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Gonorrhoea is an important sexually transmitted notifiable condition. This paper describes findings from two gonorrhoea enhanced surveillance programs operating during the 2000s in Queensland: one in the remote Torres and Northern Peninsula Area (T&NPA); the other in an urban region. The overall response rate in the T&NPA (2006-2011) was 82% (723 of 879), and in Brisbane Southside and West Moreton (BSWM) (2003-2011), it was 62% (1,494 of 2,401 notifications). In the T&NPA, cases were young (80% <25 years), Indigenous (97%) and 44% were male. In the BSWM, cases were predominantly male (76%), non-Indigenous (92%) and 42% were aged less than 25 years. Co-infection with chlamydia was found in 54% of males and 60% of females in the Torres, and in 18% of males and 35% of females in the BSWM. In the BSWM 35% of the men without a syphilis test recorded had reported sexual contact with men; similarly 34% of the men without an HIV test recorded had reported sexual contact with men. Compliance with recommended treatment (ceftriaxone) was greater than 90% in all years except 2008 (84%) in the T&NPA. Treatment compliance increased significantly, from 40% in 2003 to 84.4% in 2011 (P<0.0001) in the BSWM cohort. The proportion of contacts with a documented treatment date increased significantly in the T&NPA from 56% in 2009 to 76% in 2011 (P=0.019), after a system for follow-up with the clinician became routine. Gonorrhoea epidemiology and management challenges vary across Queensland populations. Enhanced surveillance allows public health authorities to monitor epidemiology and reminds clinicians to prioritise effective sexually transmitted infection treatment for their clients., (This work is copyright. Apart from any use as permitted under the Copyright Act 1968, no part may be reproduced by any process without prior written permission from the Commonwealth. Requests and inquiries concerning reproduction and rights should be addressed to the Commonwealth Copyright Administration, Attorney General's Department, Robert Garran Offices, National Circuit, Barton ACT 2600 or posted at http://www.ag.gov.au/cca.)

Epidemiologic research has demonstrated convincingly that certain pigmentary characteristics are associated with increased relative risks of melanoma; however there has been no comprehensive review to rank these characteristics in order of their importance on a population level. We conducted a systematic review of the literature and meta-analysis to quantify the contribution of pigmentary characteristics to melanoma, estimated by the population-attributable fraction (PAF). Eligible studies were those that permitted quantitative assessment of the association between histologically confirmed melanoma and hair colour, eye colour, skin phototype and presence of freckling; we identified 66 such studies using citation databases, followed by manual review of retrieved references. We calculated summary relative risks using weighted averages of the log RR, taking into account random effects, and used these to estimate the PAF. The pooled RRs for pigmentary characteristics were: 2.64 for red/red-blond, 2.0 for blond and 1.46 for light brown hair colour (vs. dark); 1.57 for blue/blue-grey and 1.51 for green/grey/hazel eye colour (vs. dark); 2.27, 1.99 and 1.35 for skin phototypes I, II and III respectively (vs. IV); and 1.99 for presence of freckling. The highest PAFs were observed for skin phototypes 1/II (0.27), presence of freckling (0.23), and blond hair colour (0.23). For eye colour, the PAF for blue/blue-grey eye colour was higher than for green/grey/hazel eye colour (0.18 vs. 0.13). The PAF of melanoma associated with red hair colour was 0.10. These estimates of melanoma burden attributable to pigmentary characteristics provide a basis for designing prevention strategies for melanoma.

