects 15 to 65 years old. The sensitivity and specificity of the scales were tested in patients with motor neuron disease, amyloidosis, or diabetes, with or without neuropathy. The questionnaire was useful in detecting neuropathy and staging severity, and in recognizing patterns that may have diagnostic implications.
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PMID:Neuropathy Symptom Profile in health, motor neuron disease, diabetic neuropathy, and amyloidosis. 376 34

Fixed anionic charges in the mammalian glomerulus, on both the basement membrane and the epithelial cell foot processes, are believed to form an important part of the glomerular filtration barrier. There is good evidence that their loss causes proteinuria. The charges can be visualized ultrastructurally using cationic dyes, but the requirement of these techniques for perfusion or immersion of fresh tissue has largely confined such studies to experimental models. We have extended the widely used polyethyleneimine technique, to study the charge of glomerular basement membranes in human tissue reprocessed out of paraffin blocks up to 10 years old. We studied selected cases of glomerular disease, where the diagnosis was not in any doubt. In the majority of diseases studied, a continuous charge layer persisted despite severe abnormalities of the basement membrane. Two exceptions were found. In amyloidosis, accumulation of fibrils was associated with a considerable decrease or loss of stainable basement membrane charge. In S.L.E., numerous small defects in the charge layer were noted. The persistence of charge is contrary to reported findings in several animal models of glomerular disease, including puromycin nephrosis, Heymann nephritis and streptozotocin diabetes. Although this method is not subject to precise quantitative analysis, we conclude that in the majority of cases, proteinuria in man is not caused by an extensive loss of glomerular basement membrane anionic charge.
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PMID:Basement membrane charge in human glomerular disease. 380 84

We have observed three cases of carpal tunnel syndrome (CTS) complicated by cutaneous ulcerations and acroosteolysis. Although our first patient had a mild case of CTS, he had a concomitant amphetamine addition. This led to a mania for gnawing away at the digits in the territory of the median nerve. Our other two patients had severe cases of CTS. One suffered from diabetes and the other from primary amyloidosis. Surgical decompression of the median nerve was carried out in these two cases and led to rapid healing of the cutaneous lesions. The latter patients suffered from the entity known in the french literature as carpal tunnel "ulcero-mutilating" (ulcero-osteolytic CTS). This paper discusses possible mechanisms for its pathogenesis. In one of our cases, for example, we were struck by the role played by the patient's behavioral habits whether it be conscious or subconscious in the self-perpetration of the cutaneous and osseous lesions.
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PMID:[Loss of digital tissues and carpal canal syndrome. Apropos of 3 cases]. 381 97

The high dose intravenous glucose tolerance test and concurrent immunoreactive serum insulin and glucagon levels were measured and the results related to the presence or absence of pancreatic insular amyloid in 16 cats, seven of which were known to be diabetic. Control values for all parameters were established using seven additional clinicopathologically normal cats. Nine of the 16 cats had normal fasting blood glucose levels (less than 120 mg/dl) and impaired glucose tolerance. These cats had attenuated (3/9) or normal (6/9) 0 to 5 minute glucose-stimulated insulin secretion, rising 45 to 60 minute insulin secretion (7/9), low mean insulin/glucose ratio, and normal mean serum glucagon. Three of the nine cats with impaired glucose tolerance had insular amyloidosis. These three cats had significantly higher mean blood glucose levels during the glucose tolerance test than did cats with impaired glucose tolerance and no insular amyloid deposits. Also, these three cats accounted for three of the four longest glucose disappearance one-half times (T1/2S), three of the four lowest glucose disappearance coefficients, and three of the four lowest 0 to 5 minute insulin responses. The seven diabetic cats (fasting blood glucose levels greater than 120 mg/dl) had either low to low normal (6/7) or above normal (1/7) fasting insulin levels, no insulin response to intravenous glucose stimulation (6/7), and elevated mean serum glucagon levels. Insular amyloid was present in six of the seven diabetic cats. Three diabetic cats with marked insular amyloid deposits had glucose disappearance T1/2 and K (coefficient) values, serum insulin levels, serum glucagon levels, and insulin/glucose ratios which were not significantly different from the other three diabetic cats with slight to moderate insular amyloidosis. These results confirm a strong association between the occurrence, but not the extent of insular amyloidosis and diabetes mellitus in adult diabetic cats, although amyloid replacement of pancreatic islets does not appear to be the primary diabetogenic event. Rather, these results appear to be consistent with our hypothesis that insular amyloid deposition is a morphologic marker of primary B-cell dysfunction that is basic to the pathogenesis of the diabetic condition, and is reflected clinically by impaired glucose tolerance.
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PMID:High dose intravenous glucose tolerance test and serum insulin and glucagon levels in diabetic and non-diabetic cats: relationships to insular amyloidosis. 389 Mar 45

