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Level Qualifying studies
A Systematic review or meta-analysis of human trials
B Human RDBPC trials. ≥ 2 studies and/or 1 study with ≥ 50 subjects
C Human RDBPC trials or RCTs. 1 study < 50 subjects
D Human trials or in-vivo animal trials
G No significant nutrient depletion research was found

Results for Hydrochlorothiazide: 10

Evidence Rating Scale

Chloride

Summary: Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium.

Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium.

All patients who were maintained on this medication developed a mild hypochloremia, but no significant changes in serum sodium or potassium were observed. No deleterious hematologic or renal changes occurred.

Folate

Summary: Chronic diuretic use is associated with a significant increase in serum homocysteine concentration, a significant decrease in RBC folate concentration, and no significant change in concentrations of vitamins B6 and B12.

Chronic diuretic use is associated with a significant increase in serum homocysteine concentration, a significant decrease in RBC folate concentration, and no significant change in concentrations of vitamins B6 and B12.

Chronic diuretic use is associated with a significant increase in serum homocysteine concentration, a significant decrease in RBC folate concentration, and no significant change in concentrations of vitamins B6 and B12.

In a small trial of 27 patients assigned to treatment with either hydrochlorothiazide (HCT) or an ACE inhibitor, Westphal et al (2003) measured homocysteine, creatinine, folate, vitamins B6 and B12 before and after 4–6 weeks of treatment. HCT raised homocysteine concentrations by 28%, creatinine by 12% and decreased folate levels nonsignificantly by 26%.

Iron

Summary: The results showed that for most of the trace elements investigated (zinc, iron, copper, manganese and cobalt) no relevant changes were seen. Only serum iron values (medians) showed a slight drop (p less than 0.05) with 6 mg piretanide twice daily. The results indicate that a three-months’ therapy with piretanide or with a thiazide-potassium sparer diuretic combination is safe without producing any disturbances in the serum levels of trace elements.

The results showed that for most of the trace elements investigated (zinc, iron, copper, manganese and cobalt) no relevant changes were seen. Only serum iron values (medians) showed a slight drop (p less than 0.05) with 6 mg piretanide twice daily. The results indicate that a three-months’ therapy with piretanide or with a thiazide-potassium sparer diuretic combination is safe without producing any disturbances in the serum levels of trace elements.

Magnesium

Summary: Baseline vs treatment mean serum potassium levels were 4.24 vs 4.47 mEq/L for amiloride, 4.24 vs 3.86 mEq/L for the combination, and 4.15 vs 3.56 mEq/L for hydrochlorothiazide. The changes in serum potassium level from the baseline for amiloride plus hydrochlorothiazide were significantly different from those for hydrochlorothiazide throughout the study (except for week 6).

Baseline vs treatment mean serum potassium levels were 4.24 vs 4.47 mEq/L for amiloride, 4.24 vs 3.86 mEq/L for the combination, and 4.15 vs 3.56 mEq/L for hydrochlorothiazide. The changes in serum potassium level from the baseline for amiloride plus hydrochlorothiazide were significantly different from those for hydrochlorothiazide throughout the study (except for week 6).

It can be concluded that 25 mg of hydrochlorothiazide is as effective in lowering blood pressure as higher doses of the diuretic. Higher doses of thiazides will in some patients cause adverse metabolic reactions of which the fall in serum potassium and magnesium is effectively hindered by triamterene.

Serum potassium and magnesium concentrations were reduced in the hydrochlorothiazide group and serum sodium concentration in the hydrochlorothiazide plus amiloride group. Our results suggest that in elderly hypertensive subjects, a higher proportion of patients could be managed with the low dose hydrochlorothiazide plus amiloride regimen than with the low dose hydrochlorothiazide regimen.

The occurrence of premature ventricular contractions correlated significantly with the decrease observed in serum potassium (r = 0.71, p less than 0.001) and in serum magnesium (r = 0.68, p less than 0.001). Thiazide therapy appears to cause both potassium and magnesium depletion, and decreases in both correlate well with the appearance of ventricular ectopic depolarizations.