Epidemiologic research has shown convincingly that certain phenotypic attributes are associated with increased relative risks of melanoma. Although such findings have intrinsic utility, there have been few attempts to translate such knowledge into estimates of disease burden suitable for framing public health policy. We aimed to estimate the population attributable fraction (PAF) for melanoma associated with melanocytic nevi using relative risk estimates derived from a systematic review and meta-analysis. We identified eligible studies using citation databases, followed by manual review of retrieved references. Of 49 studies identified, 25 and 23, respectively, were included in meta-analyses of atypical and common nevi. For people with > or =1 atypical nevi, the summary relative risk was 3.63 (95% confidence interval, 2.85-4.62), with a PAF of 0.25. The relative risk increased by 1.017 (95% confidence interval, 1.014-1.020) for each common nevus; however, significant heterogeneity in risk estimates was observed. We estimated that 42% of melanomas were attributable to having > or =25 common nevi (PAF 25-49 nevi = 0.15; PAF > or =50 nevi = 0.27), whereas PAFs for low nevus counts were modest (PAF 0-10 nevi = 0.04; PAF 11-24 nevi = 0.07). We modeled PAF under scenarios of varying nevus prevalence; the highest melanoma burden was always among those with high nevus counts (PAF range of 0.31-0.62 for > or =25 common nevi). Patients with > or =25 common nevi and/or > or =1 atypical nevi are a high-risk group, which might be targeted for identification, screening, and education. This work is the necessary first step in designing targeted preventive strategies for melanoma, which must now be overlaid with information about cost and utility.

Melanoma commonly clusters in families, and the recent identification of numerous genotypes predicting higher risks of melanoma has led to the widespread perception that this cancer is predominantly a genetic disease. We conducted a systematic review of the literature and meta-analysis to quantify the contribution of familial factors to melanoma, estimated by the population attributable fraction (PAF). Eligible studies were those that permitted quantitative assessment of the association between histologically confirmed melanoma and family history of the disease; we identified 22 such studies using citation databases, followed by manual review of retrieved references. We calculated summary RRs using weighted averages of the log RR, taking into account random effects, and used these to estimate the PAF. Overall, family history was associated with a significant 2-fold increased risk of melanoma (odds ratio, 2.06; 95% confidence interval, 1.72-2.45); however, there was significant heterogeneity (P = 0.01). The pooled estimate for population-based studies (n = 11) was 2.03 (1.70-2.43), and 2.51 (1.55-4.07) for clinic/hospital-based studies (n = 11), both with significant heterogeneity (P = 0.049 and P = 0.013, respectively). Two studies used record linkage to verify family history in relatives; the pooled risk estimate from these two studies was 2.52 (2.11-3.00) with no evidence of heterogeneity (P = 0.258). Estimates of PAF associated with a positive family history ranged from 0.007 for Northern Europe to 0.064 for Australia (0.040 for all regions combined). Our findings suggest that only a small percentage of melanoma cases (always <7%) are attributable to familial risk; the majority of melanomas are presumably attributable to other factors.

Objective: To assess whether the rates of Down syndrome births in Queensland vary according to rurality (ie, whether the mother lives in a rural or urban area) and type of antenatal care provider, and to consider any implications for antenatal care., Design and Setting: Population-based study of Down syndrome births in Queensland between 1990 and 2004, stratified by rurality and type of antenatal care provider (private obstetrician, public hospital or shared care)., Results: Since 2000, there has been a large fall in maternal-age-adjusted rates of Down syndrome births among mothers living in urban areas (-14.3% per year; 95% CI, -22.7%, -5.0%) and among mothers receiving their antenatal care from private obstetricians (-27.5% per year; 95% CI, -37.6%, -15.8%). Similar decreases have not occurred among mothers living in rural areas (0.0%; 95% CI, -11.7%, 13.1%) or among mothers receiving antenatal care from public hospitals (+2.9%, 95% CI, -10.3%, 17.9%)., Conclusion: Possible reasons for the observed trends include unequal access to antenatal screening; confusion about screening guidelines and protocols; late presentation for antenatal care; and differences in attitudes to screening and termination of pregnancy among expectant parents, such that they may choose not to have screening or not to act on a positive screening test result.

