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N Satz

Publications and source records attributed to N Satz.

8 recordsLinked to original sources

[Immunology and diagnostic test results in Lyme borreliosis].

Borrelia burgdorferi (B. burgdorferi), the etiologic agent of Lyme borreliosis, shows both a variety of outer surface proteins with molecular weights between 16 and 100 kiloDalton (kD) and a 41 kD flagellar protein, which induce the immunologic response. Lipopolysaccharides, another constituent of the bacterial capsule, are responsible for the inflammatory reaction, constitutional symptoms and for the Jarisch-Herxheimer reaction. First a vigorous T-cell immune response develops, followed later by a more slowly evolving humoral B-cell immune response. The delayed onset of the humoral immune response may explain why antibodies against B. burgdorferi could not be detected early in the course of the disease. But the antibody titers increase with duration of the illness. The humoral response shows the usual pattern of IgM appearing first, followed by IgG and IgA. The IgM titer normalizes after recovery while the IgG titer could persist over years or decades. It is hardly possible to detect B. burgdorferi microscopically or by cultivation from blood, joint or cerebrospinal fluid. For routine diagnosis the fluorescent antibody staining and the ELISA methods are available which detect IgM or IgG antibodies against B. burgdorferi. But the sensitivity and specificity of these tests are still unsatisfactory. Other methods such as the ELISA-capture method, complement binding reaction, passive hemagglutination or the polymerase chain reaction are not yet established for routine purposes. Western blot analysis did not yield an essential diagnostic advantage but may be helpful in long term observation or in special cases. The measurement of the cellular immune response by T-cell proliferation tests remains controversial. First of all Lyme borreliosis has to be diagnosed by clinical findings and by elimination through differential diagnosis. An elevated antibody titer or a positive T-cell proliferation test may confirm the diagnosis but cannot prove it. Without consistent clinical findings they are of no practical significance. Some general guidelines for interpretation of laboratory results are given.

Antibodies, Bacterial

[Rheumatic fever. Its current status based on 4 cases].

We report on 4 patients with rheumatic fever hospitalized and investigated in our clinics within a 12 month period between 1990 and 1991. In each case a clinically non-severe sore throat preceded the outbreak of rheumatic fever. In three cases diagnosis was according to the revised Jones criteria. Polyarthritis was the only major symptom in these cases. One patient suffered from monarthritis. Minor symptoms were fever, arthralgia, elevated blood sedimentation rates and elevated values for CRP and for antistreptolysin O. The joint symptoms were treated with nonsteroidal drugs and subsided. One of the patients had a recurrence 9 months after the first attack even though correct secondary prophylaxis with a 4-weekly intramuscular regimen of 1.2 million units of benzathine penicillin was carried out. We discuss some epidemiological aspects and diagnostic difficulties resulting from a changing clinical pattern of the disease, and emphasize the need for streptococcal sore throat treatment and continuous secondary prophylaxis to prevent recurrences.

Adult

[Arrhythmia and swelling of all extremities].

A 54-year-old patient complained about palpitations secondary to ventricular arrhythmias over a period of several years and severe fatigue for months. Later on arthralgia of the left shoulder and diffuse swelling of both hands and feet appeared. An elevated B. burgdorferi antibody titer and later on in the course the characteristic cutaneous aspect of acrodermatitis chronica atrophicans supported the diagnosis of Lyme-Borreliosis with affection of multiple organs. Under intravenous antibiotic treatment with 2 g Ceftriaxone per day for two weeks the symptoms regressed completely. The clinical findings occurring in this patient are discussed.

Arrhythmias, Cardiac

Complementary directed modifications of nucleic acids and oncogene-directed mutagenesis in vivo.

