Midfoot and Hindfoot Bone Marrow Edema Identified By Magnetic Resonance Imaging in Feet of Subjects With Diabetes and Neuropathic Ulceration Is Common but of Unknown Clinical Significance

OBJECTIVE

We conducted a retrospective cohort study assessing the prevalence and clinical and radiological outcome of remote areas of bone marrow edema on magnetic resonance imaging (MRI) in the feet of subjects with diabetes and neuropathic foot ulceration.

RESEARCH DESIGN AND METHODS

MRIs performed over 6 years looking for osteomyelitis associated with neuropathic lesions were assessed for remote areas of signal change.

RESULTS

Seventy MRI studies were assessed. Remote areas of signal change were present in 21 (30%) subjects, involved midfoot or hindfoot in 20 subjects, were associated with younger age and renal replacement therapy, and did not predict future Charcot neuroarthropathy or infection at that site. Repeat MRIs in 11 subjects with such areas found that none had progressed, six had improved, and two had resolved; in 29 subjects without such areas, five had developed new areas.

CONCLUSIONS

Bone marrow edema in the midfoot and hindfoot of subjects with diabetes and neuropathic lesions is common, often transient, and of unknown significance.We have previously described the value of magnetic resonance imaging (MRI) to assess for osteomyelitis in association with neuropathic foot lesions in subjects with diabetes whereby the MRI criteria for diagnosis require bone signal change to be in direct contiguity with signal change in the soft tissue adjacent to the area of ulceration (1). We have often incidentally observed hyperintensity on T2-weighted images, consistent with bone marrow edema, remote from the area of neuropathic ulceration (Fig. 1) that often involves the midfoot and hindfoot and is usually not associated with adjacent clinical or radiological signs of infection, clinical signs suggesting acute Charcot neuroarthropathy, or pain. We performed a retrospective cohort study to assess the prevalence of such remote areas of signal change and their subsequent clinical and radiological outcome.Open in a separate windowFigure 1Sagittal T2 fat-saturated magnetic resonance image shows remote areas of signal change in the talus and calcaneum (arrows).     

The influence of small doses of paracetamol on rabbit liver.

Paracetamol has properties that make it useful in many kinds of drugs that are readily available to users. These drugs are often used for extensive periods of time without a doctor's supervision, which might lead to unexpected overdose. The aim of this work was to assess the extent of liver damage in rabbits after administering them with paracetamol for approximately 2 months. The results we obtained suggest that paracetamol administered for a long time causes liver function impairment. It was, however, not possible to determine the impairment by measuring the activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or gamma-glutamylotranspeptidase (GGTP). It was determined by measuring the concentration of ketone bodies and arterial ketone body ratio (AKBR) value. Even when taken in small doses, paracetamol causes changes in liver metabolism when taken for an extended period of time.     

Salt-sensitive blood pressure--an intermediate phenotype predisposing to diabetic nephropathy?

BACKGROUND: Family studies point to important genetic determinants of diabetic nephropathy (DN). Blood pressure (BP) is higher in offspring of patients with type 2 diabetes and DN, but the pathomechanisms involved have not been elucidated. METHODS: We examined the salt sensitivity of BP after 5 days equilibration on a low (20 mmol/day) vs high salt diet (220 mmol/day) in three matched groups of 15 subjects each: (i) control individuals; (ii) offspring of type 2 diabetic parents without DN (DN-); and (iii) offspring of type 2 diabetic parents with DN (DN+). Ambulatory BP and hormones involved in sodium homeostasis [plasma renin activity (PRA), aldosterone and atrial natriuretic peptide (ANP)] as well as the tetrahydrocortisol + 5-allotetrahydrocortisol/tetrahydrocortisone (THF + 5alphaTHF)/THE) ratio in the urine as an index of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) activity were analysed. RESULTS: In offspring of DN+ patients on a high salt diet, systolic and diastolic BP was 137/82+/-10/8 mmHg vs 125/77+/-12/8 mmHg in offspring of DN- patients (P<0.01 for systolic BP). The salt-induced difference in mean BP between high and low salt diet was 5.2+/-3.3 mmHg in offspring of DN+ patients vs 0.7+/-4.7 mmHg in offspring of DN- patients (P<0.002). The proportion of 'salt-sensitive' individuals was 67% in offspring of DN+ patients vs 20% in offspring of DN- patients (P<0.05). In all groups, a high salt diet caused a comparable decrease of PRA and p-aldosterone accompanied by an increase in ANP. The urinary (THF + 5alphaTHF)/THE ratio was 1.23+/-0.36 in salt-sensitive individuals and 0.99+/-0.33 (P<0.03) in salt-resistant subjects, consistent with increased activity of 11betaHSD2. CONCLUSIONS: BP is more salt sensitive in offspring of type 2 diabetic patients with diabetic nephropathy. The salt sensitivity of BP may be an intermediate phenotype in individuals with a high risk of future diabetic nephropathy.     

