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A dohányzás számos krónikus betegség, a szívérrendszeri események, a daganatos megbetegedések, a krónikus obstruktív tüdőbetegségek és a halálozás fontos kockázati tényezője. Kevésbé ismert, hogy a dohányzás szerepet játszhat a 2-es típusú cukorbetegség kialakulásában is, amiben mind a béta-sejteket károsító, mind pedig az inzulinrezisztenciát fokozó hatása szerepet játszik. Számos adat szól ma már amellett is, hogy a dohányzás elősegíti a cukorbetegség nemcsak makro‑, de mikrovaszkuláris szövődményeinek kialakulását és progresszióját. A szerzők alábbi összefoglaló közleményükben ismertetik a dohányzás és a szénhidrátanyagcsere-zavar összefüggéseit, valamint a dohányzás szövődményekre gyakorolt hatásait, részletesen kitérve a dohányzás és a diabéteszes neuropathia kapcsolatára.

A diabeteses neuropathia létrejöttének pontos mechanizmusa folyamatosan bővülő ismereteink ellenére teljesen még ma sem tisztázott. A patogenetikai háttér feltárásában az utóbbi évek jelentős előrelépést hoztak – különösen gyors fejlődés zajlik a molekuláris biológiai mechanizmusok megismerése terén –, egyes részkérdések azonban még ma sem teljesen ismertek. A cukorbetegek egy részében súlyos fokú neuropathia fordulhat elő tartósan kedvező anyagcserehelyzet mellett, más betegekben – ritkábban – a tartósan kedvezőtlen anyagcserehelyzet sem jár érdemi idegbántalommal. Ennek hátterében elsősorban genetikai eltérések szerepe tételezhető fel. Ez utóbbiakról viszonylag kevés információ áll rendelkezésre, a szerzők ezeket foglalják össze közleményükben.

A szerzők egy 72 éves, évtizedek óta 2-es típusú cukorbetegségben szenvedő férfi esetét ismertetik, diabeteses polyneuropathiája 30 éve ismert. Az évek során makrovaszkuláris szövődmények következtében több alkalommal történt coronarographia, alsó végtagi PTA és stentimplantáció. Aktuális klinikai felvételére kedvezőtlen szénhidrátanyagcsere-helyzet (HbA1c: 11%), ismételt elesések miatt került sor. Az obezitásban (BMI: 39,2 kg/m2) is szenvedő beteg esetében a korábban beállított SGLT-2-gátló, illetve GLP-1-receptor-agonista kezelés dózisát emelték, aminek hatására vércukorértékei céltartományba kerültek. Mind a négy végtagra kiterjedő, disztális túlsúlyú fájdalmas neuropathiás panaszai kapcsán a beteg már évek óta kombinált oki és tüneti kezelésben részesült: alfa-liponsav és benfotiamin, valamint duloxetin és pregabalin szedése mellett is típusos alsó végtagi, dominálóan éjszakai neuropathiás fájdalmai jelentkeztek. Neuropathiavizsgálat során súlyos hypaesthesiás típusú szenzoros károsodás volt igazolható mind a négy végtagon a Neurometerrel (Neurotron Inc, Baltimore, USA) mért áramérzet-küszöbértékek, a Vibratip, a Tiptherm, a kalibrált hangvilla és a monofilamentum, továbbá a Q-Sense (Medoc Ltd., Yamat Rishai, Israel) készülékkel mért hőérzet-küszöbértékek tekintetében is. Közepesen súlyos fokú kardiovaszkuláris autonóm neuropathia is fennállt. A gyakori elesések hátterében kóroki tényezőként egyrészt a súlyos fokú szenzoros hypaesthesia, másrészt az ortosztatikus hipotónia (32 Hgmm) volt igazolható. Az eddigiekben alkalmazott négyes kombináció nem kielégítő terápiás effektusára való tekintettel kiegészítő kezelésként plazmaferezist alkalmaztak, emellett a kezelést opioid származék adásával egészítették ki. Következtetés: A neuropathia diabetica egyes ritka esetekben járhat egyidejűleg extrém mértékű neuropathiás károsodással és neuropathiás fájdalommal. A kezelésben alapvető a megfelelő glikémiás kontroll és fontos az oki és tüneti szerek alkalmazása. Az eset arra hívja fel a figyelmet, hogy emellett egyes esetekben szükséges lehet a terápia opioid készítményekkel, valamint plazmaferezissel történő kiegészítése.

