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Polyarteritis Nodosa Ann Rheum Dis: first published as 10.1136/ard.47.5.428 on 1 May 1988. Downloaded from Annals of the Rheumatic Diseases, 1988; 47, 428-430 Case report Acute confusional state and hyponatraemia due to inappropriate antidiuretic hormone secretion in polyarteritis nodosa J S H GASTON, D G I SCOTT, AND P A BACON From the Department of Rheumatology, The Medical School, University of Birmingham, Birmingham SUMMARY An acute confusional state, which developed in a patient with polyarteritis nodosa (PAN), proved to be secondary to inappropriate secretion of antidiuretic hormone and consequent hyponatraemia. This is a very unusual complication of PAN and may well reflect a direct stimulation of the supraoptic nuclei owing to cerebral vasculitis. Key words: cerebral vasculitis. copyright. The syndrome of inappropriate antidiuretic hor- and immobility. He was treated with anti- mone secretion (SIADH) is well described in inflammatory drugs but continued to deteriorate association with chest diseases (malignant or in- and after two months was referred to this hospital. flammatory), disorders of the central nervous sys- In addition to the presenting symptoms, direct tem, and certain drugs.'-3 In contrast, there have questioning disclosed anorexia and jaw claudication,http://ard.bmj.com/ only been two reports of SIADH arising in the but he did not complain of headache or visual context of vasculitic disease; one concerned two disturbance. Examination showed a depressed man patients with temporal arteritis who developed in considerable pain, but with the exception of a hyponatraemia and an associated confusional state,4 small, cool effusion in the right knee, there was no whereas the other described a patient with polyar- evidence of synovitis, and all joints moved normally. teritis nodosa (PAN) who only had asymptomatic The temporal arteries were non-tender and pulsa- were as follows: erythrocyte hyponatraemia. In this report we describe a patient tile. Laboratory values on September 27, 2021 by guest. Protected with systemic necrotising arteritis characteristic of sedimentation rate 125 mm/h, C reactive protein 139 PAN who developed an acute confusional state and mg/l (normal <4 mg/l), white cell count 26-1 x 109/l the typical electrolyte disturbances of SIADH, and (70% neutrophils), platelets 771 x 109/l, albumin 22 who responded rapidly to treatment with high dose g/l, globulins 46 gll, alkaline phosphatase 403 IU/l corticosteroids. (normal range 70-350), creatinine 125 tmol/l, urea 11*6 mmol/l, creatine kinase normal. Rheumatoid Case report factor was positive (Rose-Waaler titre 1/128); anti- bodies to nuclear antigens, extractable nuclear A 64 year old retired engineer presented to his antigens, and to hepatitis B were all negative; general practitioner with an acute onset of arthral- cryoglobulins were not detected; and protein elec- gias involving both peripheral and central joints, trophoresis did not show a monoclonal band. stiffness in the siioulder girdle and lumbar region, Electromyography was normal. A clinical diagnosis of polymyalgia rheumatica was considered and treatment started empirically Accepted for publication 4 November 1987. which resulted in the Correspondence to Dr J S H Gaston, Department of Rheumatol- with prednisolone 15 mg/day, ogy, The Medical School, University of Birmingham, Birmingham complete resolution of his stiffness and jaw claudica- B15 2TJ, UK. tion, but after two weeks there was continuing 428 Ann Rheum Dis: first published as 10.1136/ard.47.5.428 on 1 May 1988. Downloaded from Acute confusional state in polyarteritis nodosa 429 malaise, weight loss, and low back pain severe enough to require readmission to hospital. Muscle stiffness and jaw claudication had not recurred. On examination there were no new signs other than w;.~- -' increased muscle wasting and epigastric tenderness. Two days later he became restless, confused, and ~~~t~~~~~~~~~~$__~~~I disorientated over a four to six hour period. j<K^.s.s. .-w..e ^ > . M Cultures of blood, urine, and cerebrospinal fluid were negative, but hyponatraemia was noted (Table 1). At this time the urine had an inappropriately high osmolality (771 mmol/kg) and contained 73 mmol/l sodium. A diagnosis of SIADH was con- sidered and fluid restriction started. While awaiting A~~~~~~~~~~~~~~~~~~~~A the results of bacteriological culture he received intravenous cefuroxime without improvement over 12 hours. Corticosteroid dosage was then increased by substituting hydrocortisone 100 mg six hourly * X S ... - w.) &t intravenously for the prednisolone. After two doses £'*s,. Xe %* .