Search PubMed⌕ Search

Biomedical subjects

C Lichtig

Publications and source records attributed to C Lichtig.

At least 91 records · Page 5Linked to original sources
PubMed1980

Subacute bacterial endocarditis.

Two patients in whom various immunological phenomena obscured and delayed the diagnosis of subacute bacterial endocarditis (SBE) are described. Immunological abnormalities usually correlate well with the chronicity and severity of the disease, as is demonstrated here. The mechanisms underlying the various immunological phenomena are discussed. The importance of alertness to the possibility of SBE in cases of disease manifesting itself as an immunological disorder, thus achieving early diagnosis and early antimicrobial treatment, is stressed.

Adult↗
PubMed1980

The quantification and significance of mast cells in lesions of Behçet's disease.

Mast cells in the upper dermis and mucosal subepithelial layer were counted in thirty consecutive light microscopy oil-immersion fields of the following: thirty-four skin and oral specimens from lesions in patients with active Behçet's disease, eight specimens of apparently uninvolved skin of the same patients, and 102 lesions of a variety of other skin diseases. The results revealed a significant increase in the number of mast cells in Behçet's lesions. Furthermore, the histamine content of five reactive lesions showed a two-fold increase compared with that in apparently uninvolved skin of patients with active Behçet's disease. It is suggested that mechanisms similar to cutaneous basophil hypersensitivity may be involved in the production of Behçet's lesions.

Behcet Syndrome↗
PubMed1980

ASdult Fanconi's syndrome with renal tubular acidosis in association with renal amyloidosis: occurrence in a patient with chronic lymphocytic leukemia.

In a patient with chronic lymphocytic leukemia, multiple renal tubular defects developed in association with urinary excretion of K light chain proteins and peritubular deposits and casts of amyloid. Proximal tubular dysfunction, resembling adult Fanconi's syndrome, was suggested by an increased urinary loss of phosphate and urate and glycosuria. Renal tubular acidosis with hypokalemia and a marked impairment of the urinary concentrating mechanism were also observed.

Acidosis, Renal Tubular↗
PubMed1980

Amyloidosis in immunoblastic lymphadenopathy.

A case of immunoblastic lymphadenopathy and systemic amyloidosis in a 21-year-old man is presented. The basic defect in immunoblastic lymphadenopathy is believed to be an abnormal immune reaction, most probably of the B cell system. Although systemic amyloidosis is common in some disorders of the B cell system, no cases of systemic amyloidosis complicating immunoblastic lymphadenopathy have been previously reported. Immunoblastic lymphadenopathy includes elements known to be associated with amyloidosis and we believe that this association is not merely coincidental.

Adult↗
PubMed1979

Ultrastructural pathology with normal light microscopy of liver in Wilson's disease. A case report.

Light microscopy findings in early Wilson's disease (hepatolenticular degeneration) may be normal even when special cytochemical stains are used. We present a case of Wilson's disease in which light microscopy was negative, while electron microscopy showed the characteristic changes in the hepatocytes. Since low serum ceruloplasmin levels and high urinary copper excretion are not by themselves definite proof of Wilson's disease, and since copper content of the liver is not universally measured, electron microscopy examination of liver tissue appears to be a worthwhile additional tool for the early diagnosis of Wilson's disease.

Adult↗
PubMed1979

Extracranial bone metastases from intracranial meningiomas.

Distant bone metastases in cases of intracranial meningiomas are uncommon. Two patients with meningiomas showing malignant histological features are described, in both of whom bone metastases were observed many years after cranial surgery.

Adult↗
PubMed1978

Cholestatic jaundice caused by D-penicillamine.

D-penicillamine is not generally considered to cause hepatic damage. Cholestatic jaundice developed in a patient with rheumatoid arthritis 4 weeks after penicillamine was added to his regimen, and he died in acute renal failure. The probability that penicillamine caused the cholestasis is discussed.

Arthritis, Rheumatoid↗
PubMed1977

Premature coronary atherosclerosis in a 5-year-old with corticosteroid-refractory nephrotic syndrome.

We report the case of a 5-year-old girl who died two years after onset of the idiopathic nephrotic syndrome, which failed to respond to treatment with corticosteroid and cyclophosphamide. Severe atherosclerotic changes were noted in both coronary arteries. Prolonged hyperlipidemia in patients with long-standing nephrotic syndrome may represent a major risk factor predisposing to premature coronary atherosclerosis in children who are also destined to develop chronic renal failure.

Adrenal Cortex Hormones↗
PubMed1977

Systemic lupus erythematosus, Sjögren's syndrome and glomerular nephritis.

The combination of systemic lupus erythematosus, Sjögren's disease and severe diffuse glomerular nephritis has only rarely been reported. A 14-year-old girl is described with lupus nephritis in whom co-existent clinical and histological features of Sjögren's syndrome were found. These include bilateral parotid enlargement, xerostomia, increased serum amylase, reduced salivary secretion and lymphocyte infiltration of both salivary glands and kidneys. The co-existence of systemic lupus erythematosus with Sjögren's syndrome is discussed together with a consideration of pathogenesis.

