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C Grönhagen-Riska

Publications and source records attributed to C Grönhagen-Riska.

132 records · Page 8Linked to original sources
PubMed1979

Angiotensin converting enzyme. IV. Changes in serum activity and in lysozyme concentrations as indicators of the course of untreated sarcoidosis.

The mean values of serum angiotensin-converting enzyme (ACE) activities and lysozyme (LZM) concentrations measured during different phases of sarcoidosis coincided well with the clinical evaluation of the state of the disease. However, both enzymes, especially LZM, decreased before improvement was detected. Changes in these enzymes were in accord with the simultaneous clinical development in three fourths of cases. Incompatibility between clinical observations apnd LZM fluctuations was most frequently seen during active stable or inactive disease. LZM often decreased during the active stable phase and fluctuated irregularly during inactive disease. During the former phase LZM decrements possibly reflect decreasing activity of granulomatous macrophages and, in fact, precede detectable improvement. During inactive disease, on the other hand, cells were not connected with the disease process dominate LZM production. ACE changes paralleled the clinical development more often than corresponding LZM changes during stable sarcoidosis. This may have been misleading and due to a delayed reaction of serum ACE, compared with LZM, inreflecting the activity of granylomatous cells. This delayed reaction was also observed in connection with erythema nodosum. Stable ACE activity during inactive sarcoidosis indicated the usefulness of measurements when trying to predict a relapse. We conclude that ACE may be a secondary feature of sarcoidosis rather than a primary funtion of macrophage activity.

Humans↗
PubMed1978

Predisposing factors in hepatitis induced by isoniazid-rifampin treatment of tuberculosis.

Seventy-five patients who developed mild hepatic reactions (serum transaminase concentrations of 45 to 149 units per liter) and 50 patients who showed more serious liver damage (serum transaminase values greater than 150 units per liter) were compared with 261 consecutive patients who had no liver reactions during treatment with rifampin and isoniazid. Generally, liver toxicity occurred in 18 per cent of patients receiving combined anti-tuberculous drug therapy. Small increases in transaminase occurred in 14 per cent of the patients; large increases occurred in 4 per cent. Elderly women comprised a risk group. Among patients exhibiting a more serious hepatic lesion (transaminase values greater than 150 units per liter), alcoholics, mostly men, formed another risk group, together with other patients with a history of previous liver or biliary disease. Of 261 patients who did not develop a liver reaction, 57 per cent were slow INH acetylators. In this study, the groups with small and large increases in transaminase were clearly separated; in the former group there was no preponderance of phenotype, whereas in the latter group, slow acetylators clearly dominated among early (first 4 weeks of treatment) hepatic reactions (P less than 0.01). Studies of single-drug regimens of isoniazid have shown that neither slow nor rapid acetylation has any causal influence on isoniazid-induced hepatitis. Because the metabolism of rifampin is independent of the acetylation process, rifampin and isoniazid in combination seem to cause a toxic hepatitis that differs from the hepatitis induced by either drug separately.

Acetylation↗
PubMed1978

Angiotensin-converting enzyme and lysozyme in silicosis and asbestosis.

Serum angiotensin-converting enzyme (ACE) activity and lysozyme (LZM) concentration in 22 silicosis and 18 asbestosis patients were studied. These patients were compared with 57 untreated and 36 treated sarcoidosis patients. In all groups significantly raised ACE and LZM mean values were noted. Untreated sarcoidosis patients had the highest values. Raised ACE activity in silicosis and asbestosis has not been reported before, and weakens the differential diagnostic value of this enzyme determination for sarcoidosis. The similar patterns of increased ACE and LZM mean values in all three diseases suggest that these enzymes have a common source.

Adult↗
PubMed1976

Bronchiolar adenomatosis. A case report.

A case of bronchiolar adenomatosis (benign pulmonary adenomatosis) with unusually widespread pulmonary changes is presented. This disease is rare and occurs equally in both sexes. The tumourous growth is slow and can easily be mistaken for alveolar cell carcinoma, alveolar proteins, tuberculosis, sarcoidosis, or malignant pulmonary adenomatosis. The diagnosis can be made on a histological specimen from the affected lung. In spite of a benign histological picture, the disease may ultimately run an unfavourable course because of its malignant potentialities. A distinction between benign and malignant pulmonary adenomatosis may therefore only be made with certainty by a complete and careful postmortem examination.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMedDate not supplied

Is renin substrate an erythropoietin precursor?

The biogenesis of erythropoietin is incompletely understood. One hypothesis maintains that erythropoietin is synthesized primarily in the kidney while according to another theory an erythropoietin precursor present in plasma is activated by a renal factor, erythrogenin. An attractive candidate for the erythropoietin precursor is renin substrate (angiotensinogen) which has chemical similarities with erythropoietin. We show here that purified renin substrate from human plasma is immunologically related to human erythropoietin. Moreover, purified renin substrate, like erythropoietin, causes the dose-dependent increase of haemoglobin F in cultured human erythroid leukaemia K562 cells. We conclude that renin substrate is a likely precursor of erythropoietin.

Angiotensinogen↗