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PubMed1977

Trial of the prophylactic effect of diazoxide in the treatment of familial periodic hypokalemia.

Five patients suffering from familial periodic paralysis with hypokalemia (FPP) were exposed to standard paralysis induction trials which elicited total paralyysis and hypokalemia. In all cases the serum potassium fell to or below 2.6 mmol/1. After being pre-treated with diazoxide for 72 h, the same five patients were exposed to the same standardized paralysis induction procedure. None of them developed any demonstrable symptoms or signs of paralysis. In one the serum potassium dropped to 3.2 mmol/1, but in all the others the levels were higher. The serum glucose level was significant higher (P less than 0.01), the serum insulin level was significant lower (P less than 0.01) when induction of paralysis was attempted under diazoxide cover than during the untreated stimulation phase. Three patients were put on prophylactic diazoxide medication. After a few months, without paralytic episodes or other prophylactic drugs, adaptation to the diazoxide occurred and the previous, frequent paralytic episodes returned in unchanged severity. This experimental prophylactic effect of diazoxide supports the hypothesis that the glucose deposition in muscles is a major step in eliciting the parese attacks in FPP.

Acute Disease↗

PubMed1977

Mechanical and metabolic effects of diazoxide in rat uterus.

Diazoxide relaxed both polarized and depolarized rat uterus. The drug also conteracted the contractions elicited by Ca2+ in a competitive manner. The relaxing effect was associated with an increase in the tissue level of cyclic AMP. This metabolic effect of diazoxide was inhibited by propranolol-treatment and in preparations from reserpinized animals, while the mechanical effects were only partially reduced. Diazoxide was also found to increase the release of tritium from preparations preloaded with [3H]-noradrenaline. It is suggested that diazoxide may induce some of its mechanical and metabolic effects by releasing the adrenergic transmittor substance noradrenaline. An effect of diazoxide on the Ca2+-metabolism is also probable.

Animals↗

PubMed1985

The biological relevance of the protein binding of diazoxide.

The biological importance of the binding of diazoxide to serum protein was studied in vitro. Contractions in the rings of the rabbit pulmonary artery evoked by electrical field stimulation or exogenous noradrenaline (NA) were studied in the absence and presence of serum albumin (45 g/l) in Krebs-Henseleit (K-H) solutions. Diazoxide concentrations up to 128 micrograms/ml in the K-H solution and to 256 micrograms/ml in albumin K-H solutions diminished the contractions and albumin reduced this diminishing effect. Because of an apparent binding of exogenous noradrenaline to albumin only the experiments with electrical field stimulation were used to assess the biological importance of the protein binding of diazoxide. At 2 micrograms/ml of diazoxide the free drug fraction determined by ultrafiltration was 5% but determined by our biological method the free (active) fraction was 65%. In accordance with a previous clinical study we conclude that the binding of diazoxide to serum protein is important for the transportation of the drug to the arteriolar wall which apparently has a much higher affinity for the drug than serum albumin.

Animals↗

PubMed1975

Intravenous diazoxide in treatment of hypertension associated with recent myocardial infarction.

Twenty patients with blood pressure over 180/110 mm Hg one hour after admission to a coronary care unit with recent acute myocardial infarction were given intravenous diazoxide in a bolus of 300 mg. The average blood pressure before diazoxide was 194/122 mm Hg. Blood pressure fell considerably in all patients, though six patients required two injections. The average fall was 58 mm Hg systolic and 40 mm Hg diastolic. No patient became severely hypotensive. The heart rate increased by an average of 10 beats/min. In nine patients the electrocardiographic changes immediately after the administration of diazoxide suggested an increase in myocardial injury. Though none of the patients seemed to deteriorate clinically from the diazoxide the electrocardiographic changes suggested that the use of intravenous diazoxide to lower blood pressure in patients with acute myocardial infarction might possibly be deleterious.

Acute Disease↗

PubMed2005

Acute and chronic effects of glucose and carbachol on insulin secretion and phospholipase C activation: studies with diazoxide and atropine.

