Biomedical subjects
Josef Finsterer
Publications and source records attributed to Josef Finsterer.
Loss of taste is loss of weight.
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Why is venous thrombosis only rarely detected in patients with suspected paradoxical embolism?
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HFE Genotypes and iron overload in patients with suspected coronary heart disease but normal angiograms.
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Amyotrophic lateral sclerosis with very slow progression.
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Influence of disposable, concentric needle electrodes on muscle enzyme and lactate serum levels.
Several studies addressed the question whether needle-EMG causes elevation of muscle enzymes [aspartate-aminotransferase, alanine-aminotransferase, lactate-dehydrogenase, creatine-phosphokinase (CPK), isoenzyme-MB, aldolase] and lactate with conflicting results. However, these studies used sterilizable needle electrodes and different protocols and methods to record EMGs and determine muscle enzymes. This study examined if muscle enzymes are elevated immediately after or 24 h following EMGs with disposable, concentric needle-electrodes, and if they are dependent on age, sex, muscle, number of investigated sites and previous CPK-elevation. In 53 subjects, 24 woman, 29 men, aged 17-88 years, muscle enzymes were determined before, immediately after and 24 h following EMG with disposable, concentric needle-electrodes. Muscle enzymes were not different before, immediately after and 24 h following the EMG. Muscle enzymes were not different between patients 60 years of age. Apart from higher CPK in men than women, muscle enzymes were not different between the genders. Apart from CPK, muscle enzymes were not different between the brachial biceps and anterior tibial muscle. Muscle enzymes were not different if 20 sites were investigated and were independent on pre-EMG CPK-levels. In conclusion this study shows that muscle enzymes do not increase immediately or 24 h following EMG with disposable, concentric needle-electrodes, irrespective of age, gender, muscle, number of investigated sites and pre-EMG CK-levels.
Lactate stress testing in 155 patients with mitochondriopathy.
OBJECTIVE: Few data are available about the diagnostic yield of the lactate stress test (LST) in a large group of patients with mitochondriopathy (MCP). METHODS: Serum lactate was determined once before, three times during, and once after a 15-minute, constant 30W workload on a bicycle in 62 controls, aged 17 to 84 years, 155 patients with MCP, aged 17 to 87 years, and 31 patients with neurological disorders other than MCP. RESULTS: Lactate's upper reference limits at rest, 5, 10, 15 minutes after starting, and 15 minutes after finishing the exercise were 2.0, 2.1, 2.1, 2.1 and 1.8 mmol/l respectively. The test was regarded abnormal if more than two of the five lactate values exceeded the cut-off levels. Among the 103 patients with abnormal LST, 64 (62 %) had normal resting lactate. The sensitivity of the test was 67% and the specificity 94%. CONCLUSION: The LST proved to have a high sensitivity and specificity in the detection of patients with MCP, being thus a simple but powerful tool to assess the impaired oxidative metabolism in MCP patients.
Problems, interventions and complications in long-term oral anticoagulation therapy.
BACKGROUND: If problems, interventions and complications occurring during oral anticoagulation (OAC) are related with age, indication for OAC, hypertension, diabetes, previous stroke, and number of additional drugs. MATERIAL AND METHODS: Clinical characteristics, additional drugs, problems, interventions and complications of outpatients whose OAC was controlled between two years were registered. Potential gastrointestinal and urologic bleeding sources were eliminated prior to initiation of OAC. Five-hundred-seventy-nine patients (mean age 65 years, 44% female) were observed for 590 patient-years. RESULTS: Medical problems occurred in 352/100 patient-years (% p-y), organisational problems in 276% p-y, interventions in 636% p-y and complications in 13.8% p-y. Patients >65 years had less organisational problems (254 vs. 302% p-y, p = 0.0092) and interventions (574 vs. 713% p-y, p = 0.0003) than patients < or =65 years. The 35 patients with heart valve prosthesis had more life-threatening and fatal complications (12% p-y) than the 360 patients with atrial fibrillation (1.0% p-y), 128 patients with venous thromboembolism or 56 patients with other indications (0.0% p-y, p = 0.0024). Problems, interventions and complications were not related with hypertension (n = 297), diabetes (n = 97) or previous stroke (n = 90). Patients with >3 additional drugs/day had a higher complication rate than patients with < or =3 drugs/day (21 vs. 8.7% p-y, p = 0.0238). Patients with complications had more headache (27 vs. 20% p-y, p = 0.0036), chest pain (45 vs. 27% p-y, p = 0.0150), abdominal pain (25 vs. 15% p-y, p = 0.0350) and pain in the limbs (55 vs. 42% p-y, p = 0.0044) than patients without complications. CONCLUSIONS: By careful monitoring, eliminating potential bleeding sources, treating pain adequately and minimizing additional drugs the complications of OAC can be kept low.
Mitochondriopathy as a differential diagnosis of amyotrophic lateral sclerosis.