- s< s - of hydrocortisone he became rational, alert, and +z*X<.;ix, < -t - orientated, with no memory for the confusional episode. The serum sodium rapidly returned to Fig. 1 Haematoxylin and eosin stained section ofa small normal (Table 1). intramuscular artery showingfibrinoid necrosis. A mixed Further investigation to elucidate the nature of inflammatory cell infiltrate which includes polvmorphs and the underlying disease included a muscle biopsy, lymphoid cells extends through the vessel wall. The which showed necrotising vasculitis of small muscu- surrounding skeletal muscle show evidence of fibres copyright. lar arteries characteristic of PAN (Fig. 1). In regeneration. addition, there was a markedly raised level of factor VIII related antigen in the serum (over three times normal), consistent with the active endothelial cell cell count, platelets, haemoglobin) after four damage seen in acute vasculitis.6 Arteriography of months' follow up. the coeliac axis and renal vessels did not show aneurysms; cerebral angiography was not performed Discussion http://ard.bmj.com/ because of extensive atheroma at the origin of the carotid arteries. Other normal or negative investiga- Some of the presenting features in this case (pain, tions included chest radiographs, barium meal and stiffness, jaw claudication) were suggestive of follow through, and both computed tomographic polymyalgia rheumatica or giant cell arteritis, and and ultrasound scans of the abdomen. A diagnosis these symptoms responded rapidly to low doses of of PAN was made, and the patient was treated, steroids. The overall illness, however, continued to therefore, with intermittent pulses of cyclophospha- progress rapidly, and the diagnosis of PAN was mide and steroids, with a rapid improvement in all made from the muscle biopsy, which showed typical on September 27, 2021 by guest. Protected of his clinical symptoms, including significant weight necrotising arteritis of small muscular arteries. Very gain. He has remained completely well with normal high levels of factor VIII related antigen are more renal function and normal blood parameters (white often seen in PAN than in other vasculitides.6 The markedly raised white cell count and the increased alkaline phosphatase are also compatible with this Table 1 Laboratory values before and after treatment diagnosis. It is of interest to speculate whether a biopsy of the temporal arteries (which were always Date Na K Urea Creatinine normal on examination) would also have shown a (mmol/1) (mmoli) (mmolll) (Wnolll) necrotising arteritis rather than giant cell arteritis; this has been First admission 130 4-6 11-6 125 reported previously in some patients Second admission 129 5-2 7-8 109 with PAN.78 Confusional state 122 4-8 7-4 87 SIADH has been defined as the occurrence of 36 Hours after hyponatraemia, which reflects hypo-osmolality, at a steroid treatment 129 3-3 6-6 65 60 Hours after time when the kidneys continue to excrete both a steroid treatment 134 3-8 6-0 57 concentrated urine and sodium. Normal renal and adrenal function, with no clinical evidence of Ann Rheum Dis: first published as 10.1136/ard.47.5.428 on 1 May 1988. Downloaded from 430 Gaston, Scott, Bacon volume depletion, are also required. 1-3 Our patient this was not shown by arteriography, and in the clearly fulfilled this definition: the urine was hyper- presence of normal urinary sediment and renal tonic with a high concentration of sodium, hypovo- function, renal biopsy was not considered justified. laemia was absent clinically (no diuretics were being The rapidity of the recovery of the hyponatraemia taken, and the serum urea decreased with the suggests that it was not due to fluid restriction alone, hyponatraemia), and the patient had already been but was more likely to reflect treatment with high treated with corticosteroids. Renal function was dose steroids. A similarly rapid response to steroid mildly impaired at presentation, but serum creati- treatment was reported in a patient with SIADH nine was in the normal range when SIADH was and temporal arteritis, who regained consciousness diagnosed. after 24 hours' treatment with high dose hydrocorti- There are two principal mechanisms by which sone and had a normal serum sodium by 48 hours.4 hyponatraemia might have been produced in this Patients with SIADH complicating chest infection patient. Firstly, ADH production may have been also show a rapid recovery when the infection is truly 'inappropriate', caused by pathological treated3; thus recovery may be dependent on the stimulation of the supraoptic/hypophyseal path- treatment of the underlying condition, rather than ways, possibly owing to local cerebral vasculitis. on a direct effect of steroids on ADH secretion. The presence of jaw claudication at presentation This is the first report of SIADH as a major suggests vasculitis of extracranial vessels, but complication of PAN. We suggest that the most unfortunately we were prevented from trying to likely aetiology in this case was a local cerebral demonstrate cerebral vasculitis arteriographically. vasculitis stimulating ADH secretion directly and The report of SIADH in patients with temporal responding rapidly to treatment with cortico- arteritis, one of whom also had jaw claudication,4 steroids. supports such a hypothesis, and the rapid response of the hyponatraemia to high dose steroids in our the expected allevia- We are grateful to Dr G Kondratowicz, Department of Pathology, patient could be explained by University of Birmingham, for reviewing the pathological findingscopyright. tion of cerebral vasculitis by such treatment.
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