The acute and chronic effects of 20 mM glucose and 10 microM carbachol on beta-cell responses were investigated. Acute exposure of rat islets to 20 mM glucose increased glucose usage rates and resulted in a large insulin-secretory response during a dynamic perifusion. The secretory, but not the metabolic, effect of 20 mM glucose was abolished by simultaneous exposure to 100 microM diazoxide. Glucose (20 mM) significantly increased inositol phosphate (IP) accumulation, an index of phospholipase C (PLC) activation, from [(3)H]inositol-prelabeled islets. Diazoxide, but not atropine, abolished this effect as well. Unlike 20 mM glucose, 10 microM carbachol (in the presence of 5 mM glucose) increased IP accumulation but had no effect on insulin secretion or glucose (5 mM) metabolism. The IP effect was abolished by 50 microM atropine but not by diazoxide. Chronic 3-h exposure of islets to 20 mM glucose or 10 microM carbachol profoundly reduced both the insulin-secretory and PLC responses to a subsequent 20 mM glucose stimulus. The adverse effects of chronic glucose exposure were abolished by diazoxide but not by atropine. In contrast, the adverse effects of carbachol were abolished by atropine but not by diazoxide. Prior 3 h of exposure to 20 mM glucose or carbachol had no inhibitory effect on glucose metabolism. Significant secretory responses could be evoked from 20 mM glucose- or carbachol-pretreated islets by the inclusion of forskolin. These findings support the concept that an early event in the evolution of beta-cell desensitization is the impaired activation of islet PLC.

Animals↗

PubMed2001

Dual roles of mitochondrial K(ATP) channels in diazoxide-mediated protection in isolated rabbit hearts.

Whether the mitochondrial ATP-dependent potassium (mK(ATP)) channel is the trigger or the mediator of cardioprotection is controversial. We investigated the critical time sequences of mK(ATP) channel opening for cardioprotection in isolated rabbit hearts. Pretreatment with diazoxide (100 microM), a selective mK(ATP) channel opener, for 5 min followed by 10 min washout before the 30-min ischemia and 2-h reperfusion significantly reduced infarct size (9 +/- 3 vs. 35 +/- 3% in control), indicating a role of mK(ATP) channels as a trigger of protection. The protection was blocked by coadministration of the L-type Ca(2+) channel blockers nifedipine (100 nM) or 5-hydroxydecanoic acid (5-HD; 50 microM) or by the protein kinase C (PKC) inhibitor chelerythrine (5 microM). The protection of diazoxide was not blocked by 50 microM 5-HD but was blocked by 200 microM 5-HD or 10 microM glybenclamide administrated 5 min before and throughout the 30 min of ischemia, indicating a role of mK(ATP) opening as a mediator of protection. Giving diazoxide throughout the 30 min of ischemia also protected the heart, and the protection was not blocked by chelerythrine. Nifedipine did not affect the ability of diazoxide to open mK(ATP) channels assessed by mitochondrial redox state. In electrically stimulated rabbit ventricular myocytes, diazoxide significantly increased Ca(2+) transient but had no effect on L-type Ca(2+) currents. Our results suggest that opening of mK(ATP) channels can trigger cardioprotection. The trigger phase may be induced by elevation of intracellular Ca(2+) and activation of PKC. During the lethal ischemia, mK(ATP) channel opening mediates the protection, independent of PKC, by yet unknown mechanisms.

Adenosine Triphosphate↗

PubMed1983

Sodium reabsorption during intrarenal diazoxide infusion in the dog.

Infusion of diazoxide, a potent benzothiazide antihypertensive, into the renal artery results in diuresis and natriuresis. The site within the nephron of decreased reabsorption has been controversial. Thus free flow recollection micropuncture studies of the superficial proximal tubule of the dog were undertaken to determine if diazoxide decreased sodium reabsorption from this part of the nephron. Renal blood flow, monitored by an electromagnetic flow meter, was increased by about 15% with the diazoxide infusion. Systemic blood pressure and hematocrit remained unchanged. Glomerular filtration rate increased significantly from 26 +/- 2 to 34 +/- 3 ml/min, urine flow and sodium excretion also increased (0.13 +/- 0.01 to 0.33 +/- 0.06 ml/min and 5.5 +/- 0.90 to 35.5 +/- 11.0 microEq/min, respectively). Decreased sodium reabsorption from the proximal tubule was demonstrated by a decrease in the tubular fluid to plasma inulin ratio (1.62 +/- 0.1 1.47 +/- 0.1) thus giving a reduction in fractional sodium reabsorption to the site of micropuncture (36.1 +/- 4.3 to 29.5 +/- 5.1%, p less than 0.05). To examine peritubular effects of diazoxide infusion, capillary protein concentration and pressure were measured; the former increasing significantly (9.17 +/- 0.32 to 9.80 +/- 0.35, p less than 0.05) and the latter did not change (13.1 +/- 1.0 vs. 15.2 +/- 1.4 mm Hg). Thus intrarenal diazoxide causes whole kidney vasodilatation with diuresis, natriuresis and decreased sodium reabsorption from the superficial proximal tubule. Additional studies provided no data to indicate that changes in peritubular physical factors account for the changes in sodium handling.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1981