In conclusion, CA-SPAK mice exhibit normomagnesemia, despite increased NCC activity and Na+ reabsorption. Thus, Mg2+ reabsorption is not coupled to increased thiazide-sensitive Na+ reabsorption, suggesting a similar process explains normomagnesemia in Gordon syndrome. Further research is required to unravel the molecular underpinnings of this phenomenon and the more pronounced Mg2+ excretion after prolonged HCTZ administration.

Thiazide therapy appears to cause both potassium and magnesium depletion, and decreases in both correlate well with the appearance of ventricular ectopic depolarizations.

Mild hypomagnesemia develops in about one fifth of normal subjects during short-term thiazide treatment. Relyte can readily correct it.

With respect to dose, those receiving 100 mg/d of hydrochlorothiazide had the lowest Mg++ concentrations and the greatest prevalence of hypomagnesemia (12%), defined as Mg++ less than 0.75 mmol/L (1.5 mEq/L). Serum Mg++ need not routinely be determined in patients with uncomplicated hypertension who are receiving triamterene-containing diuretics or low-dose (50 mg/d or less) hydrochlorothiazide.

Potassium

Summary: Patients with thiazide-induced hyponatraemia were characterized by advanced age, female gender, inappropriate saliuresis and mild hypokalaemia. Low BMI was not found to be a significant risk factor, despite previous suggestions. The time from thiazide initiation to presentation with hyponatraemia suggests that the recommended practice of performing a single investigation of serum biochemistry 7-14 days after thiazide initiation may be insufficient or suboptimal. Further larger and more systematic studies of thiazide-induced hyponatraemia are required.

Patients with thiazide-induced hyponatraemia were characterized by advanced age, female gender, inappropriate saliuresis and mild hypokalaemia. Low BMI was not found to be a significant risk factor, despite previous suggestions. The time from thiazide initiation to presentation with hyponatraemia suggests that the recommended practice of performing a single investigation of serum biochemistry 7-14 days after thiazide initiation may be insufficient or suboptimal. Further larger and more systematic studies of thiazide-induced hyponatraemia are required.

The magnitude of the observed change in fasting plasma glucose associated with low-dose thiazide diuretic use, while statistically significant, does not appear to place patients at clinically significant risk. On the other hand, the observed change in serum potassium was also statistically significant, and may be clinically significant in patients whose baseline potassium concentration is low or low-normal, and could predispose at-risk patients, such as those with ischemic heart disease, to ventricular arrhythmias.

In conclusion, using thiazide-like diuretics is superior to thiazide-type diuretics in reducing blood pressure without increasing the incidence of hypokalemia, hyponatraemia and any change of blood glucose and serum total cholesterol.

KMgCit is equally effective as potassium chloride in correcting thiazide-induced hypokalemia. In addition, KMgCit, but not potassium chloride, produces a small but significant increase in serum magnesium concentration by delivering a magnesium load, and it confers alkalinizing and citraturic actions.

Magnesium citrate significantly increased 24-hour urinary magnesium after the first week of supplementation and maintained this increase throughout the study. Potassium magnesium citrate and potassium citrate, but not magnesium citrate, significantly increased urinary pH and citrate values. Potassium magnesium citrate not only corrects thiazide-induced hypokalemia, but also may avert magnesium loss while providing an alkali load.

Ten patients receiving hydrochlorothiazide developed hypokalemia compared with only two receiving hydrochlorothiazide with amiloride. Relatively low doses of hydrochlorothiazide (25 to 50 mg/d) effectively reduce blood pressure in elderly hypertensive patients. Hypokalemia may occur with hydrochlorothiazide alone but is much less common when hydrochlorothiazide is combined with amiloride.

The proportions of patients in the two groups with hypokalemia (14% and 29% respectively), defined as a serum potassium level below 3.5 mmol/L, differed significantly (p = 0.0026), whereas the proportions with a potassium level exceeding 4.5 mmol/L (4.5% and 3.9% respectively) were similar. Thus, the combination drug reduced the blood pressure to the same extent as hydrochlorothiazide alone but significantly less often caused hypokalemia. In light of growing concerns about the cardiovascular complications of hypokalemia, hydrochlorothiazide-amiloride appears preferable to hydrochlorothiazide alone for the treatment of some patients with hypertension.

The cumulative incidence of hypokalemia of 8% for the furosemide group compared to that of 62% for the hydrochlorothiazide group.