Adolescent↗
PubMed1977

Postoperative intrahepatic cholestasis.

Postoperative jaundice is an occasional complication of major surgery. Four illustrative cases are described and a mechanism of development is suggested. The jaundice may seem to be biochemically of the obstructive type. Most of the bilirubin is of the conjugated type. The disturbance of liver function can be caused by several factors, including massive transfusion, hematoma in tissues, shock, heart failure, anoxia, infection and perhaps medications. Postoperative jaundice by itself is not of cardinal importance in deciding the prognosis of the patient.

Acute Kidney Injury↗
PubMed1976

Histohogical and direct immunofluorescence study of cutaneous hyperreactivity in Behçet's disease.

The mechanism of skin hyperreactivity (pathergy) in Behçet's disease is unknown. It has been suggested that the response is due to an Arthus-like reaction. In 18 patients with active Behcet's disease, pathergy was induced and the skin biopsied after 24 h. The histological reaction was that of mold to intense round cell infiltration. perivascular in type. Direct immunofluorescence failed in all 18 patients to demonstrate the local presence of immunoglobulins and complement at the site of lesion. A marked increase in the number of mast cells was observed at the site of reaction and scattered throughout the dermis, the role of which is to be further investigated. The study failed to demonstrate a humoral mechanism in the production of the cutaneous hyperactivity.

Adult↗
PubMed1975

A new method for determination of postmortem left ventricular volumes: clinico-pathologic correlations.

A description is presented of a new and simple procedure for ventricular volume determination by means of pressure fixation of the heart and preparation of plastic molds of the ventricles which can be used to displace water in a graduated cylinder to determine the volume of the mold. Correlations between postmortem ventricular volume as measured by this method and antemortem stroke volume or clinical cardiac status indicate that a large left ventricular volume is often correlated with a low cardiac output and cardiogenic shock.

Autopsy↗
PubMed1975

Myocardial ultrastructure and function during progressive early ischemia in the intact heart.

Regional contraction of ischemic anterior and normal lateral left ventricular myocardium was measured with isometric force gauges after 5, 10, 15, and 20 minutes of anterior descending coronary artery occlusion-each followed by 10 minutes of reperfusion. Multiple myocardial biopsies of both regions were taken at these same intervals and examined by electron microscopic techniques. Mean contraction of the ischemic area fell significantly in 15 to 30 seconds and returned to an average of 68, 51, 40, and 28 per cent, respectively, after 5, 10, 15, and 20 minutes of ischemia. Simultaneously, focal morphologic changes were detected after 5 and 10 minutes, were more clear and widespread at 15 minutes, and diffuse and unequivocal at 20 minutes, when return of local contraction was minimal. The changes of myocardial morphology in the ischemic area as seen by electron microscopy were: reduced content of glycogen granules and mitochondrial changes. The latter began to appear at 5 minutes and consisted of swelling, disruption of cristae, and reduction of matrix. This study indicates a qualitative correlation between ultrastructural changes in regionally ischemic myocardium and diminished regional function in the intact heart. At 5 and 10 minutes the mitochondrial changes were focal, requiring multiple samples, while at 15 and 20 minutes they became more widespread, making the occasional sample more representative.

Animals↗
PubMed1975

Myocardial ultrastructure and contraction during short periods of experimental ischemia.

The relationship of structure and function of the intact myocardium during the early minutes of experimental ischemia was studied in the anesthetized, open-chest pig. Regional contraction of ischemic and normal myocardium was measured, using isometric strain gauges on the anterior and lateral left ventricle. Biopsies for electron microscopy were taken consecutively 5, 10, 15, and 20 minutes after anterior descending artery occlusion-each followed by 10 minutes of reperfusion. Contraction of the ischemic area fell significantly within 15 to 30 seconds following occlusion, returning to 68, 50, 40, and 28%, respectively, after 5, 10, 15, and 20 minutes fo ischemia. In contrast, slight morphological changes were detected only after 5 and 10 minutes of ischemia, becoming more clear after 15 minutes, and unequivocal after 20 minutes-when return of contraction was minimal. The morphologic alterations in the ischemic area as seen by electron microscopy were: reduction of glycogen granules and specific changes in the mitochondria. The latter, consisting of swelling, disruption of cristae, and reduction of matrix, began to appear at 5 minutes and were more evident after 10 minutes of ischemia. These changes, although present, were not always proportional to sequential ischemic periods. This apparent lack of correlation between contraction and morphology could be due to sampling problems or to the focal nature of the ischemic process. However, it could imply that the changes seen by electron microscopy are a "late" phenomenon as compared to the loss of function. Morphologic corroboration of the immediate decrease of contraction of ischemic myocardium still escapes the perception of current morphological techniques. It is hoped that more refined stereological measurements will help bridge the present gap between function and morphology in early myocardial ischemia.

Animals↗