An Unusual Cause Of Eosinophilia


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An Unusual Cause Of Eosinophilia

  1. 1. An Unusual Cause Of Eosinophilia? Or much ado about nothing?
  2. 2. The mysterious case of Mrs H’s Malaise……… <ul><li>69 Year old lady presented with chest pain ? Acute coronary syndrome. </li></ul><ul><li>She had a past medical history of asthma and high cholesterol. </li></ul><ul><li>incidentally gave a 5/12 history of general malaise, “sickliness” & weight loss. </li></ul><ul><li>MI screen negative, WCC normal, eosinophils of 4.9 (32%), Na 2+ 132. </li></ul><ul><li>CXR revealed apical fibrosis ~ ? tuberculosis </li></ul><ul><li>Treated as TB with Rifinah, Ethambucol, Pyrazinamide & Isoniazid and discharged with follow up ~ awaiting AAFB results </li></ul>
  3. 3. The Mysterious case of Mrs H’s Malaise…… <ul><li>Readmitted 8/7 later, with worsening nausea and vomiting. Thought to be dehydrated & BP low </li></ul><ul><li>Eosinophils 1.7, Na 2+ 124. </li></ul><ul><li>Given iv fluids and symptomatically improved, then Na 2+ results seen </li></ul><ul><li>Bendrofluazide stopped, fluid restricted and given antiemetics. </li></ul><ul><li>Initially pyrazinamide stopped as most likely cause of nausea & vomiting. </li></ul><ul><li>Fluid restriction stopped to allow for formal plasma/urinary osmolality & electrolytes to be sent. </li></ul>
  4. 4. The mysterious case of Mrs H’s malaise….. <ul><li>Plasma Osmolality 263 </li></ul><ul><li>Urine Osmolality 165 </li></ul><ul><li>Not SIADH ~ however Na 2+ </li></ul><ul><li>continues to drop & trough’s </li></ul><ul><li>at 117. </li></ul>Mrs H was again fluid restricted despite previous results. Rpt osmolalities:Plasma 231, Urine 160, urinary Na 2+ <10. Definitely not SIADH!! No peripheral oedema Only other drugs aspirin, ramipril, atorvastatin TFTs & random cortisol normal Autoimmune screen negative AAFBs x 3 negative IgG 12.6 IgM 1.1 IgA 1.51 IgE 672
  5. 5. The Mysterious Case Of Mrs H’s Malaise….. <ul><li>On closer questioning, Mrs H believed that her non-specific symptoms could be linked to the time that her GP commenced atorvastatin. </li></ul><ul><li>All medicines were stopped except her inhalers. </li></ul><ul><li>Her symptoms then gradually improved so that she felt well enough to go home 21/7 after her re-admission. </li></ul><ul><li>On discharge Na 2+ was 133, Eosinophils 2.4. </li></ul>. <ul><li>CXR reviewed ~ appearances significantly better so unlikely to be TB. </li></ul><ul><li>She was rehydrated and treated with antiemetics </li></ul>
  6. 6. The Mysterious Case Of Mrs H’s Malaise…… <ul><li>We postulated that her symptoms are down to medicine SE’s ~ likely atorvastatin. Our aim was to rechallenge if her eosinophils returned to normal. </li></ul>CSM reports 1 case of pulmonary eosinophilia with atorvastatin, 1 case of peripheral eosinophilia with ramipril & 3 of hyponatraemia with ramipril.
  7. 7. Pulmonary Eosinophilia
  8. 8. Pulmonary Eosinophilia <ul><li>Range from the very mild simple pulmonary eosinophilias to the often fatal polyarteritis nodosa. </li></ul>
  9. 9. