Enzymatic Therapy

Enzymatic Therapy — Capsule, St. John s Wort (0.3% hypericin, 3% hyperforin)... 

Garlinase 4000 — Enzymatic Therapy, extract equivalent to 4 g fresh garlic (3.4% allicin)... 

Greenberger NJ. Enzymatic therapy in patients with chronic pancreatitis. Gastroenterol Clin North Am 1999 28 687-693. 

One major concern in developing an oral enzymatic therapy is the retention of enzyme activity with passage through the gastrointestinal tract, especially the acidic pH environment of the stomach. To be useful the enzyme must retain its activity to act in the near-neutral pH environment of the small intestine. Thus, immobilized bilirubin oxidase was... 

Pain is the other cardinal symptom of chronic pancreatitis. The rationale for its treatment with pancreatic enzymes is based on the principle of negative feedback inhibition of the pancreas by the presence of duodenal proteases. The release of cholecystokinin (CCK), the principal secreta-gogue for pancreatic enzymes, is triggered by CCK-releas-ing monitor peptide in the duodenum, which normally is denatured by pancreatic trypsin. In chronic pancreatitis, trypsin insufficiency leads to persistent activation of this peptide and an increased release of CCK, which is thought to cause pancreatic pain because of continuous stimulation of pancreatic enzyme output and increased intraductal pressure. Delivery of active proteases to the duodenum (which can be done reliably only with uncoated preparations) therefore is important for the interruption of this loop. Although enzymatic therapy has become firmly entrenched for the treatment of painful pancreatitis, the evidence supporting this practice is equivocal at best. 

The immobilization of enzymes with the formation of insoluble forms is usually intended for the development of specific catalysts for technical purposes. Here, we consider another medico-biological problem of the preparation of insoluble enzymatic systems based on crosslinked polyelectrolytes, used in the replacement therapy for oral administration. 

Improving giycaemic control may not only reduce the rate of non-enzymatic glycosyiation and monosaccharide autooxidation, but lower polyol pathway activity. In addition, it should have a beneficial effect on other haemodynamic and hormonal factors involved in the development of diabetic vascular disease. However, in studies of diabetic retinopathy, rapid control of glucose levels by intensive insulin therapy has been shown to worsen vascular disease initially and it could be postulated that a sudden improvement in retinal blood flow promotes further free-radical damage as part of a reperfusion-ischaemic injury. 

Figure 13.7 Outline of antibody-directed enzyme prodrug therapy (ADEPT). Subsequent to its enzymatic activation, the active drug is taken up by the cell, upon which it exhibits a cytocidal effect. Refer to text for specific detail...

The specific therapy consists in concurrent use of two antidotes differing by mechanism of action cholinolytics eliminating anticholinesterase effects on CNS, and cholinesterase reactivators (ChR) ensuring the restoration of inhibited enzymatic activity. 

Langer R, Linhardt RJ, Hoffberg S, Larsen AK, Cooney CL, Tapper D, Klein M (1982) An enzymatic system for removing heparin in extracorporeal therapy. Science 217 261-263. 

Drug/Lab test interactions False-positive urine glucose reactions may occur with penicillin therapy if Clinitest, Benedict s Solution, or Fehling s Solution are used. It is recommended that enzymatic glucose oxidase tests (such as Clinistix or Tes-Tape) be used. Positive Coombs tests have occurred. High urine concentrations of some penicillins may produce false-positive protein reactions (pseudoproteinuria) with the P.870... 

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