The present review draws attention to the diversity of islet lesions seen in human type 1 and type 2 diabetes. This heterogeneity of islet changes is best demonstrated by immunocytochemistry. In type 1 diabetes the endocrine pancreas is characterized by selective loss of B cells, which most likely results from a slowly acting autoimmune process depending on the presence of both genetic and environmental factors. The process starts years before overt diabetes develops and manifests when the B-cell volume is reduced by about 80%. In type 2 diabetes B cells are always present, regardless of the duration and severity of the disease, but lack any signs of functional activity. This reflects a secretory defect of the B cells which obviously becomes evident under the conditions of obesity, hyperinsulinism and insulin resistance. Obese but non-diabetic subjects show, in parallel to their hyperinsulinism, an increased B cell volume, suggesting that under prediabetic conditions the B cells have still the capacity to respond to increased functional demands by enhanced proliferation. In manifest diabetes the B cells have lost their proliferative potential. Whether this is due to an inherent defect or the consequence of a functional disturbance, is not clear. The development of islet amyloidosis most likely represents an associated functional abnormality of the B cell.
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PMID:Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. 2471 75

A 51-year-old man with diabetes mellitus and the nephrotic syndrome on renal biopsy was found to have diabetic glomerulosclerosis, amyloidosis and membranous glomerulopathy. The presence of three distinct glomerular diseases in the same patient is unique. Possible factors involved in their pathogenesis are discussed and the literature on concomitant glomerular diseases is reviewed.
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PMID:Concomitant presence of three different glomerular diseases in the same patient. Report of a case and review of the literature. 634 70

A recent study has demonstrated secondary amyloidosis in dogs treated with continuous intravenous insulin infusion. Since elevated levels of serum amyloid A protein (SAA) and diminished amyloid fibril degrading activity (AFDA) are associated with amyloidosis, we measured SAA and AFDA in ten type I diabetics treated with continuous subcutaneous insulin infusion and in five conventionally treated patients. Only one pump- and one conventionally treated patient had detectable but low SAA levels, comparable with these seen in healthy controls. In patients with secondary amyloidosis the mean SAA level was 24-fold higher than in controls (P less than 0.001). Similarly, in both diabetic groups, AFDA was normal whereas it was reduced by 41% in patients with amyloidosis (P less than 0.001). Furthermore, no local amyloidosis was seen at the infusion site in any of the patients studied. Thus, our data fail to provide any evidence of secondary amyloidosis in patients treated for 3-40 mo with continuous subcutaneous insulin infusion.
Diabetes 1983 Jan
PMID:No evidence of amyloidosis in type I diabetics treated with continuous subcutaneous insulin infusion. 684

Autonomic dysfunction leads to a variety of clinical disorders involving all parts of the gut. These neural disorders are distinct from the four other recognised categories of disorders involving myogenic function, myoelectric activity, hormonal regulation and abnormal humoral factors. Criteria for establishing that a disorder has a neurogenic aetiology vary in different diseases. Absence of a neural mediated response with intact muscle function has been the major criterion used in most studies. Neural mediated responses of peristalsis, sphincteric relaxation and intestinal contraction following distension or feeding are the major parameters of assessment. Abnormalities in neural function have been demonstrated in achalasia, symptomatic diffuse oesophageal spasm, diabetes mellitus, amyloidosis, scleroderma and chronic idiopathic intestinal pseudoobstruction. The anatomical site and type of gut neurological disorder varies in each condition. Morphological studies have been helpful in demonstrating specific intranuclear inclusion bodies in some pseudoobstruction patients, and vagal and ganglionic lesions in achalasia. Intact muscle ad myoelectric function as well as normal responsiveness to drugs acting directly upon muscle may be established by morphological study. Advancement in basic technology should provide a rewarding area for future study of the pathogenesis and treatment of the gut neurological disorders.
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PMID:Clinical aspects of autonomic nerve dysfunction of the gut. 695 Dec 65

After grading into 4 groups of severity the extent of amyloidosis of the islets of Langerhans was investigated in 60 patients with diabetes and in 60 without. Distinction of 3 stages of diabetes according to clinical parameters showed clear connections between the stage of diabetes and the extent of amyloidosis. Development of amyloid locally may be evidence for progressive B cell insufficiency in diabetes of adults.
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PMID:[Amyloid of islets of Langerhans and its relation to diabetes mellitus (author's transl)]. 700 25


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