Inappropriate secretion of ADH in a patient with systemic lupus erythematosus.код для вставкиСкачать
237 LETTERS her scalp. trunk, and left leg, indicating hematologic dissemination. Over the next week her skin rash and joint pains completely resolved and she has been well since. She has remained asymptomatic for the last 6 months. Herpes zoster was confirmed by a greater than fourfold rise in her serum complement fixation titer. Discussion. The joint involvement in this patient probably occurred from spread along nerves arising from the dorsal root of L2. Both the femoral and obturator nerves arise from the dorsal root of L2, 3,4. and supply branches to the hip joint. In the previously reported case ( I ) in which both knees were involved, it was postulated that arthritis in one knee resulted from spread along the nerves. However, in the other knee where there was no vesicular rash in the same dermatome distribution, hematogenous spread was suspected. If hematogenous spread does occur, it is surprising that arthritis is not more frequent in generalized herpes zoster infection. The current patient had obvious hematogenous spread causing disseminated zoster but there was no involvement of other joints. Disseminated zoster occurs in 2-10% of patients. The incidence increases, especially in malignancy, usually lymphomas. In a study (3) on the incidence of herpes zoster with lymphoma, there were 21 disseminated cases in 129 patients. Arthritis was not reported in any of these. If hematogenous spread resulted in arthritis. it would have been expected to occur more commonly in this group with severe disseminated disease. However, an immune complex mediated mechanism must also be considered since this may account for those cases where there is no dermal eruption in contiguous dermatomal distribution to that supplying the joint. The most likely mechanism remains that of direct inflammation of the synovium via viral spread along the nerves arising from the activated dorsal root. In all cases reported to date. the arthritis has resolved rapidly, with no sequelae. after the appearance of the skin rash. Perhaps because of severe pain in the dermatome involved with herpes zoster, other cases of synovitis have been masked and not diagnosed. The transient nature of the arthritis also makes diagnosis difficult. The major difficulty remains that of excluding a bacterial arthritis in these patients . M.D. Devereaux, MB. BS K.A. Hazelton, MRCP(UK), FRACP Princess Alexandra Hospitol Brishane, Australia 1. Cunningham AL. Frdser JKE, Clarris BJ. Hobbs JB: A study of synovial fluid and cytology in arthritis associated with herpes zoster. Aust NZ J Med 9:W. 1979 2. Priest JR. Urick J U , Groth KE. Balfour H H Jr: Varicellaarthritis documented by isolation of virus from joint fluid. J Pediatr 9390. 1978 3. Goffinet DR. Gladsteon EJ. Merigan TC: Herpes zoster varicella infections and lymphoma. Ann Intern Med 76:235. 1972 Inappropriate secretion of ADH in a patient with systemic lupus erythematosus To the Editor: Inappropriate secretion of antidiuretic hormone (SIADH) has been reported in a wide variety of disorders, and in diseases involving the central nervous system (CNS) in particular (Zerbe R. Stropes L, Robertson G: Vasopressin function in the syndrome of inappropriate diuresis. Annu Rev Med 31:315-327, 1980). Surprisingly. there is only one report of SlADH in a patient with systemic lupus erythematosus with CNS involvement, but that patient had tuberculosis during her illness (Kaplan AP. Curl FD, Decker JL: Central hyperventilation and inappropriate antidiuretic hormone secretion in systemic lupus erythematosus. Am J Med 48:661-667, 1970). We would like to report a case of SlADH occurring as a sole consequence of active lupus. Our patient, a 26-year-old white male homosexual, was admitted to St. Clare's Hospital on December 29, 1981 with a 3-day history of fever to 103°F. nausea, vomiting. diarrhea. For the past 6 months he had experienced muscle and joint pains. In August 1981 he developed a malar rash after sun exposure at the beach. History was remarkable for a positive test for syphilis 7 years previously, which, although he was asymptomatic, had resulted in treatment with penicillin. His father died from multiple sclerosis. On examination. the patient was lethargic and notably dehydrated. An atrophic, scaly rash was noted on the malar areas, forehead, eyebrows, bridge of the nose, and ears. Initial hematocrit count was 33%, erythrocyte sedimentation rate 45 mm/hour, white blood count 2,700, blood urea nitrogen (BUN) 40 mg%. creatinine 1.2 mg%, serum sodium 147 mEqlliter; other electrolytes were normal. Intravenous hydration was begun with the patient receiving a total of 3,000 cc on the first hospital day, 2,000 cc of which was D5W and 1.OOO cc of normal saline. On the second hospital day, with the same intravenous intake and an additional 500 cc orally, the serum sodium fell to I20 mEq/ liter and the BUN to 28 mg%. On the third hospital day the patient had a grand ma1 seizure. Serum sodium was noted to have fallen to I10 mEql liter. An additional 500 cc of 3% (hypertonic) saline was administered. Although the patient was very confused and disoriented, there were no localizable neurologic signs, and spinal tap results were negative. Other laboratory values of note were a platelet count of 13O,OOO,antinuclear antibodies positive at a titer of 1/80 with a peripheral pattern, 3 positive lupus preps. latex fixation 1/80, VDRL test positive 112. fluorescent treponemal antibody-absorption test negative, C4 and C3 normal, cryoglobulins positive 1/20, and cold agglutinins. hepatitis-associated antigen. cytomegalovirus. and Monotest all negative. Urine was 1 + for protein. White blood count was 2.550 and red blood count, 50-100. Serum osmolality was 260 mOsm/liter, urine osmalality. 