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Correspondence

Case 32-2001: Interstitial Pneumonitis and Rheumatoid Arthritis

N Engl J Med 2002; 346:866-867March 14, 2002

Article

To the Editor:

The anatomical diagnosis presented in Case 32-2001 (Oct. 18 issue)1 is “usual interstitial pneumonitis with acute exacerbation, associated with rheumatoid arthritis,” apparently one of the forms of rheumatoid lung disease. Yet the only evidence of the presence of rheumatoid arthritis is the statement that it had begun a year and a half before admission.

No mention is made of a history of joint pain or morning stiffness, no information about a physical examination or radiographs of the joints is provided, we are not told whether rheumatoid nodules were present, and none of the tests that one would want to perform in order to support the putative diagnosis are reported. Dr. Hollingsworth, the discussant, does state that “the finding of hypergammaglobulinemia is consistent with the presence of rheumatoid arthritis,” but this finding is much less helpful than information about rheumatoid factor and rheumatoid nodules, both of which are usually present in patients with rheumatoid interstitial lung disease.2 The treatment of this unfortunate patient might have been the same whether he had interstitial lung disease alone or in association with rheumatoid arthritis, but these two diagnoses warrant different discussions.

Harvey E. Golden, M.D.
Rush Medical School, Chicago, IL 60612

2 References
  1. 1

    Case Records of the Massachusetts General Hospital (Case 32-2001). N Engl J Med 2001;345:1193-1200
    Full Text | Web of Science | Medline

  2. 2

    Luthra HS. Extraarticular rheumatoid arthritis. In: Koopman WJ, ed. Arthritis and allied conditions: a textbook of rheumatology. 14th ed. Vol. 1. Philadelphia: Lippincott Williams & Wilkins, 2001:1187-201.

To the Editor:

Dr. Hollingsworth provides an instructive discussion of a patient with rheumatoid arthritis who presented with acute dyspnea and renal failure, but there is little mention of the accompanying renal failure. Dr. Hollingsworth appropriately considered and then eliminated the possibility of a hemorrhagic pulmonary–renal syndrome and suggested several other causes. With one exception, none are tenable. Mild hypertension does not cause acute renal failure. There were no documented hypotensive episodes before the decline in renal function. Neither lisinopril nor indomethacin was a recent addition to the patient's medical regimen. Interstitial nephritis secondary to treatment with ampicillin is a possible diagnosis, but the very rapid recovery of renal function argues against it.

Urinalysis is not mentioned in the case presentation. As pointed out in the discussion of a previous Case Record,1 urinalysis is essential in evaluating unexplained renal failure, so much so that clinical nephrologists still examine the urine themselves. In this case, an examination of the urine would probably have shown renal tubular cells, muddy-brown granular casts, or both — as are typically seen in acute tubular necrosis — perhaps caused by a systemic inflammatory response syndrome. The absence of red-cell casts would have strengthened Dr. Hollingsworth's conclusion that this patient did not have glomerulonephritis.

Aaron Spital, M.D.
Rochester General Hospital, Rochester, NY 14621

1 References
  1. 1

    Case Records of the Massachusetts General Hospital (Case 28-1978). N Engl J Med 1978;299:136-145
    Full Text | Web of Science | Medline

Author/Editor Response

Dr. McNeely, an Associate Editor of the Case Records, replies:

To the Editor: The letters about Case 32-2001 raise two issues. One is the lack of information about urinalysis. A urinalysis (showing 0 to 5 red cells) was performed at the referring hospital, and another (showing ++ protein, 20 to 50 red cells, and 0 to 2 granular casts, without cellular casts or eosinophils) was performed at Massachusetts General Hospital. Although the results of both urinalyses were included in the abstract provided to the discussant and to those who attended the conference, these findings were not published because of space constraints.

The other issue is that there was no mention of rheumatoid nodules (although the case presentation does note that rheumatoid arthritis was diagnosed 18 months earlier and was managed with indomethacin and hydroxychloroquine). Nodules were not mentioned in the records for this extremely ill patient, who died on the eighth hospital day.

William F. McNeely, M.D.
Massachusetts General Hospital, Boston, MA 02114