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

A 59-year-old man with an 8-years history of diabetes mellitus had an acute onset of sharp pain in the anterior part of right lower leg. One month later, the pain changed to deep dull nature in the deeper site of the peroneal region. The pain increased, when he stood up, walked, and stayed in the cold room and decreased by rest. It was more painful in the evening than in the morning. The first sharp pain was thought to be caused by ischemia due to diabetic vascular neuropathy. The next dull pain was considered to be originated from ephaptic transmission between sympathetic efferent fibers to group IV and afferent ones from the skeletal muscle. The latter dull pain was selectively suppressed by nerve block when it became effective to the branch of deep peroneal nerve to extensor digitorum longus muscle. The hypothesis of ephaptic transmission was supported by meaningful decrease of muscle sympathetic activity detected by microneurography before and after the dosage of L-DOPS, which effectively suppressed the pain as well as other alpha-stimulant, midodrine hydrochloride. We concluded that the ephaptic pain caused by muscle sympathetic activity could be suppressed by the vasoconstrictive drugs through the mechanism of baroreflex control.
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PMID:[Pain caused by ephaptic transmission occurring in the recovery phase of diabetic vascular mononeuropathy was effectively suppressed with L-threo-3,4-dihydroxyphenyl-serine]. 959 2

Postprandial hypotension (PPH) is defined as a decrease of systolic blood pressure by more than 20 mmHg after meals. Severe PPH is a troublesome diabetic complication, which has no established means of treatment. We encountered a patient who had diabetes mellitus complicated by severe PPH and attempted to treat this problem using several medications (octreotide, midodrine hydrochloride, and acarbose). A 58-year-old male with diabetic triopathy complained of orthostatic dizziness and vertigo after meals. The blood pressure was monitored for 24 h with an ambulatory blood pressure monitor, revealing that the systolic blood pressure decreased markedly after breakfast and dinner by 45 and 50 mmHg, respectively. PPH was not improved by a subcutaneous injection of octreotide. Administration of midodrine hydrochloride reduced the frequency of hypotensive episodes from twice to once daily, but the magnitude of the postprandial fall in blood pressure was still around 30 mmHg. After the patient started to receive acarbose therapy, the postprandial fall in blood pressure was diminished to 18 mmHg and his symptoms largely disappeared. For the treatment of PPH in diabetic patients, our experience suggests that it may be appropriate to try first on alpha-glucosidase inhibitor like acarbose.
J Diabetes Complications
PMID:Acarbose improved severe postprandial hypotension in a patient with diabetes mellitus. 1135 85

Orthostatic hypotension (OH) may be dependent upon various neurogenic and non-neurogenic disorders and conditions. Neurogenic causes include the main autonomic failure syndromes, primary (multiple system atrophy, pure autonomic failure, and autonomic failure associated with Parkinson's disease) and secondary (central nervous system diseases, peripheral neuropathies and systemic diseases). Non-neurogenic causes of OH include cardiac impairment, fluid and electrolyte loss, vasodilatation, and old age. A number of drugs may also cause OH, through their vasoactive action or by interfering with the autonomic nervous system. Symptoms of OH are debilitating, often confining patients to bed, and longitudinal studies have shown that OH increases the risk of stroke, myocardial ischemia and mortality. The therapeutic goal is to decrease the incidence and severity of postural symptoms, rather than restore normotension. In non-neurogenic OH, treatment of the underlying cause may be curative. In neurogenic OH a combination of non-pharmacological and pharmacological measures is often needed. Patient education and non-pharmacological measures represent the first step; among these interventions, fluid repletion and physical countermanoeuvres have been proven very effective. Pharmacological treatment comprises a number of agents acting on blood vessels, on blood volume or with other pressor mechanisms. The drugs most currently used are fludrocortisone and midodrine. Fludrocortisone expands the extravascular body fluid volume and improves alpha-adrenergic sensitivity. Midodrine is a peripheral, selective alpha1-adrenergic agonist that causes arterial and venous vasoconstriction. Despite the wide use of these drugs, multicentre, randomised and controlled studies for the treatment of OH are still scarce and limited to few agents and groups of patients. Pharmacological management of OH substantially improves the quality of life of patients, although it may be problematic. The development of supine hypertension and subsequent congestive heart failure should be avoided, especially in those patients with a pre-existing cardiovascular risk, such as in diabetes or ischemic heart disease.
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PMID:Orthostatic hypotension: evaluation and treatment. 1734 29

Renal dysfunction in cirrhosis is mostly related to the development of acute kidney injury (AKI), precipitated by either an acute disturbance of hemodynamics, or acute structural damage to the kidneys. The incidence of chronic renal failure is rising, due to increasing prevalence of conditions such as diabetes, viral hepatitis, which can be associated with renal damage. AKI is defined as a rise in serum creatinine of 0.3 mg/dL in <48 hours or by 50% from baseline within the past 3 months without setting a threshold for the final serum creatinine. Stages 1, 2, and 3 of AKI are defined as 150%, 200% and 300% of baseline serum creatinine respectively, which allows for assessment of AKI progression. Chronic kidney disease (CKD) is defined as an estimated glomerular filtration rate of <60 mL/min for >3 months. Treatment of AKI consists of removal of precipitating factors and replenishment of the intravascular volume using colloids such as albumin. Frequently, AKI can be reversed using these measures alone. Non-responders to removal of precipitating factors and volume challenge can receive vasoconstrictors such as terlipressin or norepinephrine together with albumin. Midodrine is inferior in efficacy as a vasoconstrictor when compared to terlipressin. Liver transplantation is the definitive treatment for type 1 hepatorenal syndrome with liver failure. Delay in receiving a liver transplant can result in non-recovery of renal function post transplant. Treatment of CKD in cirrhosis is unsatisfactory, mostly aimed at optimizing management of comorbid conditions, or treating the underlying refractory ascites in patients with type 2 hepatorenal syndrome.
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PMID:Diagnosing and treating renal disease in cirrhotic patients. 2709 2