Five subjects receiving amiloride-hydrochlorothiazide (12%) and two subjects receiving triamterene-hydrochlorothiazide (5%) had hypokalemia (serum potassium level less than 3.5 mEq/l) at week 9. The average decrease in serum potassium levels during amiloride-hydrochlorothiazide therapy (-0.33 +/- 0.08 mEq/l) was greater than that after triamterene-hydrochlorothiazide (- 0.08 +/- 0.07 mEq/l).

For end-stage renal disease patients on CAPD, the combination of furosemide, hydrochlorothiazide, and spironolactone results in higher urine output and better volume control compared to furosemide alone.

In contrast, patients on HCTZ developed volume contraction, hypokalemia associated with an increase in fractional sodium and potassium excretion, and an increased urine osmolality associated with a decreased free-water clearance.

The combination of the 2 drugs decreased supine diastolic BP to goal levels in about 56% of the patients not achieving goal with either drug alone. Adverse effects were minimal with either drug alone and in combination, except for hypokalemia, which increased with thiazide alone and in combination.

In this study population, combination therapies with VAL/HCTZ were associated with significantly greater BP reductions compared with either monotherapy, were well tolerated, and were associated with less hypokalemia than HCTZ alone.

All active treatments were well tolerated. There was a trend towards a higher incidence of hypokalemia in patients treated with HCTZ, alone or in combination, compared to those receiving ibopamine alone or placebo.

By contrast, HCTZ-based therapy provided significantly smaller mean reductions in BP from baseline in obese patients vs. nonobese patients (P < 0.05). Aliskiren-based therapy was generally well tolerated in obese patients, and was associated with a significantly lower incidence of hypokalemia (1.0 vs. 14.0%, P < 0.0001) than HCTZ-based therapy.

In the majority of hypertensive patients, treatment with 50 mg/d of hydrochlorothiazide does not cause marked hypokalemia or ventricular arrhythmias. However, because some individuals will develop hypokalemia after starting diuretic therapy, serum potassium levels should be monitored and potassium-sparing strategies should be used when indicated.

In addition, the effect of each drug on blood chemistry differed markedly: indapamide failed to alter significantly the serum ionic composition, whereas hydrochlorothiazide was associated with both hyponatremia and hypokalemia.

The absolute value of serum potassium was significantly lower on hydrochlorothiazide than on lisinopril therapy. Neither treatment had an effect on serum magnesium concentrations, nor was there any significant effect of either treatment on urine volume or urinary excretion of sodium, potassium or magnesium. There was a trend towards increased total body potassium concentration on lisinopril compared with a decrease in total body potassium on hydrochlorothiazide. However, this difference was just outside the range of statistical significance.

The results showed that blood pressure control was comparable in both treatment groups but hydrochlorothiazide alone caused a statistically significant reduction in serum potassium levels compared to the drug combination. Apart from 1 patient who developed hypokalaemia on hydrochlorothiazide alone, no other side-effects of treatment were reported.

Mild hypokalemia (less than 3.5 mEq/L) occurred in approximately half of the patients and was unrelated to treatment group. Serious arrhythmias were infrequent, though some patients had large numbers of extra beats. The incidence of arrhythmia appeared unrelated to serum potassium concentration. We conclude that mild hypokalemia associated with low-dose diuretic therapy for hypertension is not arrhythmogenic.

Both treatments were clinically well tolerated; however, the tendency of hypokalemia was more pronounced in the hydrochlorothiazide group. This could be hazardous in patients who receive a concomitant cardiac glycoside, especially when no clear-cut benefit of concomitant digitalis therapy is demonstrated.

Serum potassium values were significantly (P < 0.001) reduced by hydrochlorothiazide but there was no correlation between changes in potassium levels and changes in ventricular ectopic activity. The results of the study suggest that hydrochlorothiazide and cilazapril were equally effective in reducing blood pressure, but only cilazapril reduced left ventricular hypertrophy and suppressed ventricular ectopic activity.

Nicardipine caused no significant changes in blood chemistry, whereas HCTZ caused statistically significant decreases (P < 0.001) in sodium and potassium and increases (P < or = 0.01) in glucose, BUN, creatinine, uric acid, cholesterol and LDL compared with baseline. In 12.7% of the patients in the HCTZ group, serum potassium dropped to levels < 3.5 meq/l, which occurred in only 1.4% of the patients who used nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS).