The effect of glucagon and diazoxide on the normal and obstructed upper urinary tract.

The effect of diazoxide and glucagon were studied on the freely draining upper urinary tract and after varying periods of obstruction in dogs. Without obstruction, diazoxide produced longer inactive periods than glucagon and recovery was associated with less retrograde activity. Following obstruction for 5--10 min, 6 and 24 h, diazoxide decreased renal pressure and the effect was greatest when the upper tract was obstructed for the shortest period. Glucagon also produced an overall reduction in pressure after 5--10 min and 6-hour periods of obstruction, but there was an initial rise in pressure after 5--10 min of obstruction. At 24 h there was an increase, but no overall decrease in pressure after glucagon. Diazoxide produced a greater fall in pressure after 5--10 min and 24 h of obstruction, and a faster fall in pressure after 5--10 min and 6 h of obstruction as compared to glucagon. Diazoxide may be a more effective therapeutic agent in the management of ureteral calculus disease than glucagon.

Animals↗

PubMed2003

Cardioprotective effect of diazoxide is mediated by activation of sarcolemmal but not mitochondrial ATP-sensitive potassium channels in mice.

BACKGROUND: We recently demonstrated that the sarcolemmal ATP-sensitive potassium (sarcK(ATP)) channel plays a key role in cardioprotection against ischemia/reperfusion injuries in Kir6.2-knockout (KO) mice. In the present study, we evaluated the effects of diazoxide, a mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel opener, on ischemia-induced myocardial stunning in sarcK(ATP) channel-deficient mice. METHODS AND RESULTS: Langendorff-perfused hearts of wild-type (WT) and KO mice were subjected to global ischemia/reperfusion. Diazoxide improved the recovery of contractile function in WT hearts but not in KO hearts. Treatment with HMR1098 (a sarcK(ATP) channel blocker) but not 5-hydroxydecanoate (a mitoK(ATP) channel blocker) abolished the cardioprotective effect of diazoxide in WT hearts. In coronary-perfused WT ventricular muscle preparations, action potential shortening during ischemia was accelerated in the presence of diazoxide. CONCLUSIONS: Diazoxide enhances action potential shortening during ischemia by activating sarcK(ATP) channels and provides cardioprotection in mouse hearts.

Action Potentials↗

PubMed1979

Safety of intravenous diazoxide in children with severe hypertension.

The safety and efficacy of diazoxide administered intravenously in the treatment of children with acute severe hypertension have been evaluated by a collaborative study. Observations of the response of blood pressure in 36 patients, ranging in age from two months to 18 years, during the initial episode of hospitalization reveal diazoxide treatment to be effective in lowering blood pressure in 94 per cent of the cases. No serious adverse circulatory, fluid and electrolyte, metabolic or hematologic effects were observed. Symptomatic and subjective reactions observed with diazoxide administered intravenously to children were identical with those described in adults. Reinstitution of other means of antihypertensive therapy is safe and effective when delayed until the transiently induced period of hypotension has passed. Repeated use of diazoxide for subsequent recurrence of severe hypertension was equally effective and safe in 93 per cent of the instances. The results lead us to recommend the use of intravenous diazoxide for treatment of children with severe symptomatic hypertension especially when it is refractory to control by other hypertensive agents.

Adolescent↗

PubMed2003

Diazoxide attenuates glucose-induced defects in first-phase insulin release and pulsatile insulin secretion in human islets.

