Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235886 (leg edema)
 674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We encountered a patient with diabetes mellitus due to the 3243 mitochondrial tRNA mutation(DM-Mt3243), who developed insulin edema and hepatic dysfunction after starting insulin. Such a rare phenomenon was unlikely to be a fortuitous coincidence in mitochondrial diabetes, as none in 197 non-mutant NIDDM patients had same episode. Moreover, similar leg edema was noticed in another DM-Mt3243 patient, and other two DM-Mt3243 patients had leg edema which responded to coenzyme Q10. These observations suggest further a role of mitochondrial function on leg edema. The mechanism of his insulin edema may involve vasomotor changes induced by the rapidly glycemic control, because our case of insulin edema had a prominent increase of strong succinate dehydrogenase reactive vessels. Alternatively, myocardial dysfunction might have produced leg edema and hepatic dysfunction, because he had subclinical myocardial dysfunction, judged by imaging with beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid. The third explanation is that a rapid improvement of glycemic control might have induced hepatic reoxygenation and the production of reactive oxygen species in the liver that contributed to cell damage. Thus, although we cannot draw definite conclusion, our experiences here suggest that mitochondrial dysfunction is important in the etiology of insulin edema.
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PMID:Insulin edema in diabetes mellitus associated with the 3243 mitochondrial tRNA(Leu(UUR)) mutation; case reports. 859 1

Edema is an adverse event associated with thiazolidinedione therapy The potential for mild-to-moderate peripheral edema with thiazolidinedione is known, especially in patients who have heart failure or use insulin. Our experience reveals that patients who do not have heart failure or do not use insulin also can develop moderate-to-severe edema that necessitates discontinuation of the thiazolidinedione. A 77-year-old man developed ankle, hand, and facial swelling 2 weeks after starting rosiglitazone. After discontinuing the drug, his edema resolved. A 75-year-old man developed bilateral lower leg edema 6 months after switching from troglitazone to pioglitazone. He was hospitalized for 51 days and, after aggressive diuresis and discontinuation of pioglitazone, was discharged with a weight loss of 30 pounds. A 53-year-old man developed lower leg edema 4 weeks after rosiglitazone was increased from 4 mg once/day to 4 mg twice/day. Rosiglitazone was discontinued and the edema resolved. Until the mechanism of action responsible for fluid overload is known, we suggest that thiazolidinediones be administered with caution in all patients.
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PMID:Thiazolidinedione-induced edema. 1212 25

Short-acting insulin analogue has previously shown to be equal to short-acting human regular insulin regarding in vitro characteristics, immunogenicity, and safety. But in the present study, we experienced seven patients who had mild to moderate side effects due to short-acting insulin analogue. These side effects could be divided into two types based on the appearance time; one with early onset and the other with late onset. Early onset side effects include rash, disturbances in walking and general fatigue that can not be explained by the swing in glucose levels. These symptoms appeared 2-3 days after the use of short-acting insulin analogue and disappeared several hours after switching short-acting human regular insulin. The late onset side effect is bilateral leg edema, which appeared 1-2 months after the induction of short-acting insulin analogue and disappeared after several hours by changing to short-acting human regular insulin. We should monitor the early and late onset side effects as diligently as possible when we use short-acting insulin analogue on diabetic patients.
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PMID:Early and late onset side effects of short-acting insulin analogue in seven Japanese diabetic patients. 1730 2

A 29-year-old woman was diagnosed as having type 1 diabetes mellitus and received insulin aspart and NPH insulin (NovolinN). On day 22, she had leg edema and right abdominal pain. The serum hepatobiliary enzyme levels were markedly elevated. Computed tomography revealed gallbladder edema. After an injection of human regular insulin and NPH insulin (HumacartN), the elevated liver enzyme levels were no longer observed. Challenge testing demonstrated that protamine was the cause of her allergy. Furthermore, tests revealed increased VEGF levels. This is an extremely rare case with a delayed-type protamine allergy caused by NovolinN resulting in gallbladder edema.
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PMID:Gallbladder edema in type 1 diabetic patient due to delayed-type insulin allergy. 1972 1

A 50-year-old female patient, who had had a long-term history of myelodysplastic syndrome and type II diabetes mellitus, had developed acute myelogenous leukemia and received allogeneic bone marrow transplantation (BMT). She was being treated with tacrolimus, methotrexate and prednisolone for prophylaxis and treatment of graft-versus-host disease, and with intensive insulin therapy for better glycemic control. The patient suddenly developed marked leg edema at 27 days after starting intensive insulin therapy (on day 40 after BMT) without coexistence or exacerbation of apparent causes such as renal failure, cardiac dysfunction or leg thrombosis around the onset of leg edema. Interestingly, the leg edema regressed soon after daytime hyperglycemia and intensive insulin therapy were performed. Histopathological examination revealed slight dermal edema and small bullae with little inflammatory infiltration but no signs of autoimmune blistering diseases or vasculitis. These findings indicate that the present case may be considered a form of so-called insulin edema occurring during intensive insulin therapy after BMT.
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PMID:Case of insulin edema occurring during intensive insulin therapy after bone marrow transplantation. 2195 Dec 68