It can be concluded that 25 mg of hydrochlorothiazide is as effective in lowering blood pressure as higher doses of the diuretic. Higher doses of thiazides will in some patients cause adverse metabolic reactions of which the fall in serum potassium and magnesium is effectively hindered by triamterene.

It can be concluded that 25 mg of hydrochlorothiazide is as effective in lowering blood pressure as higher doses of the diuretic. Higher doses of thiazides will in some patients cause adverse metabolic reactions of which the fall in serum potassium and magnesium is effectively hindered by triamterene.

Serum potassium and magnesium concentrations were reduced in the hydrochlorothiazide group and serum sodium concentration in the hydrochlorothiazide plus amiloride group. Our results suggest that in elderly hypertensive subjects, a higher proportion of patients could be managed with the low dose hydrochlorothiazide plus amiloride regimen than with the low dose hydrochlorothiazide regimen.

However, patients developed adverse reactions, including muscle cramps (n = 2), biological (n = 7) or symptomatic hypovolemia (n = 1), hypokalemia (n = 4), and hyponatremia (n = 1), which all corrected after treatment withdrawal. HCTZ doses greater than 0.4 mg/kg/d decreased calcium excretion, but were associated with significant adverse events. Thiazide diuretic therapy should be considered with caution in children with Dent disease.

Although the administration of the diuretics increased potassium excretion in all groups, the response of the zinc-deficient rats was attenuated.

Length of hospital stay, hospital cost, and MR were higher in elderly with CAH. Female gender, hydrochlorothiazides, loop diuretics, and ≥2 comorbid diseases are the leading risk factors associated with CAH in elderly.

These qualitative changes resemble those induced by hydrochlorothiazide but did not achieve quantitative significance, either because the constituent diuretic dose was too small or because acebutolol compensated for some of its effects.

Hypokalemia occurred frequently in both groups: 71.4% and 83.3% in the oral hydrochlorothiazide and intravenous chlorothiazide groups, respectively (p=0.21).

Changes in serum potassium and serum glucose levels were not correlated in individuals receiving hydrochlorothiazide monotherapy; thus maintenance of normal potassium levels may not attenuate the risk of thiazide diuretic-induced hyperglycemia.

The incidence and severity of side effects were similar for both drugs. Three patients receiving doxazosin and 6 receiving HCTZ were withdrawn due to drug-related clinical side effects including 2 patients receiving HCTZ who were withdrawn because of laboratory test abnormalities. Eight HCTZ- and 1 doxazosin-treated patients developed hypokalemia and 6 HCTZ-treated patients developed hyperuricemia. These findings indicate that doxazosin and HCTZ provide comparable antihypertensive efficacy after 6 months of treatment using a once-daily regimen, but doxazosin produces a beneficial effect on the serum lipid profile as well as fewer biochemical aberrations.

The high dose produced a mean 0.7 mEq/L reduction in serum potassium while the low dose caused no change. Both doses produced similar changes in serum lipoproteins. Statistically significant elevations were seen in total cholesterol (approximately 12%), LDL cholesterol (approximately 20%), cholesterol: HDL ratio (approximately 15%), and apolipoprotein B (approximately 20%). Apolipoprotein A1 was significantly reduced (approximately 6%). These results support the use of low doses of HCTZ in mild hypertension to avoid hypokalemia, but suggest that adverse changes in serum lipids will occur.

Thiazide therapy appears to cause both potassium and magnesium depletion, and decreases in both correlate well with the appearance of ventricular ectopic

Thus, although many elderly women taking diuretics may have hypokalemia routine potassium supplementation for all non-digitalized geriatric patients receiving diuretics does not seem to be indicated.

Sodium

Summary: Patients with thiazide-induced hyponatraemia were characterized by advanced age, female gender, inappropriate saliuresis and mild hypokalaemia. Low BMI was not found to be a significant risk factor, despite previous suggestions. The time from thiazide initiation to presentation with hyponatraemia suggests that the recommended practice of performing a single investigation of serum biochemistry 7-14 days after thiazide initiation may be insufficient or suboptimal. Further larger and more systematic studies of thiazide-induced hyponatraemia are required.