620 mOsm/ liter. Urine electrolytes were normal. The patient began a treatment program of fluid 238 restriction, prednisone 100 mg daily, and Dilantin 300 mg daily. Urine output increased from 600 cc to 1,800 cc daily. The serum sodium rose to 142 mEq/liter. His mental status improved dramatically, and there was no further seizure activity. The subsequent course was complicated by a proximal myopathy that involved the shoulder and pelvic girdles and was attributed to high-dose corticosteroid therapy, but the patient was discharged in good condition on February 9, 1982, with his prednisone decreased to 30 mg daily. Bertrand Agus, MD Sudha Nayar, MD Dipti J. Patel, MD Michael McGrath, MD St. Clare’s Hospital New York, N Y Systemic lupus erythematosus, gout, and Paget’s disease To the Editor: Two short communications concerning the occurrence of crystal induced deposition disease as a cause of arthritis in patients with systemic lupus erythematosus (SLE) have been published (Moidel RA, Good AE: Coexistence of gout and systemic lupus erythematosus. Arthritis Rheum 24:967-971, 1981), (Rose EP, Alves LE: Coexistent gout and systemic lupus erythematosus. Arthritis Rheum 25:713-714, 1982). By and large the majority of articular flare-ups in patients with SLE can be accounted for by the disease itself. However, other etiologies should be ruled out in the usual fashion especially if the patient lacks other manifestations suggestive of active SLE. We wish to report another patient with SLE and gout, who also happened to have Paget’s disease of bone, which made the interpretation of her symptoms more complicated. A 52-year-old black woman was admitted to the hospital on January 7, 1982 with a 2-day history of chest pain. Medical history was pertinent for hypertension, hypertensive cardiovascular disease, insulin dependent diabetes metlitus, hyperparathyroidism secondary to parathyroid adenoma (removed in 1978), and hyperuricemia. Cholecystectomy and hysterectomy had been performed in the past. The diagnosis of SLE was made when at age 38 she was admitted to another hospital with fever, polyarthralgias, pleurisy, skin rash, photosensitivity, and positive antinuclear antibody. Treated with various doses of prednisone ever since, she was first admitted to our medical center at age 48; bone pains were a prominent part of her complaints. Her SLE was inactive. Hyperparathyroidism was diagnosed and she underwent parathyroidectomy; her bone survey showed skull and pelvic lesions diagnostic of Paget’s disease of bone. She was found to be hyperuricemic. It was believed that her bony aches were primarily related to her Paget’s disease and thus a trial of calcitonin gave relief from pain. However, LETTERS calcitonin had to be stopped because of the cost involved. At age 49, and ever since, the patient experienced episodes of acute oligoarthritis in addition to persisting bone pain. Her SLE remained quiescent. Two weeks before admission the patient developed chest pain which was believed to be skeletal in origin and, because of persistence of that symptom, she was admitted. Shortly afterward acute left ankle arthritis was noted; aspiration yielded a yellow turbid fluid with a white blood cell count of 22,400, negative Gram stain and cultures, and no crystals. Three days later minimal effusion developed in the right knee. A few drops of synovial fluid were obtained and typical urate crystals were observed under the polarized scope. Serum urate was 18 mg/100 dl and a 24-hour uric acid excretion was 448 mg. Because the patient was already taking 50 mg Indocin twice daily, she was given 1 mg intravenous colchicine to which she responded dramatically. Thereafter she was placed on oral colchicine with complete resolution of her arthritis. It was thought that her SLE was not responsible for her present symptoms and thus prednisone was tapered. Her problems illustrate the complexity of patients with systemic lupus erythematosus. Graciela S. Alarcon, MD Gene V. Ball, MD Paul M. Goldfarb, Jr, MD University of Alabama Birmingham, Alabama Pancreatitis and systemic lupus erythematosus: a case report To the Editor: Pancreatitis may sometimes be seen in the course of systemic lupus erythematosus (SLE), but the role of SLE in the pathophysiology of the pancreatitis is often obscured by the concomitant use of drugs that are known to cause pancreatitis or by coexistent medical problems. We report a case of recurrent pancreatitis in a young woman with SLE. In this patient, there appeared to be a direct relationship between episodes of pancreatitis and SLE activity. Endoscopic retrograde cannulation of her pancreatic duct revealed normal pancreatic anatomy. The patient is a 30-year-old white woman who has had SLE since 1971. In early 1980, while she was receiving prednisone 10 mg per day, intermittent diarrhea and recurrent episodes of severe coexistent abdominal pain occurred. During one such episode in May 1980, her serum amylase was elevated (Figure I). Results of an oral cholecystogram and an ultrasound study of the gall bladder and pelvis were normal, and computerized tomogram of the abdomen showed diffuse pancreatic enlargement. She responded well to conservative therapy with nasogastric suction and intravenous hydration. Prednisone was continued at 10 mg per day.