Humans with type-2 diabetes mellitus (TTDM) have hyperglycemia ( approximately 11 mM) and impaired glucose-mediated insulin secretion characterized by impaired first-phase insulin release (FPIR) and pulsatile insulin release. Culture of islets from nondiabetic humans in very high glucose concentrations ( approximately 20-30 mM) for 96 h causes impaired FPIR. We sought to determine 1). whether human islets cultured at a glucose concentration of approximately 11 mM (comparable to TTDM) recapitulates impaired insulin secretion in TTDM, specifically impaired FPIR and insulin pulse mass with an increased proinsulin/insulin (PI/I) secretion ratio; and 2). whether these changes can be attenuated by addition of diazoxide to islets cultured with 11 mM glucose. Islets cultured with 11 mM glucose for 96 h had 75% depleted insulin stores (P < 0.05), decreased FPIR and insulin pulse mass (P < 0.05), and an approximately 3-fold increase in the ratio of PI/I islet content and in secretion ratio (P < 0.05). Addition of diazoxide to islets cultured with 11 mM glucose decreased insulin secretion during static incubation, leading to relative preservation of insulin stores and enhanced insulin secretion during subsequent perifusion; FPIR increased by 162% (P < 0.05) and insulin pulse mass by 150% (P < 0.05) vs. no diazoxide. The mean islet PI/I content and islet PI/I secretion ratio were also decreased by approximately 70% (P < 0.05) by prior addition of diazoxide to islets during culture with 11 mM glucose. FPIR and insulin pulse mass were related to islet insulin stores (P < 0.001 for FPIR and P < 0.001 for pulse amplitude). In conclusion, the pattern of defects of insulin secretion present in TTDM (impaired FPIR and pulsatile insulin secretion, increased PI/I ratio) can be recapitulated in human islets cultured with 11 mM glucose for 96 h. These defects can be at least partially offset by concurrent inhibition of insulin secretion by diazoxide, which also preserves insulin stores. Defective insulin secretion in TTDM may be, at least in part, due to depletion of available insulin stores secondary to chronic increased demand (insulin resistance and hyperglycemia) in the setting of a decreased beta-cell mass.

Cells, Cultured↗

PubMed1986

Long-term treatment with diazoxide in childhood hyperinsulinism.

This paper reviews the outcome in 12 children with hyperinsulinaemic hypoglycaemia who first developed symptoms between the ages of 2 and 8 months and who were treated with diazoxide (5-20 mg/kg/day) for 2-13 years. Two cases required subtotal pancreatectomy at the ages of 5 and 10 years because of recurrent hypoglycaemia and one girl with severe retardation died at the age of 6 years while still on diazoxide therapy. Two patients aged 3.5 and 9 years are still on treatment and in 7 cases diazoxide was discontinued between the ages of 2.5 and 14 years, indicating that spontaneous remission can be expected in a high proportion of children with post-neonatal hyperinsulinaemic hypoglycaemia. Of the 9 children who started diazoxide within 3 months of the onset of symptoms, 5 are of normal intelligence and 4 are moderately retarded (IQs 63-71). In 3 children diazoxide was started 8 months to 3 years after the onset of symptoms; two are retarded (IQs 60-70) and the third was severely retarded and died aged 6 years.

Diazoxide↗

PubMed1998

Leptin levels in women with polycystic ovary syndrome before and after treatment with diazoxide.