It is widely believed that the cerebral salt-wasting syndrome (CSWS) exists as an entity distinct from the syndrome of inappropriate ADH secretion, and that it is characterized by evidence of severe renal salt wasting that results in volume depletion and hyponatremia. Proof of the existence of CSWS as an entity requires documentation of renal salt wasting and volume depletion. The present review has been undertaken to examine the evidence that the CSWS is a separate entity. In this effort, we have discussed various methods of documentation of volume depletion, and then reviewed reported cases of CSWS to determine whether volume depletion and renal salt wasting have been clearly demonstrated. Our review has led us to conclude that not one case of purported CSWS has demonstrated clear evidence of volume depletion and renal salt wasting. If renal salt wasting had been proven in these cases, we would conclude that the likely site of renal salt transport was the proximal tubule. The proximal site of salt transport defect has been suggested by the absence of hyperreninemia and hypokalemia, which would be a distinguishing feature of Bartter's syndrome and Gitelman's syndrome.

This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.

Objective: Discussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis, diagnosis, and treatment., Data Sources: Relevant literature in the English language and the authors' clinical experience., Study Selection: No special study has been carried out for the present discussion., Data Extraction: The information from the literature and the data from the authors' clinical experience have been used to illustrate important points in the discussion., Data Synthesis: A most important aspect in the approach to hypernatremia is determination of the mechanism responsible for impaired water intake. Various mechanisms of abnormal water loss can be determined from measurement of urine osmolality. Hypernatremia is treated by water replacement and measures to reduce abnormal water loss. In most instances, hyponatremia is caused by inappropriate concentration of urine because of either appropriate or inappropriate antidiuretic hormone secretion. The determination of appropriateness of antidiuretic hormone secretion requires the assessment of effective arterial volume. Treatment depends on the pathogenetic mechanism., Conclusions: Abnormal plasma sodium concentration results from abnormal water intake or water output. Treatment is guided by determining the pathogenetic mechanism.

The release of potassium from platelets is a well-known cause of pseudohyperkalemia in thrombocytosis. In predicting the magnitude of pseudohyperkalemia associated with thrombocytosis, previous investigations considered only the amount of potassium released from platelets during blood clotting, although the increment in serum potassium during blood clotting depends on the quantity of potassium released from platelets as well as the volume of distribution of the released potassium, which is inversely proportionate to the hematocrit. The present study proposes a new mathematical formula to predict the magnitude of increase in serum potassium during blood clotting, and accuracy of this formula has been tested in a patient with thrombocytosis.

The purpose of the present investigation was to determine whether dexamethasone, an agent known to preserve the blood-brain barrier, and colchicine, an agent that impairs mobilization of macrophages, can prevent demyelinating lesions associated with rapid correction of hyponatremia in the experimental animal. Hyponatremia was induced in rats with Pitressin and water. After 4 days hyponatremic rats received hypertonic saline alone or hypertonic saline plus dexamethasone or colchicine. All of the 9 rats that received only 5% NaCl developed demyelinating disease, while 3 of 6 rats treated with dexamethasone and 5 of 15 rats treated with colchicine showed no CNS abnormality. The results of our investigation might help understand the pathogenetic mechanism of central pontine myelinolysis in humans, a disease attributed to rapid correction of hyponatremia.

Potassium filtered at the glomerulus is almost completely reabsorbed before the distal tubule; it must therefore be secreted into the collecting duct. The rate of potassium secretion is determined by a number of factors, notably aldosterone, distal sodium delivery, and serum potassium. Normal serum potassium is maintained by the interplay of passive leak of potassium from the cells and its active return to the cells. Transmembrane potassium distribution is influenced largely by acid-base equilibrium and hormones including insulin and catecholamines. In the diabetic with ketoacidosis hyperkalemia, in the face of potassium depletion, is attributable to reduced renal function, acidosis, release of potassium from cells due to glycogenolysis, and lack of insulin. Chronic hyperkalemia in diabetics is most often attributable to hyporeninemic hypoaldosteronism but other conditions including urinary tract obstruction may also contribute. A variety of clinical situations (e.g., volume depletion) and drugs (e.g., nonsteroidal antiinflammatory agents, and heparin) may acutely provoke hyperkalemia in susceptible individuals.