OBJECTIVES: To assess how often mitochondrial myopathy (MMP) mimics amyotrophic lateral sclerosis (ALS) and the phenotypic similarities and differences between these two disorders. METHODS: Records of 123 MMP patients and 59 ALS patients, diagnosed during five years (1996-2000), were retrospectively evaluated. RESULTS: Re-evaluation revealed that 8 patients, initially diagnosed as ALS had actually MMP (13.6%). Among the MMP patients, 6.5% were initially misdiagnosed as ALS. None of the MMP patients actually had ALS. Common features of ALS and MMP were weakness, wasting, upper motor neurone signs, bulbar abnormalities, and a neurogenic EMG. Features differentiating MMP from ALS were ptosis, sensory disturbances, multi-system involvement, slowly progressive disease course, abnormal lactate stress test, histological and biochemical abnormalities, and mtDNA analysis. CONCLUSIONS: In a small number of cases MMP may clinically and electrophysiologically mimic ALS, particularly in the early stages of the disease. Patients with suspected ALS, but slow progression and multi-organ involvement, should undergo lactate stress testing and muscle biopsy. ALS should be diagnosed only if MMP has been excluded.
Positive malignant hyperthermia susceptibility in vitro test in a patient with mitochondrial myopathy and myoadenylate deaminase deficiency.
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Role of infectious and immune factors in coronary and cerebrovascular arteriosclerosis.
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Histological appearance of left ventricular hypertrabeculation/noncompaction.
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Hypothyroidism and muscular respiratory failure successfully treated with liothyronine.
After total thyroidectomy because of hyperthyroidism, hypothyroidism developed in a 78-year-old woman. Despite replacement therapy with levothyroxine sodium in continuously increasing doses, worsening hypothyroidism led to respiratory failure, necessitating artificial ventilation. The addition of liothyronine resulted in complete recovery. Impaired conversion of thyroxine to triiodothyronine by the dejodase was responsible for the manifestations of hypothyroidism.
Neurologic and cardiac progression of glycogenosis type VII over an eight-year period.
Little is known about the progression of phosphofructokinase deficiency (glycogenosis type VII, Tarui's disease). We describe a 66-year-old woman who had this disease diagnosed in 1997. Initial manifestations had included simple partial seizures since 1977, anginal chest pain since 1982, and muscle cramps since 1983. To prevent recurrent myocardial infarction, anticoagulation therapy with phenprocumon was initiated. Cardiac involvement progressed over an 8-year period, manifesting as low-voltage electrocardiogram (ECG), ectopic supraventricular tachycardia, thickened mitral valve, mitral valve insufficiency, enlarged left atrium, left ventricular hypertrophy, and diastolic dysfunction. Progression of neurologic involvement manifested as complex partial seizures, double vision, reduced tendon reflexes, central facial palsy, bradydiadochokinesia, and distal weakness of the upper extremities. Discontinuance of oral anticoagulation after 19 years, initiation of enalapril therapy, and administration of carbamazepine markedly improved the patient's condition.
Diabetic atrial fibrillation patients: mortality and risk for stroke or embolism during a 10-year follow-up.
BACKGROUND: To compare in atrial fibrillation patients with and without diabetes, (1) baseline characteristics, (2) additional risk factors for stroke or peripheric or visceral embolism (hypertension, previous stroke, age >75 years), (3) mortality, (4) stroke or embolism, and (5) oral anticoagulation in the year 2000. METHODS: Included were 409 outpatients with nonrheumatic atrial fibrillation (62 +/- 12 years, 36% female). All underwent transthoracic and transesophageal echocardiography. Patients with thrombi received oral anticoagulation; patients without thrombi received aspirin until the follow-up in 1995; afterwards, oral anticoagulation according to risk factors for stroke or embolism was recommended. Patients were contacted during the year 2000. RESULTS: Type 2 diabetes was diagnosed in 73 patients (18%). Sixteen (22%) diabetic and 169 (50%) nondiabetic patients had no other risk factors for stroke or embolism (p < 0.0001). Diabetic patients were older, had more frequent heart failure, hypertension, myocardial infarction, left ventricular dysfunction, valvular abnormalities, left atrial or appendage thrombi, larger left atria, and left atrial appendages than nondiabetic patients. Mean follow-up was 115 months. Diabetic patients had a higher mortality than nondiabetic patients (7%/year versus 4%/year, p < 0.0001). The rate of stroke or embolism of diabetic (3%/year) and nondiabetic patients (2%/year) was similar. The rate of oral anticoagulation was higher in diabetic than in nondiabetic patients (p = 0.0066). CONCLUSIONS: Diabetic patients with atrial fibrillation frequently have additional risk factors for stroke or embolism, and thus should be treated with oral anticoagulation. Whether in the rare cases of atrial fibrillation, in whom diabetes is the only clinical risk factor, oral anticoagulation is indicated cannot be answered by the present study.
Familial left ventricular hypertrabeculation in two blind brothers.
So far, left ventricular hypertrabeculation (LVHT) has been described to occur only sporadically. In a 49-year-old man with Leber's hereditary optic neuropathy (LHON) due to the primary LHON mutation G3460A, arterial hypertension was reported since 2000 and palpitations since 1995. ECG revealed Wolff-Parkinson-White syndrome. Transthoracic echocardiography and cardiac MRI showed myocardial thickening and LVHT. Pindolol markedly improved the cardiac abnormalities. Surprisingly, LVHT was also found in the 50-year-old brother of the index patient who also had LHON and also carried the G3460A mtDNA mutation. This brother also had Wolff-Parkinson-White syndrome and myocardial thickening, but without hypertension. It is concluded that LVHT, previously described to occur only sporadically, may be hereditary in single cases.