Elevated serum dipeptidyl peptidase IV (CD26, EC 3.4.14.5) activity in patients with primary biliary cirrhosis

Lakatos, László; Firneisz, Gábor; Rákóczy, G; Selmeci, L.; Szalay, Ferenç

doi:10.1016/s0168-8278(99)80211-6

Cited by 20 publications

(10 citation statements)

References 5 publications

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“…The results established elevated serum DPP-IV activity as a clinically useful marker of cholestasis and demonstrate that DPP-IV levels do not change in metastatic bone disease (Lakatos et al, 1999;Perner et al, 1999) nor in allergic asthmatics, inhaling glucocorticoids or not (Van Der Velden et al, 1999). Higher activities were also found in serum of patients with osteoporosis, probably related to its severity (Gotoh et al, 1988).…”

Section: Discussionmentioning

confidence: 90%

Preoperative serum CD26 levels: diagnostic efficiency and predictive value for colorectal cancer

et al. 2000

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CD26 is an ectoenzyme with dipeptidyl peptidase IV activity expressed on a variety of cell types. Although the function of the high concentration of serum-soluble CD26 (sCD26) is unknown, it may be related to the cleavage of biologically active polypeptides. As CD26 or enzymatic activity levels were previously associated with cancer, we examined the potential diagnostic and prognostic value of preoperative sCD26 measurements by ELISA in colorectal carcinoma patients. We found a highly significant difference between sCD26 levels in healthy donors (mean 559.7 ± 125.5 μg l –1 ) and cancer patients (mean 261.7 ± 138.1 μg l –1 ) ( P < 0.001). A cut-off at 410 μg l –1 gave 90% sensitivity with 90% specificity which means that the diagnostic efficiency of sCD26 is higher than that shown by other markers, particularly in patients at early stages. Moreover, sCD26 as a variable is not related with Dukes’ stage classification, age, gender, tumour location or degree of differentiation. With a follow-up of 2 years until recurrence, preliminary data show that sCD26 can be managed as a prognostic variable of early carcinoma patients. In addition, the origin of sCD26 is discussed. © 2000 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 90%

Preoperative serum CD26 levels: diagnostic efficiency and predictive value for colorectal cancer

et al. 2000

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“…Indeed, repeated stimulation of sympathetic nerves causes depletion of NPY release [29]. Another interesting linkage to decreased splanchnic NPY action is elevated dipeptidyl-peptidase IV (DPP-IV) activity in cirrhosis [30]. DPP-IV acts on the extracellular metabolism of peptides at/near endothelial and smooth muscle cell surface receptors [31].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the proteolytic processing of NPY leads to selective activation of presynaptic Y2 receptors via NPY 3-36 [32]. Therefore, the observed Y2 receptor-associated decrease of NA release might be more pronounced in cirrhosis because of the above mentioned elevated DPP-IV-activity [30] and thus increased proteolytic processing of NPY with subsequent selective presynaptic Y2 receptor stimulation. Moreover, cholinergic M3 receptor-induced vasodilation in the perfused rat mesentery is well known [46].…”

Section: Discussionmentioning

confidence: 99%

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dietrich¹,

Moleda²,

Kees

et al. 2013

Journal of Hepatology

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“…62 Another linkage to decreased splanchnic NPY action is elevated dipeptidyl-peptidase IV (DPP-IV) activity in cirrhosis. 63 Dipeptidyl-peptidase IV proteolytically processes NPY 64 so that elevated DPP-IV activity may reduce NPY activity. Additionally, in the rat mesenteric bed, endothelins (ET-1, ET-3) inhibited NPY release.…”

Section: Neuropeptide Ymentioning

confidence: 99%

Molecular mechanisms of circulatory dysfunction in cirrhotic portal hypertension

Huang

2015

Journal of the Chinese Medical Association

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Acute or chronic insults to the liver are usually followed by a tissue repairing process. Unfortunately, this action, in most cases, is not effective enough to restore the normal hepatic structure and function. Instead, fibrogenesis and regenerative nodules formation ensue, which are relatively nonfunctioning. The common final stage of the process is liver cirrhosis with increased intrahepatic resistance to portal venous blood flow. Throughout the entire course, the extrahepatic circulatory dysfunction, including increased splanchnic blood flow, elevated portal venous blood flow and pressure, decreased splanchnic and peripheral vascular resistance, tachycardia, and increased cardiac output, are noted and denoted as portal hypertension with hyperdynamic circulatory dysfunction. When such a condition is established, patients may suffer from fatal complications such as gastroesophageal variceal hemorrhage, hepatic encephalopathy, or hepatorenal syndrome. The cause of such a circulatory dysfunction is not fully elucidated. Nevertheless, clarification of the pathophysiology definitely contributes to the control of portal hypertension-related complications. Herein, the molecular mechanism of this intriguing disaster is reviewed and discussed.

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Elevated serum dipeptidyl peptidase IV (CD26, EC 3.4.14.5) activity in patients with primary biliary cirrhosis

Cited by 20 publications

References 5 publications

Preoperative serum CD26 levels: diagnostic efficiency and predictive value for colorectal cancer

Preoperative serum CD26 levels: diagnostic efficiency and predictive value for colorectal cancer

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Molecular mechanisms of circulatory dysfunction in cirrhotic portal hypertension

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