To determine the mechanism of hyperchloremic acidosis during recovery from diabetic ketoacidosis (DKA), serial measurements were made in eight patients of serum and urinary electrolytes and organic acids, and of urinary net acid. On admission, the average decrease in serum total CO2 was 17.5 mmol/L, corresponding to the excess anion gap, 18.5 meq/L, and the serum organic acids, 17.1 meq/L. With the treatment, the anion gap and organic acids decreased by 16.1 and 14.7 meq/L, respectively, but the serum CO2 increased only by 8.4 mmol/L; serum electrolyte balance was maintained by increase in chloride concentration. Fluid retention was insufficient to explain the disparity between the increase in CO2 and the decrease in organic acids. Renal loss of bicarbonate precursors during treatment was modest and was exceeded by renal bicarbonate production. The disparity between the increase in serum CO2 and the decrease in organic acids during treatment of DKA may be explained to a large extent by a difference in volume of distribution between bicarbonate and organic anions. The renal loss of ketone anions before admission, however, is ultimately responsible for the persistence of substantial metabolic acidosis.

The proper approach to diagnosis and management in patients with a first episode of a calcium-containing kidney stone is controversial, and we have reviewed the literature in a search for objective information. Six large retrospective studies show the "natural cumulative recurrence rate of renal stones" to be 14% at 1 year, 35% at 5 years, and 52% at 10 years. Randomized studies of the use of either thiazides or allopurinol suggest a modest beneficial effect of about 35% over placebo. Considering that the risk of this specific therapy is about 5%, the morbidity associated with renal stones is limited, and relatively less invasive procedures can often replace nephrolithotomy, we conclude that use of specific drug therapy, namely thiazides or allopurinol, is not warranted in patients with a first kidney stone and, therefore, that extensive metabolic evaluation is unnecessary.

Bartter's syndrome is generally attributed to a primary defect in salt reabsorption either in the ascending limb of Henle's loop or in the proximal tubule. 2 siblings presented here have all the clinical and biochemical features of Bartter's syndrome but seem to have defective salt reabsorption in the distal convoluted tubule. A surreptitious use of diuretics was ruled out. Free water clearance was reduced in both patients and also was low after the addition of furosemide when compared with controls. Urine osmolalities following overnight dehydration were 883 and 1,000 mosm/l. The reduced maximal free water clearance argues against a proximal defect, and the normal urine concentration against a Henle's loop defect. Low free water clearance after furosemide suggests a defect in the distal convoluted tubule.

A 77-year-old diabetic man with a creatinine clearance of 23--27 ml/min developed hyperkalemia while receiving heparin for peripheral arterial insufficiency. Discontinuation of this agent led to resolution of hyperkalemia as the plasma aldosterone concentration multiplied by sixfold. Renal insufficiency may have predisposed this patient to the development of hyperkalemia when heparin therapy suppressed aldosterone synthesis.

Measurement of solute concentrations in biologic fluids by an osmometric technique has been described previously. Here, we describe an osmometric technique for measuring CO2 in gas samples. A solution of NaOH is injected into a graduated syringe containing the gas sample and CO2 is trapped in the reaction: 2NaOH + CO2 leads to Na2CO3 + H2O. The decrease in osmolality of the NaOH solution allows estimation of pCO2 in the original gas sample.

A 56-year-old woman received a kidney transplant and presented subsequently with evidence of volume contraction, hyponatremia and hyperkalemia. Urinary sodium excretion was inappropriately high for the degree of volume contraction and urinary potassium excretion inappropriately low for the degree of hyperkalemia. Marked elevation of plasma renin activity and plasma aldosterone suggested that the renal tubules were unresponsive to mineralocorticoids. The defect was shown to be transient. The mechanisms leading to the defect are discussed.