A szerzők fiatal, 1-es típusú cukorbetegség szövődményeként diabeteses neuropathiában szenvedő betegük lábsérülésének következtében kialakult Charcot-láb kórtörténetét mutatják be esettanulmányukban. A 25 éves nőbeteg felvételére a szénhidrát-anyagcsere egyensúlyának rendezése céljából került sor. Klinikai felvételekor jobb oldali nem gyógyuló talpi fekélyre és következményesen kialakult Charcot-lábra derült fény. Inzulinadagjainak módosítását követően vércukorértékei közel normális tartományba kerültek. A vizsgálatok közepes fokú, hypaesthesiás típusú szenzoros neuropathiát igazoltak. A röntgen- és CT-vizsgálat a jobb boka csontjainak szerkezeti elváltozásait, a lábboltozat deformitását igazolták. A végtag tehermentesítése mellett, 10 napos alfa-liponsav infúziós és intravénás pamidronatkezelésben részesült a beteg, ortézisének elkészítése folyamatban volt. Esetünk felhívja a figyelmet szénhidrátanyagcsere-helyzet egyensúlyban tartásának fontosságára, hiszen a diabeteses neuropathia már fiatalkorban is súlyos szövődményekhez, akár Charcot-láb kialakulásához vezethet. Cukorbetegeink figyelmét kiemelt fontosságú felhívnunk nem csak a szénhidrát-anyagcsere egyensúlyban tartására, hanem a neuropathiás fekélyek kialakulásának rizikójára, valamint időben történő szakszerű ellátására is.

The distinction between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)–related and community-acquired pneumonias poses significant difficulties, as both frequently involve the elderly. This study aimed to predict the risk of SARS-CoV-2-related pneumonia based on clinical characteristics at hospital presentation. Case-control study of all patients admitted for pneumonia at Semmelweis University Emergency Department. Cases (n = 30) were patients diagnosed with SARS-CoV-2-related pneumonia (based on polymerase chain reaction test) between 26 March 2020 and 30 April 2020; controls (n = 82) were historical pneumonia cases between 1 January 2019 and 30 April 2019. Logistic models were built with SARS-CoV-2 infection as outcome using clinical characteristics at presentation. Patients with SARS-CoV-2-related pneumonia were younger (mean difference, 95% CI: 9.3, 3.2–15.5 years) and had a higher lymphocyte count, lower C-reactive protein, presented more frequently with bilateral infiltrate, less frequently with abdominal pain, diarrhoea, and nausea in age- and sex-adjusted models. A logistic model using age, sex, abdominal pain, C-reactive protein, and the presence of bilateral infiltrate as predictors had an excellent discrimination (AUC 0.88, 95% CI: 0.81–0.96) and calibration (p = 0.27–Hosmer-Lemeshow test). The clinical use of our screening prediction model could improve the discrimination of SARS-CoV-2 related from other community-acquired pneumonias and thus help patient triage based on commonly used diagnostic approaches. However, external validation in independent datasets is required before its clinical use.

Neuropathy is one of the most important complications of diabetes. According to recent advances, vitamin D deficiency might play a role in the development and progression of diabetic neuropathy. Moreover, therapeutic vitamin D supplementation has the potential to improve this condition. The aim of the present review was to summarize new data available in this area.The PubMed database was searched for articles written in English and published through September 2021, using combinations of the following key words: vitamin D, diabetes, diabetes mellitus, diabetic neuropathy, polyneuropathy, peripheral neuropathy, cardiac autonomic neuropathy, supplementation, and therapy.A number of studies have suggested that vitamin D deficiency can play a significant role in the development of peripheral neuropathy, diabetic foot ulcers, as well as cardiovascular autonomic neuropathy in patients with type 2 diabetes. Vitamin D supplementation might serve as an effective adjuvant therapy for neuropathic pain and may slow or stop the progression of neural damage.Vitamin D therapy for diabetic complications could be a reliable option; however, further studies are needed to confirm this notion.

