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In their review, Goodfield and Millard [1] list this condition under the rubric "Cutaneous features of vascular insufficiency", and term it "cheiro-arthropathy". They indicate that enthusiastic use of the test involving approximation of the palmar surfaces of the fingers leads to detection of abnormalities in many normal people, that the joint stiffness in the fingers is a result of stiffness of the skin, and that the lack of correlation with non-enzymatic glycosylation indicates that the browning reaction is not causal. Furthermore, they suggest that the association of limited joint mobility (LJM) with chronic complications may simply reflect the fact that all of these features are more likely in those with longer duration and poorer diabetes control. None of these notions is supportable, including the classification and terminology.Firstly, considering the syndrome of LJM, particularly as it occurs in young patients [2], to be a result of cutaneous vascular insufficiency has no experimental basis. Biopsy study of the associated skin changes shows thickening of the dermis and epidermis with accumulation of collagen and loss of skin appendages, compared to control biopsies [3,4]. Biochemical study does, indeed, fail to show that skin collagen glycosylation correlates with LJM [5,6] or with microvascular complications [6]. Skin collagen glycosylation does, however, correlate with HbA1 levels, reflecting the ketoamine link, an early step in the non-enzymatic browning reaction. Thus, glycosylation in the skin simply reflects recent diabetic control and not long-standing processes that would lead to abnormalities in the connective tissue. The stable end-products of the non-enzymatic browning reaction which are thought to be responsible for increased cross-linking, packing, and stiffening of collagen are fluorescent. Monnier et al. [6] demonstrated that fluorescence of skin collagen increased linearly with age, but that 95% of 41 Type 1 (insulin-dependent) diabetes patients had abnormal increases for age, and that the degree of skin collagen fluorescence correlated with the presence of retinopathy, nephropathy, and LJM.The suggestion that cautious interpretation of LJM is needed because of its frequency in the normal population is in reference to a study [7] in older patients, in whom age and occupation-related changes in the finger joints confound interpretation, as does the presence of Dupuytren contracture. This is most definitely not the case in the young patients originally and subsequently reported by numerous investigators. Control populations of patients under 25 have been found to have an absence of any detectible limitation using the same techniques applied to age-comparable young people with diabetes having frequencies of limitation in the 30% range [2].The authors suggest that LJM results from skin stiffness. This does not appear to be the case in youngsters with LJM, most of whom do not have clinically apparent thickened skin, but periarticular connective tissue thickening on radiographs and by palpati...
In their review, Goodfield and Millard [1] list this condition under the rubric "Cutaneous features of vascular insufficiency", and term it "cheiro-arthropathy". They indicate that enthusiastic use of the test involving approximation of the palmar surfaces of the fingers leads to detection of abnormalities in many normal people, that the joint stiffness in the fingers is a result of stiffness of the skin, and that the lack of correlation with non-enzymatic glycosylation indicates that the browning reaction is not causal. Furthermore, they suggest that the association of limited joint mobility (LJM) with chronic complications may simply reflect the fact that all of these features are more likely in those with longer duration and poorer diabetes control. None of these notions is supportable, including the classification and terminology.Firstly, considering the syndrome of LJM, particularly as it occurs in young patients [2], to be a result of cutaneous vascular insufficiency has no experimental basis. Biopsy study of the associated skin changes shows thickening of the dermis and epidermis with accumulation of collagen and loss of skin appendages, compared to control biopsies [3,4]. Biochemical study does, indeed, fail to show that skin collagen glycosylation correlates with LJM [5,6] or with microvascular complications [6]. Skin collagen glycosylation does, however, correlate with HbA1 levels, reflecting the ketoamine link, an early step in the non-enzymatic browning reaction. Thus, glycosylation in the skin simply reflects recent diabetic control and not long-standing processes that would lead to abnormalities in the connective tissue. The stable end-products of the non-enzymatic browning reaction which are thought to be responsible for increased cross-linking, packing, and stiffening of collagen are fluorescent. Monnier et al. [6] demonstrated that fluorescence of skin collagen increased linearly with age, but that 95% of 41 Type 1 (insulin-dependent) diabetes patients had abnormal increases for age, and that the degree of skin collagen fluorescence correlated with the presence of retinopathy, nephropathy, and LJM.The suggestion that cautious interpretation of LJM is needed because of its frequency in the normal population is in reference to a study [7] in older patients, in whom age and occupation-related changes in the finger joints confound interpretation, as does the presence of Dupuytren contracture. This is most definitely not the case in the young patients originally and subsequently reported by numerous investigators. Control populations of patients under 25 have been found to have an absence of any detectible limitation using the same techniques applied to age-comparable young people with diabetes having frequencies of limitation in the 30% range [2].The authors suggest that LJM results from skin stiffness. This does not appear to be the case in youngsters with LJM, most of whom do not have clinically apparent thickened skin, but periarticular connective tissue thickening on radiographs and by palpati...
\s=b\ We have recorded clues to the clinical recognition of chronic insulin overdosage in 101 pediatric patients with diabetes mellitus, identified predisposing circumstances, and reconsidered the traditional strategy of slow reduction in insulin dose. Overtreatment occurred in 70%, overall, and in 90% of those referred for instability; mean overdose was 38% of the readjusted dose. The most common findings were frank hypoglycemic episodes, polyuria/nocturia/enuresis despite increasing insulin dosage, excessive appetite, hepatomegaly, weight gain, headaches, exercise intolerance, marked variation in glucosuria, mood swings, and frequent bouts of rapidly developing ketoacidosis. Overtreatment usually developed because of attempts to achieve metabolic control using glucosuria as principal criterion. One fourth of those observed became overtreated during periods of emotional turmoil when need for increased insulin to counter stressinduced hyperglycemia and ketosis led to chronic increase in dosage. Persistent glucosuria/ketonuria and exacerbation of hypoglycemic symptoms were more frequent with slow than with rapid reduction in insulin dosage.(Am J Dis Child 131: [881][882][883][884][885] 1977)
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