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INTRODUCTION: Applications of mathematical modeling may provide an insight into the timing of surveillance modalities. We aimed to determine the optimal magnetic resonance imaging (MRI) interval for the detection of surgically treated early cervical cancer asymptomatic recurrence by using a mathematical model for volumetric tumor growth time. METHODS: We assumed that tumor volume increases by a factor equal to the basis of natural logarithms (e~2.718) at constant time intervals. Using a mathematical formula, the tumor volume (V) was converted to diameter (D), which could be expressed as a function of time (t), given an initial diameter Di (corresponding to initial volume Vi) and a constant DT, where DT is the time required for volumetric tumor growth by a factor (e). Three different DTs were used for demonstration of the model, i.e. 20, 100 and 400 days. RESULTS: Assuming complete surgical clearance, a worst-case scenario for a 20-day DT indicated that a 20 µm cervical tumor would need at least 12 months to reach 10 mm in diameter, which would be detected with an annual surveillance interval MRI. Over a 5-year (60 months) follow-up, nearly five surveillance MRIs would be required if the threshold of 10 mm was desired. For a 100-day DT over a 5-year (60 months) follow-up, a single only MRI would be required, if the threshold of 10 mm was desired. In the case of an indolent tumor (DT is 400 days), the model would not recommend a surveillance MRI to detect asymptomatic recurrence. A positive linear association between optimal MRI intervals and volumetric tumor DTs was demonstrated. CONCLUSION: In the absence of evidence, we postulate annual MRI scanning is probably the shortest interval, which can be clinically useful for optimization of routine surveillance follow-up protocols in surgically treated early cervical cancer. This mathematical model requires proper verification in prospective clinical studies. Hippokratia 2016, 20(1): 4-8.

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Thalassemic patients today undergo intensive transfusion and chelation regimes that offer them prolonged survival and improved quality of life. Nevertheless, they face the consequences of chronic illness and therapies which affect multiple bodily functions. Endocrine derangements involve, among others, the GH-IGF-I axis with consequent impairment of growth. In such cases, GH release, as assessed with stimulation tests, may be normal whereas ultradian GH secretion seems to be subnormal. New GH secretagogues (GHRs) are agents that stimulate pituitary GH release by acting upon different receptors than the endogenous hypothalamic secretagogue, growth hormone-releasing hormone (GHRH). Examples are the growth hormone releasing peptides (GHRPs) GHRP-6, GHRP-1, GHRP-2, Hexarelin and the nonpeptidyl MK-0677. These can be administered by multiple routes, even per os or intranasally, thus obviating the need for injections. Their GH releasing capacity is more pronounced and prolonged than that of GHRH and their use is devoid of serious side effects. The most recently developed GHRs seem to be capable of producing sustained GH release in many cases and can thus be viewed as therapeutic candidates in cases of reduced GH secretion with intact pituitary, as seems to be the case in a group of thalassemic patients.

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The aim of this study was to access the associations between urinary albumin excretion rate (AER) and diabetic retinopathy and its major risk factors in 105 type II non-insulin-dependent diabetic (NIDDM) patients. In 44.7% of the patients, there were no signs of retinopathy (NR), whereas 30.4% had background (BR) and 24.7% proliferative retinopathy (PR). Patients with retinopathy, both BR and PR, were older and the duration of diabetes was longer, than in the group consisting of patients with NR. Patients with retinopathy had elevated AER (BR: 9.4 +/- 2.8 micrograms/min, PR: 19.3 +/- 1.7 micrograms/min; vs. NR: 4.3 +/- 2.1 micrograms/min, p < 0.001). Patients with retinopathy had a higher systolic blood pressure and the metabolic control was worse than those without retifiopathy. In the diabetic group as a whole, raised AER was correlated with the duration of diabetes (rs = 0.287, p < 0.01) and systolic blood pressure (rs = 0.269; p < 0.01).

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It has been reported that albumin excretion rate may reflect not only an indication of renal disease but also a widespread vascular damage. We studied the relationship between overnight albumin excretion rate (AER) and peripheral vascular disease (PVD), using Doppler ultrasound, and its major risk factors in 80 Type 2 (non-insulin-dependent) diabetic patients. Thirty-eight of these patients had normoalbuminuria (AER < 30 micrograms/min), 22 had microalbuminuria (30-200 micrograms/min) and 20 had macroalbuminuria (> 200 micrograms/min). Patients with macroalbuminuria were older than those with normoalbuminuria (p < 0.01) and they also had a longer duration of diabetes (p < 0.05). Patients with elevated albumin excretion rates had elevated prevalence of PVD (macroalbuminuric 40%, p < 0.01; microalbuminuric 27.2%, p < 0.05; vs normoalbuminuric 7.8%). Among the risk factors analysed, hypertension and triglyceride concentrations were higher in the proteinuric diabetics (macroalbuminuric p < 0.001, p < 0.01; microalbuminuric p = NS, p < 0.01 respectively), while HDL-C levels were found to be significantly lower in this group (p < 0.05). In the diabetic group as a whole, raised AER was correlated with PVD (p < 0.05), duration of diabetes and systolic blood pressure (p < 0.01). We conclude that the prevalence of PVD was significantly higher in Type 2 diabetic patients with elevated albumin excretion rate. Furthermore, these patients had higher blood pressure and low HDL-C.

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The effect of an intravenous calcium gluconate load (10 mg/kg over 5 min) on plasma ionized calcium concentration, parathyroid hormone (PTH), and the rate of urinary excretion of calcium, sodium, and nephrogenous cyclic adenosine monophosphate (NcAMP) was examined in 26 patients with essential hypertension and 27 age- and sex-matched normotensive subjects. Prior to calcium administration hypertensives had lower plasma ionized calcium concentration (P < .01) and higher PTH levels (P < .001) and excreted more calcium (P < .05) and NcAMP (P < .001) in the urine compared to normotensives. Following calcium infusion, plasma ionized calcium did not differ significantly between the two groups, but PTH levels remained higher in the hypertensive subjects at both 60 min (P < .001), and at 120 min (P = .02) post-load. Post-load values for both urinary calcium excretion and urinary sodium excretion were significantly higher in the hypertensive subjects than in the control group. Both before and after calcium infusion, urinary calcium excretion was positively correlated with urinary sodium excretion in each of the two groups, but for the same level of sodium excretion, hypertensives excreted more calcium in the urine, compared to normotensives, both before (P < .05) and after calcium infusion (P < .001). A positive correlation between basal plasma renin activity (PRA) values and plasma ionized calcium values obtained before (r = 0.42, P = .03) or at 60 min (r = 0.41, P = .03) and 120 min (r = 0.42, P = .03) after calcium infusion existed only in the hypertensive subject group. Post-load urinary sodium excretion values were negatively correlated to basal PRA values in both groups (r = -0.55, P < .01 and r = -0.58, P < .01 for hypertensives and normotensives, respectively), but a similar negative correlation between post-load urinary calcium excretion values and basal PRA values existed only in the hypertensive subject group (r = -0.50, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

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