A 74 éves, 2-es típusú cukorbetegségben szenvedő férfi beteg klinikai felvételére fél éven belül bekövetkező 25 kg-os fogyás, a test számos részén megfigyelhető, pörkkel fedett sebek, nagyfokú gyengeség miatt került sor. A tumorirányú vizsgálatok negatív eredménnyel zárultak. A bőrjelenségek ismételt bőrgyógyászati konzílium véleménye alapján bullosus pemphigoidnak bizonyultak. Biklonális gammopathia igazolódott, a cristabiopszia eredménye ugyanakkor nem igazolt malignus infiltrációt. Fél évvel későbbi, ismételt klinikai észlelése során motoros neuropathia tünetei kerültek előtérbe. Betegünk esetében összességében amyotrophia diabetica volt diagnosztizálható, a szerzők a differenciáldiagnosztikai aspektusok mellett a több kóroki tényező együttes fennállása mellett kialakuló, súlyos fokú neuropathia lehetőségére hívják fel a figyelmet.

Background. People with diabetic cardiovascular autonomic neuropathy (CAN) have increased cardiovascular mortality. However, the association between distal symmetric polyneuropathy (DSPN) or CAN with all-cause mortality is much less investigated. Thus, we set out to examine the effect of CAN and DSPN on all-cause mortality in a well-phenotyped cohort. Methods. All diabetes cases ( n = 1,347 ) from the catchment area of a secondary diabetes care centre who had medical examination including neuropathy assessment between 1997 and 2016 were followed up for all-cause mortality in the NHS Hungary reimbursement database until 2018. We investigated the association of CAN (Ewing tests) and DSPN (Neurometer) with all-cause mortality using Cox models stratified by diabetes type. Results. Altogether, n = 131 / 1,011 persons with type 1/type 2 diabetes were included. Of the participants, 53%/43% were male, mean age was 46 ± 12 / 64 ± 10 years, diabetes duration was 13 ± 10 / 7 ± 8 years, 42%/29% had CAN, and 39%/37% had DSPN. During the 9 ± 5 / 8 ± 5 -year follow-up, n = 28 / 494 participants died. In fully adjusted models, participants with type 1 diabetes patients with versus without DSPN had an increased mortality (HR 2.99, 95% CI 1.4-8.63), while no association with CAN was observed. In type 2 diabetes, both DSPN and CAN independently increased mortality (HR 1.32, 95% CI: 1.07-1.64, and HR 1.44, 95% CI: 1.17-1.76). Conclusions. Our results are compatible with an increased risk of mortality in people with type 1 diabetes and DSPN. Furthermore, we report a similarly strong association between DSPN and CAN and all-cause mortality in type 2 diabetes mellitus.

Cardiovascular autonomic neuropathy (CAN) is a common complication of diabetes mellitus. Cardiovascular reflex tests (CARTs) are the gold standard in the diagnosis of CAN, but the handgrip test is no longer recommended to be performed. Previously, the inverse association between the presence of hypertension and handgrip test abnormality was demonstrated and hypertension as major cause for excessive diastolic blood pressure rise during handgrip testing in diabetic individuals proposed. The aim of the present study is to describe more precisely the association between handgrip test and hypertension by performing ambulatory blood pressure monitoring (ABPM) among diabetic patients. A more comprehensive evaluation of the relationship between cardiovascular autonomic function, hypertension and the handgrip test was targeted using heart rate variability (HRV) analysis. Our study involved 163 patients with diabetes. Cardiovascular autonomic neuropathy was assessed by the CARTs and sustained handgrip test was performed. All patients underwent ABPM and HRV analysis well. CAN was diagnosed in 69 patients. Significant associations were found between the diastolic blood pressure increase in response to handgrip exercise and the 24-h (rho = 0.245, p = 0.003), daytime (rho = 0.230, p = 0.005) and night-time (rho = 0.230, p = 0.006) mean systolic and 24-h diastolic (rho = 0.176, p = 0.034) blood pressure values, systolic blood pressure load (rho = 0.252, p = 0.003) and systolic (rho = 0.236, p = 0.005) and diastolic (rho = 0.165, p = 0.047) hyperbaric impacts. Higher values of ambulatory blood pressure monitoring parameters are associated with greater increases in diastolic blood pressure during isometric handgrip exercise. Diastolic blood pressure elevations during the handgrip test are also correlated, in order to diminished heart rate variability parameters attributable to parasympathetic dysfunction highlighting the pivotal role of sympathetic overactivity in evolving handgrip test results. Our study provides further evidence on the inverse association between handgrip test abnormality and hypertension in diabetic patients.

