[Diabetic nephropathy as an excessive cardiovascular risk].
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Biomedical subjects
Publications and source records attributed to T Schleiffer.
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Disordered gastric motility occurs frequently in diabetes mellitus. Gastric emptying time is abnormal in about 50% of diabetic patients and delayed emptying time is known as an important cause for brittle diabetes in type 1 diabetes. We compared the rise in blood glucose after a standardized meal (oatmeal test) as a noninvasive screening test for diabetic gastropathy with the noninvasive measurement of gastric emptying time with ultrasound in type 1 and type 2 diabetic patients. The test result was considered pathological if the rise of blood glucose after an initial steady state did not reach 20 mg/dl in the first 20 min after the meal (prolonged blood glucose latency). We found a sensitivity of 90% (58.7-99.8) and a specificity of 100% (71.5-100) for the oatmeal test in type 1 diabetes in the gastropathy screening. In type 2 diabetes we found a sensitivity of 13% (1.5-38.3) and a specificity of 78% (60-90.7) (95% CI). In conclusion, the oatmeal test seemed to be a good, noninvasive screening test in diabetic gastropathy in type 1 diabetes, but has no diagnostic value in type 2 diabetes. The causes for such a difference may be due to a different postprandial blood glucose regulation in type 2 diabetes compared to the beta-cell-depleted type 1 diabetes.
The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnosed with chronic pancreatitis with pancreatic calcifications and pancreatic duct dilation, although she was completely asymptomatic and with no signs of steatorrhoea. She did not have gallstones and the common bile duct was normal. A possible etiopathogenic pathway for pancreatitis could be a suppressive effect of the mt 3243 mutation on the oxidative phosphorylation in affected mitochondria. Although pancreatitis and pancreatic dysfunction in association with the mt 3243 mutation, especially in patients with comorbidity of MELAS and diabetes, has previously been described as a rare manifestation, this case is specific because of the discrepancy of advanced morphological pancreatic alterations and complete lack of pancreatogenic symptoms.
BACKGROUND: Diabetes mellitus leads to a broad spectrum of symptoms and manifestations in the field of gastroenterology. BASIS: This article reviews the pathophysiology, differential diagnoses and secondary diseases of the gastrointestinal tract in diabetic patients. CLINICAL APPEARANCE: Motility disorders, infectious complications, secondary diseases of the stomach, liver, pancreas, gall bladder, small and large bowel are considered and discussed. Diagnostic and therapeutic approaches for the management of diabetic enteropathy are presented. CONCLUSION: The new strategies in diagnosis and therapy for a successful prevention or treatment of gastrointestinal complications due to diabetes mellitus need good cooperation of clinical specialties.
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The clinical course of 15 patients with Wegener's granulomatosis (WG) and eight patients with microscopic polyangiitis (MPA) from one nephrological clinical center is presented for the period from 1984 to 1993, when testing for antineutrophil cytoplasmic antibodies (ANCA) was gradually introduced into routine clinical practice. We found a high degree of prolonged time periods with symptoms attributable to WG or MPA until the specific diagnosis was made. Nine patients with WG and one patient with MPA had symptomatic prediagnostic periods of more than three years, which extended in one case up to twenty years. In these prediagnostic periods, often even severe flares of vasculitic activity resulted in spontaneous remission without immunosuppressive therapy. One patient on chronic dialysis for four months because of rapidly progressive glomerulonephritis, experienced sufficient spontaneous regain of residual renal function to stay off dialysis for 6 years. Despite a high amount of spontaneous recovery, recurrent flares of disease eventually led to death in those cases without sufficient immunosuppressive therapy. Contrary to long courses of disease, one patient with WG had a fulminate exacerbation of disease with lethal hemoptysis after a prediagnostic period of only three months. Renal disease, respiratory and other symptoms did not occur sequentially, but each could precede the other. We conclude in agreement with published former experience, that WG and MPA show a highly variable spontaneous disease course, that requires extended observational periods for evaluating maintenance therapies.