Convenience of medicine-taking and lack of side effects are two major factors that favor compliance. Using a simple and convenient once-a-day regimen of minoxidil, nadolol, and chlorthalidone, we treated successfully 30 patients with moderate to severe hypertension. All patients were previously taking at least three medications, usually three to four times a day. Treatment was started with nadolol (160 mg) and chlorthalidone (50 mg) once daily. If diastolic blood pressure remained above 90 mmHg, minoxidil was added at a starting dose of 2.5 mg/day and increased weekly until blood pressure was controlled or the maximum dose of 100 mg/day was reached. The average blood pressure decreased from 170.9/107.0 mmHg (sitting) and 174.1/110.8 mmHg (standing), before the addition of minoxidil, to 138.8/86.7 mmHg (sitting) and 140.0/89.5 mmHg (standing), at the third month of minoxidil therapy. At the sixth month of minoxidil therapy, the figures were 140.9/86.3 and 141.9/89.8 mmHg. With this single-dose program, smooth blood pressure control throughout 24 hours was documented by 24-hour ambulatory blood-pressure monitoring. Hypertrichosis was common but was bothersome only to women patients. Pericardial effusions occurred in five patients, but they were all small and asymptomatic. Subjective side effects of the regimen were usually so mild that all patients who completed the study decided to remain on the same regimen.

15 patients who had benign, uncomplicated essential hypertension, were treated with chlorthiazide (500 mg twice a day) with or without propranolol (10--20 mg 4 times a day), and the effect of the treatment on plasma renin activity (PRA), urinary aldosterone excretion, total body potassium (TBK) and plasma sodium and potassium was evaluated. TBK depletion was significant mathematically (more than 5% of TBK lost) in 7 patients, but not significant physiologically (less than 15% of TBK lost) in any except in one, who may have had other reason for TBK depletion. Although propranolol prevented the increase in PRA and aldosterone excretion, it did not prevent the modest TBK depletion. Dietary potassium intake may have some importance in the maintenance of normal body potassium during chronic treatment with thiazides for hypertension.

We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.

A group of patients whose dietary potassium was unrestricted and who received 12-18 h of Kiil dialysis twice weekly against a bath containing no potassium, had body potassium concentrations (total body potassium/intracellular volume) of 7.6% lower than normal. Despite marked hypokalemia at the end of dialysis, suprisingly few electrocardiographic changes were seen. Another group of subjects, dialyzed fro 5-6 h thrice weekly against a bath containing 1 mEq/liter of potassium in a Dow dialyzer, showed more marked electrocardiographic abnormalities despite smaller alterations in transmembrane potassium gradients. Rapidity of establishment of potassium gradients is important as well as magnitude. The following changes occur in a single dialysis: 100 mEq of cell potassium and 20 mEq of extracellular potassium leave the body; 100 mEq of extracellular sodium enter the cells and 415 mEq of extracellular sodium leave the body; 3.5 liters of water leave the extracellular fluid, 2.5 liters into the bath and 1 liter into the cells.

Preliminary results of a study of 20 patients show a combination of prazosin and polythiazide to be effective in controlling hypertension not responsive to the diuretic alone. The maximum useful dosage of prazosin was not defined, but increasing the dosage above 15 mg a day did not improve control of blood pressure.

Isotonic saline is the fluid most commonly used for treatment of asymptomatic hypotonic dehydration, but as shown in the case presented in this article, rapid increase in serum sodium may follow administration of isotonic saline, leading to the development of central pontine myelinolysis (CPM). Because the necessity of rapid correction is less, whereas the risk of CPM is greater with chronic asymptomatic hyponatremia than with acute hyponatremia, use of a half normal saline might be more appropriate than normal saline for treating certain patients with hypotonic dehydration with asymptomatic hyponatremia. The calculations indicate that half normal saline will expand the extracellular volume quite effectively, but the rate of increase in serum sodium will be considerably slower than that with normal saline.