Further evidence for the subsensitivity of striatal AMPA receptors, induced by chronic haloperidol administration: an autoradiographic study

The aim of the present study was to investigate the influence of chronic treatment with haloperidol on the striatal N-methyl-D-aspartate (NMDA), -amino-3-hydro-xy-5-methyl-4-isoxasole-propionic acid (AMPA) and dopamine D₂ receptors using a quantitative autoradiography in rats. Haloperidol was given to animals in a dose of ca. 1 mg/kg/day in drinking water for 6 weeks or 3 months and was afterwards withdrawn for 5 days. Haloperidol increased by 20–50% the binding of [³H]spiperone in different regions of the caudate-putamen. Haloperidol decreased by ca. 30% the binding of [³H]AMPA in the ventrolateral region of intermediate part of the caudate-putamen, but did not influence the binding of [³H]MK-801. The present results suggest that, apart from supersensitivity to dopamine, chronic treatment with haloperidol also induces subsensitivity of striatal AMPA receptors.     

Does reserpine induce parkinsonian rigidity?

Summary The aim of the study was to find out whether the reserpineinduced rigidity is similar to that seen in parkinsonism. Simultaneous measurements of the muscle resistance of the hind foot to passive bending and stretching in the ankle joint, as well as of the electromyographic (EMG) activity of the gastrocnemius and tibialis anterior muscles of rats were carried out. Reserpine was injected in a dose of 10 mg/kg alone or with -methyl-p-tyrosine (250 mg/kg) 1,4 and 27.5 h before the measurements. Reserpine increased the muscle resistance of the rat's hind leg to passive movements. That effect was the strongest at 1–2 h after the injections, and diminished markedly afterwards. The rigidity was accompanied with an increase in the resting, as well as in the stretch-induced short-and long-latency EMG activity in the gastrocnemius muscle. However, the intensity of the latter symptom did not change for a long period of time, which seems to correlate with the striatal dopamine depletion. The results suggest that the reserpine-increased EMG activity is a good model of parkinsonian rigidity.     

Left ventricular apical rupture caused by takotsubo cardiomyopathy--comprehensive pathological heart investigation.

An 81-year-old woman with emotionally-induced takotsubo cardiomyopathy developed a fatal left ventricular (LV) apical rupture. During the hospitalization persistent ST-segment elevation with no electrocardiographic time evolution was observed on the ECG, characteristic for takotsubo cardiomyopathy. Histopathologically, transmural myocardial necrosis with hemorrhage was found at the rupture site, but there were foci of coagulation and contraction band necrosis with mononuclear lymphocyte infiltrations in other heart regions, and the intensity and distribution of these pathological changes corresponded to the distribution of the LV contraction abnormalities seen on ventriculography. The article concludes that: the LV functional disorder in takotsubo cardiomyopathy may be caused by distracted foci of coagulation and contraction band necrosis in the myocardium; contraction band necrosis (a sign of catecholamine cardiotoxicity) may reflect the sympathetic hyperactivity in this disease; persistent myocardial damage expressed by persistent ST-segment elevation without an electrocardiographic time evolution should be carefully observed with sequential echocardiographic examinations because of the possibility of cardiac rupture.