Background and aims To assess the risk factors for sensory nerve dysfunction in subjects with isolated impaired glucose tolerance (IGT). Methods and results Seventy-two people with isolated IGT (WHO 1999 criteria) and 39 gender and age-matched healthy volunteers underwent detailed clinical and neurological assessment including quantitative sensory testing using the Neurometer device (current perception threshold measurement on four limbs at three different frequencies). Sensory nerve dysfunction was defined as at least two abnormalities on any frequencies on the upper or lower limbs. Sensory nerve dysfunction was more prevalent among subjects with IGT compared to controls (58.3 vs. 10.3%, OR: 11.23, 95%CI: 3.57–35.35). This association was not influenced by BMI, systolic and diastolic blood pressure, heart rate and autonomic neuropathy (multiple adjusted OR: 13.87, 95%CI: 3.18–60.58), but further adjustment for glycaemic measures abolished the association (OR: 1.58, 95%CI: 0.07–35.68). Assessing the components of glycaemic measures separately, the association between sensory nerve dysfunction and IGT was not affected by HbA1c (OR: 13.94, 95%CI: 1.84–105.5). It was, however, substantially attenuated by fasting plasma glucose (OR: 6.75, 95%CI: 1.33–34.27) while the significance was lost after adjustment for 120 min postload glucose level (OR: 3.76, 95%CI: 0.26–54.10). In the pooled population assessed, independent determinants of sensory nerve dysfunction were older age, 120 min glucose, higher height and cardiovascular autonomic neuropathy at near significance. Conclusions Sensory nerve dysfunction amongst subjects with IGT was not explained by cardiovascular covariates, only by glycaemic measures. In addition to 120 min glucose, cardiovascular autonomic neuropathy at borderline significance, age, and height were the independent determinants of sensory nerve dysfunction.

Objective: Historically, a set of 5 Cardiovascular Autonomic Reflex Tests (CARTs) were considered to be the gold standard in the assessment of Cardiovascular Autonomic Neuropathy (CAN). However, measuring diastolic Blood Pressure (BP) response to sustained handgrip is omitted in recent guidelines. We aimed to assess the association between the handgrip and the other 4 tests as well as to identify determinants of the handgrip test results in diabetic patients. Patients and Methods: 353 patients with diabetes (DM) were recruited (age: 60.2±7.4 years; female: 57.2%; BMI: 29.3±2.1 kg/m2; DM duration: 15.6±9.9 years; HbA1c: 7.8±1.4% (66 mmol/mol); with type 1 DM: 18.1%). CAN was assessed by 5 CARTs: the deep breathing test, Valsalva ratio, 30/15 ratio, handgrip and orthostatic hypotension test. Results: Sensitivity and specificity of the handgrip test in the diagnosis of definite CAN were 24.6% (95%CI 17.7-33.1%) and 79.4% (95%CI 73.3-84.4%), respectively. Results of the handgrip test did not show any association with those of the deep-breathing test (γ =0.004, p=0.563), 30/15 ratio ( γ=0.282, p=0.357), Valsalva ratio (γ =-0.058, p=0.436) and orthostatic hypotension (γ =-0.026, p=0.833). Handgrip test abnormality showed an independent association with higher initial diastolic BP (OR 1.05, p=0.0009) and an independent inverse association with the presence of hypertension (OR=0.42, p=0.006). Conclusion: Our data confirm that the handgrip test should no longer be part of the cardiovascular autonomic testing being highly dependent on hypertensive status and baseline diastolic BP. Exaggerated exercise pressor response is proposed as putative mechanism for the inverse association between abnormal results of the handgrip test and hypertension. Adequate CARTs are important to allow their use in clinical trials and for the prevention of DM-associated complications by initiating early treatment.

The authors review current advances in the therapy of diabetic neuropathy. The role of glycemic control and management of cardiovascular risk factors in the prevention and treatment of neuropathic complications are discussed. As further options of pathogenetically oriented treatment, recent knowledge on benfotiamine and alpha-lipoic acid is comprehensively reviewed. Alpha-lipoic acid is a powerful antioxidant and clinical trials have proven its efficacy in ameliorating neuropathic signs and symptoms. Benfotiamine acts via the activation of transketolase and thereby inhibits alternative pathways triggered by uncontrolled glucose influx in the cells comprising polyol, hexosamine, protein-kinase-C pathways and formation of advanced glycation end products. Beyond additional forms of causal treatment, choices of symptomatic treatment will be summarized. The latter is mostly represented by the anticonvulsive agents pregabalin and gabapentin as well as duloxetine widely acknowledged as antidepressant. Finally, non-pharmacological therapeutic alternatives are summarized. The authors conclude that combination therapy should be more often suggested to our patients; especially the combination of pathogenetic and symptomatic agents.