This study was carried out to investigate the renal handling of d- and l-lactate and the extent of their metabolism in men. Ten healthy male subjects were given an intravenous (IV) infusion of a racemic mixture of d- and l-lactate. At an infusion rate of 1.0 to 1.3 meq/kg body weight of each isomer, d-lactate achieved a concentration in plasma of 1.7 to 3.0 meq/L, and l-lactate 2.8 to 4.2 meq/L. At these levels, fractional excretion of d-lactate ranged from 40% to 65%, while fractional excretion of l-lactate was always less than 5%. At a higher infusion rate, 1.8 to 2.0 meq/kg/h, plasma concentrations of d- and l-lactate reached 4.5 to 6.0 meq/L, and 4.0 to 6.7 meq/L, respectively. Fractional excretion of d-lactate then ranged from 61% to 100%, while that of l-lactate ranged from 9% to 30%. At plasma concentrations of d-lactate less than 3.0 meq/L, reabsorption of l-lactate was nearly complete, but when plasma d-lactate exceeded 3.0 meq/L, reabsorption of l-lactate was considerably impaired. Similarly, for a given concentration of plasma d-lactate, its reabsorption was more efficient when the plasma l-lactate concentration and fractional excretion of l-lactate were low than when they were high. At an infusion rate of d-lactate of 1.0 to 1.3 meq/L, about 90% of the infused lactate was metabolized, and at a higher infusion rate, still more than 75% of the infused lactate was metabolized.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of change in extracellular (interstitial) volume on vascular volume (VV) is mediated through interstitial pressure. Since the effect of swollen or shrunken cells on interstitial pressure should be identical to that of changes in interstitial volume on interstitial pressure, it would be appropriate to consider that intracellular volume (ICV) as well as extracellular volume (ECV) contributes to control of VV. Total body water rather than ECV, therefore, should be considered as the fluid volume which regulates VV. Support for these conclusions has been provided by theoretical analysis of the factors that regulate capillary fluid exchange. In further support of this hypothesis, clinical examples are described, in which renal salt retention was observed despite increases in ECV (ICV was markedly decreased), and in which renal salt loss occured despite decrease in ECV (in the presence of increased cell volume).

The present study is an investigation of the role of acetate metabolism in dialysis-induced hypoxemia and of the relative roles of acetate metabolism, bicarbonate loss, and CO2 gas (g) loss in causation of hypoxemia. The loss of CO2 (g) measured in 23 patients during acetate dialysis was found to be negligible (0.21 +/- 0.01 mmol/min). The HCO-3 loss was substantial (3.4 +/- 0.5 mmol/min), but its predicted effect on dialysis hypoxemia was modest. The infusion of acetate at 4 mmol/min into 6 normal volunteers decreased the respiratory exchange ratio (R) from 0.83 +/- 0.06 to 0.71 +/- 0.06 with constant O2 consumption (VO2) and reduced net CO2 production (VCO2). In another experiment, the infusion of sodium acetate into 9 normal volunteers resulted in a similar reduction in R (from 0.82 +/- 0.04 to 0.71 +/- 0.04) and arterial pO2 (from 92.3 +/- 1.1 to 78.3 +/- 1.7 mm Hg). The results indicate that acetate metabolism can lead to reduction in R and hypoxemia and suggest that the same mechanism is responsible for hypoxemia during hemodialysis using acetate dialysate.

Platelet aggregation induced by ADP can be inhibited by plasma from uremic patients or by toxins isolated from their plasma, e.g. guanidinosuccinic acid, methylguanidine, phenol and hydroxyphenylacetic acids. Since these chemical substances can interfere with energy metabolism in tissues other than platelets and since ATP production is needed for ADP-induced aggregation, alterations in platelet energy metabolism could underlie excessive bleeding in uremic patients. Platelets incubated with idioacetate and deprived of anaerobic glycolysis produced the same quantity of ATP through respiration in the presence of all the uremic toxins studied as in their absence. Similarly, platelets incubated with cyanide and deprived of the oxidative pathway utilized anaerobic glycolysis to produce normal quantities of ATP in the presence of all the uremic toxins. The utilization of ATP, as indicated by active transmembrane potassium transport, was also unaffected by the above listed guanidines and phenols. It is concluded that the in vitro inhibition of ADP-induced platelet aggregation by the guanidines and phenols studied is not due to inhibition of production or utilization of ATP.