7 Giusti G , Gakis C . Temperature conversion factor, activation energy, relative substrate specificity and optimum pH of adenosine deaminase from human serum and tissue. Enzyme 1971; 12:417-25 8 Zuckerman SH, Olson JM, Douglas SD. Adenosine deaminase activity during in vitro culture of human peripheral blood monocytes and pulmonary alveolar macrophages. Exp Cell lies 1980; 129:281-87 9 Gakis C, Piras MA, Saba F, Romani G, Longinotti M. Rapporto 2' deossiadenosinaladenosina deaminasi nei versamenti pleurici e peritoneali: significato diagnostico. Boll Soc Ita! Bioi Sper 1981; 57:1835-41 10 Gakis C , Piras MA, Romani G, Saba F, Longinotti M. Behaviour of serum 2'deoxyadenosine/adenosine deaminase ratio in infectious diseases and haemopoietic malignacies. lot Res Commun Syst J Med Sci 1981; 9:518-19 11 Gakis C, Calia G, Cherchi GB, Andreoni G . Serum adenosine deaminase activity in brucellosis. lot Res Commun Syst J Med Sci 1983; 11:481-82
1b the Editor:
We were very interested in the communication from Gakis et al. This group has made a decisive contribution to the understanding of many problems related to ADA activity and its correlation with some cells involved in immunologic phenomena. We are very grateful for their comments on our article. It was not our aim to study the contribution of the values of ADA activity or its enzymes separately in the diagnosis of tuberculous or neoplastic pleural effusions. On the contrary, in our work we considered two groups of patients in whom these clinical situations are definitively diagnosed on the basis of clinical, bacteriologic, cytologic, and histologic elements, as we described in our Materials and Methods section. Our purpose was to investigate only an eventual correlation between ADA activity and lymphocytic populations in tuberculous and neoplastic pleural effusions. The crucial importance ofT-cell populations in the pathogenesis of tuberculous processes after stimulation by the infected macrophage is well known. So, we can assume that, notwithstanding the results of Gakis et al , the proved concentrations of ADA Tlymphocytes, associated with the great activity of these cells in tuberculosis, may contribute to the correct evaluation of our results. Manuel Fontes Baganha, M.D., F.C.C.P., Marla Alice Pego, M.D. , Maria Adelaide Lima, M .D., Ermelinda Gaspar; B. Phann. , and Antonio llobalo Cordeiro, M.D. , University ofCoimbra, Coimbra, Portugal
Unilateral Diaphragmatic Paralysis Secondary to Carbon Monoxide Poisoning 1b the Editor:
I read with interest the report by Joiner et al of a case of unilateral diaphragmatic paralysis (UDP) secondary to carbon monoxide puisoning,' which appeared in the February 1990 issue of Chest. In the discussion of this case, the authors listed the chief causes of UDP; I was struck by the fact that "unknown" was not mentioned in this list, since it is our clinical experience and that of others• that in the majority of cases of UDP no cause can be established. For instance, in the series of Piehler et al,t initial evaluation (history, clinical examination, and chest roentgenogram) failed to establish a
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cause in 142 of 247 patients with UDP (57.5 percent). In only 5 percent of the cases of "unexplained UDP" was the cause subsequently established by more extensive investigation (eg, computed tomography). While we do not comment on carbon monoxide as the probable cause of UDP in the case presented by Joiner et al, we would like to emphasize that "unknown" or "idiopathic" should be mentioned at the top of every list of causes ofUDP. Marc Noppen, M.D ., Antwerp, Belgium Reprint requem: Dr Noppen, Hooipolderlaon 4, B-2600 HobokenAntwerp. Belgium
REFERENCES 1 Joiner TA, Sumner JR, Catchings TT. Unilateral diaphragmatic paralysis secondary to carbon monoxide poisoning. Chest 1990; 97:498-99 2 Piehler JM, Pairolero PC, Gracey DR, Bernatz PE. Unexplained diaphragmatic paralysis: a harbinger of malignant disease? J Thorac Cardiovasc Surg 1982; 84:861-64
Advertising and Clinical Investigations 1b the Editor:
The exchange between Drs Ciaglia, Levi, and Ryan and Dr Petty that recently appeared in Chest (1990; 98:1309-10) touches on some potentially important issues. I recognize that Dr Ciaglia and his colleagues were appropriately concerned about the advertisement covering Dr Petty's study. However, I think that their concerns are misplaced with regard to that study, since it is commendable that practicing physicians would be organized to do an appropriately designed clinical trial. Perhaps this should be more widespread. Indeed, it is even acceptable to do "n of 1" trials for controlled comparisons in individual physicians' offices, as well as in hospitals. · (Dr Petty's, of course, was much more than an "n of I" approach.) Dr Ciaglia and his colleagues do have a valid objection to the pharmaceutical company's usage of the expression "major multicenter study." Although Dr Petty defined ''center" in a fairly narrow manner, which would be literally correct, there is no question that the pharmaceutical company meant to suggest multi-medical center, to imply that these were institutions rather than many individual offices. The criticism, I think, should be entirely directed to the pharmaceutical company.
Dovid H. Spodick, M .D .• D.Sc., F.C.C.P., St Vincent H
Errata In the article "Bronchoalveolar Lavage Cell Data in 19 Patients with Drug-associated Pneumonitis (except Amiodarone)" (Chest 1990; 99:98-104), the author in reference 13 should have been shown as "Ahmad s;· rather than "Saed A." The editors of Chest wish to thank David Lyons, M.D. , fOr pointing out that in the article "Rounded Atelectasis Complicated by Obstructive Pneumonia and Pulmonary Arterial Thrombosis" (Chest 1990; 98:1283-85}, rounded atelectasis was incorrectly referred to as "Bievosky's syndrome;· rather than "Biesovsky's syndrome," in the right-hand column of page 1283. The name Blesovsky was also misspelled in references I and 3. Communications to the Editor