Patients with thiazide-induced hyponatraemia were characterized by advanced age, female gender, inappropriate saliuresis and mild hypokalaemia. Low BMI was not found to be a significant risk factor, despite previous suggestions. The time from thiazide initiation to presentation with hyponatraemia suggests that the recommended practice of performing a single investigation of serum biochemistry 7-14 days after thiazide initiation may be insufficient or suboptimal. Further larger and more systematic studies of thiazide-induced hyponatraemia are required.

In conclusion, using thiazide-like diuretics is superior to thiazide-type diuretics in reducing blood pressure without increasing the incidence of hypokalemia, hyponatraemia and any change of blood glucose and serum total cholesterol.

For end-stage renal disease patients on CAPD, the combination of furosemide, hydrochlorothiazide, and spironolactone results in higher urine output and better volume control compared to furosemide alone.

In addition, the effect of each drug on blood chemistry differed markedly: indapamide failed to alter significantly the serum ionic composition, whereas hydrochlorothiazide was associated with both hyponatremia and hypokalemia.

Nicardipine caused no significant changes in blood chemistry, whereas HCTZ caused statistically significant decreases (P < 0.001) in sodium and potassium and increases (P < or = 0.01) in glucose, BUN, creatinine, uric acid, cholesterol and LDL compared with baseline. In 12.7% of the patients in the HCTZ group, serum potassium dropped to levels < 3.5 meq/l, which occurred in only 1.4% of the patients who used nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS).

However, patients developed adverse reactions, including muscle cramps (n = 2), biological (n = 7) or symptomatic hypovolemia (n = 1), hypokalemia (n = 4), and hyponatremia (n = 1), which all corrected after treatment withdrawal. HCTZ doses greater than 0.4 mg/kg/d decreased calcium excretion, but were associated with significant adverse events. Thiazide diuretic therapy should be considered with caution in children with Dent disease.

Elderly hypertensive patients were more likely to develop hyponatremia after age 75. Female patients had a higher frequency of hyponatremia than male patients. The main cause of hyponatremia in patients treated with diuretics was thiazide.

Our study suggests that the prevalence of hyponatremia among Saudi thiazide users is relatively high, and more so for the elderly and for those with T2DM. Early identification of this condition is important and caution should be exercised while prescribing thiazide drugs, particularly to those who are most at risk of developing hyponatremia to prevent related complications.

Hyponatremia is the most frequent and significant adverse effect of HCT, for which a close observation is mandatory in HCT application for patients with SMID.

We have presented five episodes of hydrochlorothiazide-induced hyponatremia in three elderly nursing home patients. Fortunately all our patients survived. The common use of thiazide diuretics in this population and the nonspecific symptoms that follow toxicity make it imperative to monitor closely elderly patients who are taking thiazide diuretics.

We have presented five episodes of hydrochlorothiazide-induced hyponatremia in three elderly nursing home patients. Fortunately all our patients survived. The common use of thiazide diuretics in this population and the nonspecific symptoms that follow toxicity make it imperative to monitor closely elderly patients who are taking thiazide diuretics.

The occurrence of premature ventricular contractions correlated significantly with the decrease observed in serum potassium (r = 0.71, p less than 0.001) and in serum magnesium (r = 0.68, p less than 0.001). Thiazide therapy appears to cause both potassium and magnesium depletion, and decreases in both correlate well with the appearance of ventricular ectopic depolarizations.

We report a 69-year-old man with generalized weakness beginning 2 weeks after starting hydrochlorothiazide (HCTZ). Evaluation revealed a serum sodium level of 120 mmol/L. The patient was admitted and successfully treated with free water restriction and discontinuation of the HCTZ.

Hydrochlorothiazide use was attributed in 25 (78.1%) of 32 with medication-associated hyponatraemia. Repeat renal profile (89%) was the commonest management of hypotonic hyponatraemia. Whilst hyponatraemia was common in the clinic setting, many cases were not acknowledged and had no clear management strategies. In view of mild hyponatraemia has deleterious consequences, future studies should determine whether appropriate management of mild hyponatraemia will lead to clinical improvement.