High reactivity of the polyalkylating ss oligomers that were sense or antisense 30-200-mers containing sequences complementary to E1 oncogenes of simian adenovirus SA7 and one alkylating residue -CH2CH2N(C2H5OH) (CH2)3N(Ph-p-CH2OH)CH2CH2Cl per each 25 bases of oligomers was demonstrated in vitro by alkylation of ss DNA of recombinant M 13 mp8E1 and mp9E1 phages with inserted E1 sequences of adenovirus oncogene and then by followed complete and selective elimination of E1 sequences from recombinant ss DNA. Treatment of rodent cell cultures transformed by oncogenic SA7 with polyalkylating oligomers which are complementary to the long region of the minus or plus chains of E1 DNA of SA7 revealed a rather high extent of mutant cell clones formation. The cells formed were normalized; they had lost some properties of the transformed cells. Dividing cell clones inherited the new phenotypic properties: morphology, slower and more limited proliferation, and higher dependence on bovine serum growth factors. Some of the mutant cell DNAs demonstrated different mutations in the E1A sequences of the integrated proviral oncogene. There were exchanges G to C (leu to val) in the 525 and C to A (asp to tyr) in the 555 positions of E1A oncogene. Besides a deletions in the 1057-1477 E1A region or/and a mutation in the 1457-1477 of E1A were observed. Thus the inherited cell normalization observed is performed due to oncogene-directed mutagenesis in vivo.

Adenoviridae

Perhexiline maleate-induced hepatitis.

We report on a case of perhexiline maleate-induced hepatitis secondary to a long-term administration of recommended daily dosages of 300 mg. The patient had a spectacular weight loss of 29 kg. He developed hepatitis, which subsided after drug withdrawal. Our electron-microscopic findings with the typical inclusion bodies and impaired hydroxylation capacity point to an underlying metabolic disorder as the pathogenetic mechanism.

Angina Pectoris

[Diagnostic value of various laboratory parameters in acute pancreatitis].

In 427 samples of serum and urine, collected during their stay at hospital from 40 patients affected with acute pancreatitis, the sensitivity and the specifity of total amylase and lipase in serum, total amylase and pancreas isoamylase in urine, as well as the amylase-/creatinine clearance were determined. The pancreas isoamylase in serum was used as reference value. It appeared that the sensitivity of the lipase was next to that of the pancreas isoamylase in serum, even in limit ranges. Usually the lipase stayed pathological the longest and could therefore be used to identify in the best way even an easing-off pancreatitis. The diagnostic accuracy of the total amylase in serum and urine, of the pancreatic isoamylase in urine and of the amylase-/creatinine clearance was found to be obviously less reliable. The specifity of all examined tests was reduced in patients with renal insufficiency, liver disease, alcohol abuse and in patients with abdominal pains of non pancreatic origin. Concluding form our results and with regard to the expenditure of laboratory technique and to the time required by the methods of determination, we found that of all the examined parameters, the lipase was the most convenient for both emergency and routine diagnose of an acute pancreatitis.

Acute Disease

[Left ventricular function in hypertension treated with beta blockers].

In 14 patients with essential hypertension, left ventricular function was assessed echocardiographically before and after 4 and 8 weeks of treatment with the betablocking agent atenolol. Atenolol was given orally in a dose of 100 mg/day. After 4 weeks of treatment systolic blood pressure decreased from 160 to 138 mm Hg(p less than 0.001) and diastolic pressure from 105 to 91 mm Hg(p less than 0.001). Heart rate decreased from 76 to 64 beats/min (p less than 0.05). Systolic shortening of the left ventricular transverse diameter declined from 41 to 36% (p less than 0.01), though in no instance did it fall below the lower limit of normality (30%). After 8 weeks of betablocking therapy, blood pressure and heart rate remained essentially unchanged. Systolic shortening increased slightly but insignificantly to 38%. The left ventricular enddiastolic diameter did not change throughout the study. It is concluded that longterm betablocking therapy is associated with a significant reduction of left ventricular function which improves in the later stage of treatment. Since the diminution of left ventricular function is slight, the induction of left heart decompensation is unlikely, at any rate in patients with initially normal left ventricular function.

Adrenergic beta-Antagonists

[Pancreatogenic ascites].

Pancreatic ascites is a rare disease which is often misinterpreted as ascites secondary to alcoholic cirrhosis or to intraabdominal cancer. It can be diagnosed by a high protein and amylase/lipase content of the ascitic fluid. If diagnosis and subsequent surgery occur at an early stage, the prognosis is good. The natural course, therapy, prognosis, and pathogenesis of pancreatic ascites are discussed on the basis of experience with 7 patients.

Adolescent