OBJECTIVES: To elucidate the prevalence of nondipping in 24 h blood pressure monitoring (BPM) during hospital care with respect to antihypertensive drug therapy, diabetes, renal artery stenosis, and inverse diurnal blood pressure profiles. METHODS: Prospective, consecutive categorization of routine 24 h BPM was performed according to nondipping, drug therapy, normotension, severity of hypertension, diabetes, and inverse diurnal profile for 2 years. Retrospective analysis of patients examined by intraarterial renal artery angiography were performed. Nondipping was defined as a drop in night-time blood pressure (2200-0600 h) by less than 10% of the daytime values. Normotension was considered a daytime 24 h BPM value below 135/85 mmHg without antihypertensive therapy. RESULTS: We categorized 2105 24 h BPM protocols for patients of mean age 59 years. Nondipping was found for 26% of the normotensives, 38% of hypertensive patients not being administered medication, and 48% of drug-treated hypertensives. The significant increase in nondipping among patients under drug therapy applied for patients with daytime blood pressures below and above 135/85 mmHg and was thus independent of the severity of hypertension. Among the subgroup of 561 predominantly type 2 diabetic patients the prevalence of nondipping was increased significantly only for those patients who were hypertensive and being administered antihypertensive drugs. Subgroup analysis of patients using intraarterial angiography did not find different prevalences of nondipping for patients with and without renal artery stenosis. Patients with an inverse diurnal blood pressure profile and an increase in night-time blood pressure by more than 5% of the daytime values presented as a high-risk group because of morbidity associated with renal, cardiac, and cerebral disease. CONCLUSION: Nondipping is a common phenomenon among hospital patients. Drug therapy of hypertension should be directed not only towards the daytime blood pressure, but also toward alleviation of night-time hypertension.
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This report concerns a patient with cardiac manifestation of Whipple's disease. For the first time, the gene that encodes the 16s rRNA of Tropheryma whippelii was identified in a native aortic valve by means of a polymerase chain reaction technique. DNA amplification gives evidence of Tropheryma whippelii as a causative organism in infective endocarditis.
A 36-year-old woman was delivered to our hospital with suspected aortic dissection from an outlying hospital in May 1994. She reported a history of acute and persistent thoracic and epigastric pain. The physical examination revealed a minor senso-motorical palsy of the left side as residuum after minor strokes occurring 12/93 and 4/94. Also, a marked hypertension (170/100 mm Hg) was present. The hematologic and blood chemical values were normal with a white cell count of 12,000, an erythrocyte sedimentation rate (ESR) of 19 mm/h and a c-reactive protein (CRP) of 2.2 mg/dl. The electrocardiogram was normal. Transthoracic- and transesophageal-echocardiography (TTE, TEE) revealed an eccentric thickening of the whole wall of the descending aorta up to the bifurcation with a stenosis at the side of the diaphragma. Those findings were confirmed by computed tomography. Because of the acute onset of symptoms and the results of the imaging procedures aortic dissection de Bakey type III was diagnosed and the patient was treated with beta-blockers. Symptoms were relieved over the following days. After 2 days a pleuric effusion developed and all inflammatory tests rose (fibrinogen 780 mg/dl, ESR 80 mm/hr, CRP 16 mg/dl). At this time the differential diagnosis of an arteritis was considered. A new TEE-study demonstrated no change, but now more attention was given to the fact that no dissection membrane could be visualized and all wall structures were thickened. In combination with the history of cerebral infarction due to carotid obstruction and the elevated laboratory values the diagnosis of Takayasu-aortitis was established and corticoid therapy was started. Within a few weeks the arterial changes diminshed markedly and the woman became free of symptoms. This case demonstrates the rare situation of an arteritis mimicking aortic dissection, in which the clinical course revealed the true diagnosis.
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We studied the course of a primary HIV infection in a 54-year-old woman. Probably the source of infection was sexual intercourse, since other risks, such as i.v. drug use, acupuncture and transfusion were excluded. On admission she presented with fever, a maculopapular rash, and moderate enlargement of nuchal lymph nodes. At that time the anti-HIV 1,2 enzyme immunoassay was negative. However, the HIV-p24 Ag test, which was performed in every HIV screening in our laboratory, was positive. The suspicion of an acute HIV infection was supported by a positive HIV-cDNA-PCR and confirmed by Western blot after seroconversion. As additional finding, the blood smear showed abnormal white cell differential count, indicating viral infection. Aminotransferases were slightly increased, and antibodies to hepatitis B surface and core antigens demonstrated former hepatitis B infection. It is concluded that in this case the HIV-p24 Ag test proved its suitability for early diagnosis of an acute HIV infection. In case of testing blood donors, none of the compulsory serological screening methods would have detected the HIV infection.