Thiamin

Summary: The addition of small doses of hydrochlorothiazide will readily induce an increase of water and salt excretion in rats, but does not affect the thiamine excretion. 2. Hydrochlorothiazide increases the total excretion and the concentration of thiamine in urin in healthy persons not only by normal feeding but also by increased vitamin B1 feeding. An increased liquid intake however results in a depression of thiamine concentration along with the induced increase of diurese. 3. The effect of hydrochlorothiazide on the thiamine excretion is the same in persons with a decomposed lever cirrhosis as in healthy persons and is independant of the vitamine B1 supply. 4. It is concluded in the present study that this diureticum retards thiamine reabsorption in the tubulus-system of the kidney.

The addition of small doses of hydrochlorothiazide will readily induce an increase of water and salt excretion in rats, but does not affect the thiamine excretion. 2. Hydrochlorothiazide increases the total excretion and the concentration of thiamine in urin in healthy persons not only by normal feeding but also by increased vitamin B1 feeding. An increased liquid intake however results in a depression of thiamine concentration along with the induced increase of diurese. 3. The effect of hydrochlorothiazide on the thiamine excretion is the same in persons with a decomposed lever cirrhosis as in healthy persons and is independant of the vitamine B1 supply. 4. It is concluded in the present study that this diureticum retards thiamine reabsorption in the tubulus-system of the kidney.

Vitamin C

Summary: Here we provided evidence of the involvement of oxidative stress and metabolic disorders in a rat model of HFD associated or not with HTCZ. (PhSe)2 supplementation reduced the oxidative stress and this compound should be considered for the treatment of biochemical disturbances and oxidative stress in other animal models of metabolic disorders.

Here we provided evidence of the involvement of oxidative stress and metabolic disorders in a rat model of HFD associated or not with HTCZ. (PhSe)2 supplementation reduced the oxidative stress and this compound should be considered for the treatment of biochemical disturbances and oxidative stress in other animal models of metabolic disorders.

Zinc

Summary: The available evidence suggests that use of ACE inhibitors and angiotensin 2 receptor antagonists or thiazide diuretics have the potential to reduce zinc levels in hypertensive patients. Additional research using larger participant numbers and accounting for dietary zinc intakes are required.

The available evidence suggests that use of ACE inhibitors and angiotensin 2 receptor antagonists or thiazide diuretics have the potential to reduce zinc levels in hypertensive patients. Additional research using larger participant numbers and accounting for dietary zinc intakes are required.

Hydrochlorothiazide decreased serum zinc levels (p < 0.05) and was unchanged with magnesium supplementation but the serum magnesium returned to normal values. Improvement of symptoms of sexual dysfunction was positive in one patient. This study shows that low serum zinc levels may be associated with sexual dysfunction but the definitive role of zinc in the pathogenesis of sexual dysfunction will remain controversial.

However, urinary zinc excretion was abnormally elevated in the two patient groups. In the dosage used, amiloride did not have a zinc-sparing effect.

With respect to the importance of zinc as an essential element in human metabolism and the frequency of diuretic treatment, the observed increased urinary losses of zinc deserve further attention.

Hydrochlorothiazide produced a striking and sustained increase in urinary Zn excretion, which might contribute to the efficacy of this drug in the prevention of calcific renal stones. Serum Zn levels remained normal in the majority of subjects on long term thiazide therapy, but the occasional finding of subnormal levels suggests that long term thiazide therapy carries with it the hazard of Zn deficiency.

The first four patient groups exhibited significantly increased urinary zinc/creatinine ratios when compared to the control and untreated hypertensive groups, but in the two combination regimens there was little zincuria. It is suggested that both diuretics inactivate the zincuric effect of captopril by binding to its sulphydryl group within the tubular lumen.

Treatment with losartan causes an increase in urinary Zn excretion and induces Zn deficiency in patients with hypertension. The addition of hydrochlorothiazide has an additive effect. Magnesium and nitric oxide metabolism are not affected by either treatment.

Significant zinc depletion may occur during long-term administration of DTDs, principally in conditions associated with diminished total body zinc levels such as hepatic cirrhosis, diabetes mellitus, gastro-intestinal disorders and several renal diseases. Attention to the early symptoms of zinc deficiency such as hypogeusia, hyposmia, abnormal dark adaptation and impotence and the monitoring of serum zinc levels are advisable during long-term treatment with common DTDs.

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