Introduction The aim of our study was to evaluate the relative effect of diabetes and hypertension on heart rate variability. Research design and methods Four age-matched groups including type 2 diabetic patients with and without hypertension, non-diabetic patients with essential hypertension and healthy control subjects were studied. Autonomic function was evaluated by the standard cardiovascular reflex tests and 24-hour heart rate variability measurement. Heart rate variability was characterized by the triangular index value and by the spectral components of the frequency domain analysis. Results According to the two-way analysis of variance on ranks, all parameters were influenced negatively by diabetes (heart rate variability triangular index: p

Diabetes is a widespread disease and, therefore, studies dealing with diabetes and its complications are very important for public health. Numerous reports link vitamin D deficiency to the increased risk of diabetes mellitus and complications such as neuropathy. However, there are limited and conflicting data available on vitamin D deficiency in patients with diabetic peripheral neuropathy. Studies in type 2 diabetics confirmed the relationship between vitamin D deficiency and incidence of neuropathy. Recent reports suggest a relationship between the incidence of plantar ulcers and vitamin D deficiency.A D-vitamin csontanyagcserén túlmutató hatása a tudományos figyelem középpontjába került az utóbbi években. A cukorbetegséggel és annak szövődményeivel kapcsolatos vizsgálatok pedig kiemelt népegészségügyi jelentőséggel bírnak. Egyre több adat támasztja alá a D-vitamin-hiány és a cukorbetegség kapcsolatát, a diabeteses neuropathia és a D-vitamin kapcsolatáról azonban eddig kevés és ellentmondó adat áll rendelkezésre. A többségében 2-es típusú cukorbetegek körében végzett vizsgálatok alátámasztják a D-vitamin-hiány és a neuropathia előfordulása, illetve a neuropathia okozta tünetek súlyossága közötti kapcsolatot. A legújabb tanulmányok a talpi fekélyek kialakulásában is felvetik a D-vitamin-hiány kóroki szerepét. Orv. Hetil., 2013, 154(51), 2012–2015.

In contrast to gastric dysfunction, diabetes-related functional impairments of the small and large intestine have been studied less intensively. The gastrointestinal tract accomplishes several functions, such as mixing and propulsion of luminal content, absorption and secretion of ions, water, and nutrients, defense against pathogens, and elimination of waste products. Diverse functions of the gut are regulated by complex interactions among its functional elements, including gut microbiota. The network-forming tissues, the enteric nervous system) and the interstitial cells of Cajal, are definitely impaired in diabetic patients, and their loss of function is closely related to the symptoms in diabetes, but changes of other elements could also play a role in the development of diabetes mellitus-related motility disorders. The development of our understanding over the recent years of the diabetes-induced dysfunctions in the small and large intestine are reviewed in this article.

Damage of small nerve fibers may lead to a large variety of clinical symptoms. Small-fiber neuropathy underlies the symptoms of painful diabetic neuropathy, which may decrease quality of life. It also contributes to the poor prognosis of diabetic neuropathy because it plays a key role in the pathogenesis of foot ulceration and autonomic neuropathy. Impairment of small nerve fibers is considered the earliest alteration in the course of diabetic neuropathy. Therefore, assessment of functional and morphological abnormalities of small nerve fibers may enable timely diagnosis. The definition, symptoms, and clinical significance of small-fiber neuropathy are considered in the present review. An apparently more complex interaction between small-fiber impairment and microcirculation is extensively discussed. Diagnostic modalities include morphometric and functional methods. Corneal confocal microscopy and punch skin biopsy are considered gold standards, but noninvasive functional tests are also diagnostically useful. However, in routine clinical practice, small-fiber neuropathy is diagnosed by its typical clinical presentation. Finally, prompt treatment should be initiated following diagnosis.