Plasma levels of endothelin (ET) and atrial natriuretic peptide (ANP) are known to be elevated in patients on chronic hemodialysis. Since ET and ANP plasma levels are found to be raised in nonuremic diabetic versus nondiabetic subjects, we wanted to detect a possible difference in plasma levels of these hormones in diabetic versus nondiabetic patients who were on chronic renal replacement therapy. ET is a possible marker of increased vascular atherogenic activity. We measured plasma levels of ET and ANP pre- and posthemodialysis in 23 non-insulin-dependent (NIDDM) diabetic versus 23 nondiabetic patients who were matched according to age and time of day of hemodialysis, and who did not show clinical signs of overt cardiac decompensation. Mean plasma levels of ET and ANP did not differ in diabetic from nondiabetic patients, neither pre- nor postdialysis. In both patient groups, mean ET levels were twice the upper normal limit, did not change significantly pre- versus postdialysis, and did not correlate with blood pressure or with volume ultrafiltration during dialysis. Calcium channel blocker therapy was accompanied by a significant rise of ET pre- and postdialysis in nondiabetic patients but not in diabetic patients. In diabetic patients, ET plasma levels correlated positively with fructosamine levels as an indicator of short-term blood glucose control. Mean ANP plasma levels were about three times the upper normal limit and decreased significantly during dialysis, but this decrease correlated neither with volume ultrafiltration nor with blood pressure. In conclusion, we could not find a difference in plasma levels of ET and ANP for diabetic versus nondiabetic dialysis patients, but impaired short-term blood glucose control in diabetic and calcium channel blocker therapy in only nondiabetic dialysis patients showed concomitant increases in plasma ET levels and thus possibly different mechanisms of ET regulating pathways.
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24-hour ambulatory blood-pressure measurements were obtained according to criteria of the German Hypertension League in 61 non-insulin-dependent diabetic patients after admission to hospital under clinical routine conditions. 30 patients had no signs of nephropathy; 15 patients showed signs of proteinuria of more than 0.5 g/d and/or renal insufficiency, and 16 patients were on chronic hemodialysis renal replacement therapy. Despite antihypertensive therapy, the majority of NIDDM patients with nephropathy and/or dialysis therapy were hypertensive. Hypertension of non-nephropathic patients showed a better response to therapy. About 50% of all patients with nephropathy had a higher mean arterial blood pressure at night than during the daytime. In about 25% of all diabetics with nephropathy, we found, during night time, an especially pronounced increase of both systolic and diastolic blood pressure of more than 5% above the daytime values. Diabetic patients without nephropathy already show a reduced night/daytime variation of blood pressure, however, inverse circadian rhythm as a sign of prognostically non-favorable autonomic neuropathy was found almost exclusively in the nephropathic diabetic patients.
A 53-year-old man developed a septic fever up to 40 degrees C, pancytopenia and hepatosplenomegaly after a holiday in Spain. Administration of piperacillin and amikacin was ineffective, but the fever subsided and partial haematological remission occurred when 1 mg/kg methylprednisolone daily was added. After six months his general condition worsened and pancytopenia with typical inclusion bodies in bone-marrow macrophages was noted, leading to the diagnosis of visceral leishmaniasis (Kala-Azar). The diagnosis was confirmed by serological tests. The causative organism was eliminated and the abnormal findings regressed during treatment with sodium stibogluconate, at first 600 mg/d for two weeks, then 850 mg/d over 16 days, interrupted for 14 days because of side effects.
Amiodarone-induced bilateral diffuse pulmonary fibrosis developed in a 47-year-old woman with idiopathic hypertrophic subvalvular aortic stenosis who had been treated with amiodarone (Cordarex), 300 mg daily for about 18 months. Although the drug was discontinued and cortisone treatment begun, the pulmonary fibrosis did not regress. When gentamicin (Refobacin) and cefotaxime (Claforan) were administered for suspected fibrosis-induced right-sided bronchopneumonia, gentamicin-induced acute tubular renal damage occurred, requiring dialysis. The patient died soon after of myocardial electro-mechanical dissociation. At necropsy there was, in addition to the idiopathic hypertrophic subvalvular cardiomyopathy, extensive bilateral pulmonary fibrosis, lamellar bodies in foam-cell intraalveolar macrophages, in hepatocytes and in the epithelium of the proximal and distal tubules. Although amiodarone had been discontinued three months previously, high concentrations of the drug were still present, especially in both lungs, fat tissue and the liver.