Leptin, a product of the ob gene, is a 16 kDa protein which is produced by adipocytes. In humans, obesity is a common finding in women with polycystic ovary syndrome (PCOS). The role, however, of leptin in PCOS is not clear. Some studies have reported increased levels of leptin in PCOS, while others report that they are normal. Also, insulin resistance is a common finding in PCOS. The aim of this study was to investigate further the role of insulin in leptin secretion in patients with PCOS by treating them for 10 days with diazoxide, an insulin-reducing compound. Eight women with PCOS, mean age 22.1 +/- 2.7 years, with mean body mass index (BMI) 28.4 +/- 5.7kg/m2, were studied. An oral glucose tolerance test (OGTT) was performed in all women and blood samples were taken before and at 30, 60, 90, 120 and 150 min after the administration of glucose. Glucose, insulin, leptin, free testosterone, delta4 androstenedione, sex hormone binding globulin (SHBG), LH, FSH, IGF-I and insulin-like growth factor-binding protein-3 (IGFBP-3) were measured in the sera taken before the administration of glucose, while glucose and insulin levels were measured in all samples which were collected after the administration of glucose. Diazoxide 300 mg daily was given to all women starting after the end of the OGTT for 10 days. A second OGTT was performed the day after the discontinuation of the diazoxide treatment. The same hormonal and biochemical parameters were also measured in all patients during the second OGTT. After the administration of diazoxide a reduction in sum insulin (262 +/- 147 vs 679 +/- 341 microU/ml. P<().01), leptin (18.5 +/- 10.6 vs 24.2 +/- 10.2 ng/ml, P<0.01), free testosterone (3.0 +/- 1.9 vs 5.1 +/- 1.9 pg/ml, P<0.01), delta4 androstenedione (3.8 +/- 1.9 vs 5.7 +/- 2.0 ng/ml, P<0.01) and IGF-I (219.5 +/- 69.2 vs 314.5 +/- 82.3 ng/ml, P<0.01) levels was observed. Serum SHBG (38.8 +/- 16.8 vs 27.8 +/- 12.1 nmol/l, P<0.01) and sum glucose levels (994.1 +/- 252.7 vs 711.1 +/- 166.1 mg/dl, P<0.05) were increased while IGFBP-3 (3.96 +/- 2.49 vs 3.75 +/- 2.24mg/l), FSH (6.2 +/- 1.8 vs 6.0 +/- 2.5 mU/l) and LH (18.9 +/- 6.7 vs 21.4 +/- 6.7 mU/l) concentrations did not change significantly. A significant positive correlation was found between serum leptin and BMI values before and after administration of diazoxide as well as between leptin, insulin and IGFBP-3 values. Also, sum insulin values correlated significantly with BMI. However, when multiple regression analysis was used this correlation was eliminated except that between leptin and BMI. This was most probably due to the small number of cases. The mechanism of the reduction of leptin levels is unclear. However, it is suggested that the concomitant decrease of insulin levels may play a role.

Adipose Tissue↗

PubMedDate not supplied

Pharmacokinetics and response to diazoxide in renal failure.

Diazoxide is given by rapid intravenous injection for the urgent reduction of high blood pressure in patients with all grades of renal function. Oral diazoxide produces less consistent effects. Protein binding of diazoxide is reduced in renal failure and this can be related to reduction of albumin concentration. There is a relation between impairment of renal function and the hypotensive effect of rapidly injected diazoxide. This is explicable in terms of the greater concentration of free (unbound) drug achieved after rapid injection in patients with renal failure. Renal clearance of diazoxide and its metabolites is impaired in renal failure but this is unlikely to affect its activity.

Administration, Oral↗

PubMed1994

Diazoxide causes recovery of beta-cell glucose responsiveness in 90% pancreatectomized diabetic rats.

Chronic hyperglycemia causes near-total disappearance of glucose-induced insulin secretion. The etiology has been suggested to be a nonsustainable stimulation of insulin release that causes beta-cells to become unresponsive to glucose through an undefined mechanism. We used an inhibitor of insulin secretion, diazoxide, to test this hypothesis in 90% pancreatectomized (Px) rats. Px rats were given 5 days of diazoxide (30 mg/kg orally twice a day) or tap water starting on postoperative day 8, 15, or 22. In vitro pancreas perfusions were conducted 36 h posttreatment (2, 3, or 4 weeks after surgery) using a protocol of 15 min of 16.7 mM glucose followed by 15 min of 16.7 mM glucose plus 10 mM arginine. In 2-week Px rats, insulin responses to 16.7 mM glucose and to glucose/arginine were both appropriate for the reduced beta-cell mass, i.e., no defect in beta-cell glucose responsiveness had yet occurred. Diazoxide had no affect on insulin release at this time. Between 2 and 3 weeks after pancreatectomy, insulin output to 16.7 mM glucose fell 75%, and that to glucose/arginine fell 50%. Diazoxide given at this time partially blocked the fall in glucose-induced insulin secretion and totally prevented that with arginine. The increased insulin secretion caused by diazoxide was accompanied by 1) lower nonfasting plasma glucose values, 2) improved glucose tolerance after oral glucose load, and 3) a 50% increase in pancreatic insulin content. Our results support the concept that excessive insulin secretion is a major cause of the hyperglycemia-induced loss of beta-cell glucose responsiveness. A leading candidate for the mechanism of this effect is depleted pancreatic insulin stores. Overstimulation of insulin secretion provides a new target for pharmacological therapy aimed at reducing glucose intolerance in non-insulin-dependent diabetes mellitus.