In the past few years, the effects of vitamin D that go beyond its relationship with bone metabolism have come into the focus of scientific attention. Research concerning diabetes and its complications has become a public health priority. An increasing number of reports link vitamin D deficiency to diabetes; however, so far, there has only been limited and contradictory data available on the correlation between diabetic peripheral neuropathy and vitamin D. Studies of people with type 2 diabetes confirmed the relationship between vitamin D deficiency and neuropathy incidence as well as the severity of the symptoms caused by neuropathy. The latest studies are also suggesting a relationship between the incidence of plantar ulcers and vitamin D deficiency.

The aim of our study was to evaluate the relative effect of diabetes and hypertension on heart rate variability.Four age-matched groups including type 2 diabetic patients with and without hypertension, non-diabetic patients with essential hypertension and healthy control subjects were studied. Autonomic function was evaluated by the standard cardiovascular reflex tests and 24-hour heart rate variability measurement. Heart rate variability was characterized by the triangular index value and by the spectral components of the frequency domain analysis.According to the two-way analysis of variance on ranks, all parameters were influenced negatively by diabetes (heart rate variability triangular index: p0.001; low-frequency component: p0.0001; high-frequency component: p0.001; and total power: p0.0001), whereas hypertension had a negative effect only on the low-frequency component (p0.05). The interaction between hypertension and diabetes was not significant, indicating that their effects on the heart rate variability parameters are additive. Beat-to-beat variation upon deep breathing, the most sensitive cardiovascular reflex test was also negatively influenced by both diabetes (p0.001) and hypertension, (p0.05), and their effects were additive.Diabetes appears to have a greater effect on autonomic dysfunction compared with hypertension. Patients suffering from both diabetes and hypertension are at the highest risk of reduced heart rate variability. Early assessment of the autonomic nerve function is suggested in diabetic patients with hypertension.

In this issue of the journal, Gouveri et al report on olfactory dysfunction among patients with type 2 diabetes mellitus (T2DM) and raise the question whether it might be considered as an additional manifestation of microvascular disease. 1 Diagnostic methods to assess olfactory dysfunction are well established and validated: odor-dispensing devices, so-called ‘‘Sniffin’ Sticks,’’ are used and a total threshold–discrimination–identification (TDI) score is calculated. Age was negatively associated with the TDI score. After adjusting for age, gender, various risk factors, and cardiovascular disease, only T2DM and hypertension were associated with the TDI score. Olfactory dysfunction was associated with retinopathy and diabetic peripheral neuropathy. The latter finding should be considered particularly important. We agree with the authors that olfactory dysfunction may develop due to olfactory nerve impairment. This way, it should be regarded as a novel manifestation of central neuropathy. The term ‘‘diabetic neuropathy’’ refers to disorders of the peripheral nervous system due to neuropathy. However, we now know that dysfunction of the central nervous system is also present among diabetic patients. Cognitive impairment, 2 as well as depression, 3 is well recognized in diabetes. Cranial neuropathies are less frequent, most likely often overlooked, but well established manifestations of diabetic neuropathy. The impairment of cranial nerves is defined as a form of mononeuropathy. Cranial neuropathies are more frequent in older patients with long diabetes duration. Most of these patients have several comorbidities and their glycemic control is rather poor. 4 Isolated palsy of the third, fourth, or sixth cranial nerves is a characteristic manifestation of diabetic neuropathy. The presence of multiple, painless cranial nerve palsies in diabetic patients, even without other associated neurological deficits, may represent midbrain ischemia. 5 The incidence of cranial nerve involvement is 1% in diabetic patients. 6 Isolated third nerve palsies account for the majority of patients 4 and 11% of inpatients with third nerve palsy had diabetes. 7 The onset of cranial neuropathy is usually abrupt, with progression

Aims To assess circadian blood pressure variability in people with impaired glucose tolerance and a healthy control population. Methods Seventy-five people with impaired glucose tolerance and 40 healthy volunteers (frequency matched on 10-year age bands and sex) underwent a detailed neurological assessment. Autonomic neuropathy was detected by the five standard cardiovascular autonomic tests and heart rate variability was characterized by the triangle index. Diurnal indices were assessed by 24-h ambulatory blood pressure monitoring. Systolic and diastolic diurnal indices were defined as: (mean daytime blood pressure – mean night-time blood pressure) × 100/mean daytime blood pressure. Results Mean 24-h systolic and diastolic blood pressure was significantly higher in the group with impaired glucose tolerance compared with the control group [126 ± 12 (mean ± sd) vs. 117 ± 10, 75 ± 7 vs. 71 ± 6 mmHg, both P