Animals↗

PubMed1998

Induction of beta-cell rest in type 1 diabetes. Studies on the effects of octreotide and diazoxide.

OBJECTIVE: To evaluate the inhibitory effects of octreotide and diazoxide on insulin secretion in patients with type 1 diabetes and measurable levels of circulating C-peptide. RESEARCH DESIGN AND METHODS: Diazoxide was given to six patients during a 7-day period (100 mg three times daily), followed by a 3-week washout. Subsequently, octreotide (50 micrograms, three times daily) was administered subcutaneously for 7 days. Pre- and post- prandial blood glucose and serum C-peptide concentrations were measured before medication (control) and on day 7 of each medication period. Glucagon-stimulated C-peptide was determined in the morning before medication and on the day after each treatment period. RESULTS: Diazoxide inhibited glucagon-stimulated C-peptide secretion (mean increment 0.08 nmol/l vs. 0.18 nmol/l, P < 0.05), whereas octreotide had no such effect. Both reduced the pre- and postprandial serum C-peptide concentrations (P < 0.05), octreotide being the more potent in this respect. A reduction in basal and meal-related blood glucose was observed during octreotide treatment, whereas the glucose concentrations tended to be higher during treatment with diazoxide than during the 24-h control period. CONCLUSIONS: The study indicates that the two drugs reduce insulin output by different mechanisms. Diazoxide inhibits hormonal release directly on the beta-cells, whereas octreotide exerts its effect indirectly, presumably by multiple actions on insulin sensitivity and insulin-releasing hormones. The results suggest that each drug is capable of inducing beta-cell rest in type 1 diabetes.

Adult↗

PubMed2004

Temporary preservation of beta-cell function by diazoxide treatment in childhood type 1 diabetes.

OBJECTIVE: We examined the effect of diazoxide, an ATP-sensitive K(+) channel opener and inhibitor of insulin secretion, on beta-cell function and remission in children at clinical onset of type 1 diabetes. RESEARCH DESIGN AND METHODS: A total of 56 subjects (21 girls and 35 boys, age 7-17 years) were randomized to 3 months of active treatment (diazoxide 5-7.5 mg/kg in divided doses) or placebo in addition to multiple daily insulin injections and were followed for 2 years. RESULTS: Diazoxide decreased circulating C-peptide concentrations by approximately 50%. After cessation of the treatment, basal and meal-stimulated C-peptide concentrations increased to a maximum at 6 months, followed by a decline. Meal-stimulated C-peptide concentration was significantly higher at 12 months (0.43 +/- 0.22 vs. 0.31 +/- 0.26 nmol/l, P = 0.018) and tended to fall less from clinical onset to 24 months in the diazoxide- vs. placebo-treated patients (-0.05 +/- 0.24 vs. -0.18 +/- 0.26 nmol/l, P = 0.064). At 24 months, the meal-stimulated C-peptide concentrations were 0.24 +/- 0.20 and 0.20 +/- 0.17 nmol/l, respectively. Side effects of diazoxide were prevalent. CONCLUSIONS: This study demonstrates that partial inhibition of insulin secretion for 3 months at onset of childhood type 1 diabetes suspends the period of remission and temporarily preserves residual insulin production. Further evaluation of the full potential of beta-cell rest will require compounds with less side effects as well as protocols optimized for sustained secretory arrest.

Adolescent↗

PubMed1992

Palliative treatment of hyperinsulinism with cyproheptadine and diazoxide.

Treatment for hyperinsulinism in infants and children can be difficult and has included numerous treatment modalities. This paper reports 16 months of palliative treatment with cyproheptadine and diazoxide in a child with hyperinsulinism initially diagnosed at 6 months of age (her insulin level was 80 microU/mL while her glucose level was 38 mg/dL). She continued to have episodes of staring and alteration in level of consciousness while receiving her usual doses of diazoxide (12 mg/kg) alone. Mean nocturnal glucose values, which were quite low during treatment with diazoxide alone, improved significantly with the addition of cyproheptadine to her therapeutic regimen. Fasted C-peptide values, elevated during diazoxide alone, returned to the normal range with combination treatment for 16 months. Cyproheptadine and diazoxide in combination may be useful for treatment of hyperinsulinism that presents after the neonatal period.

Blood Glucose↗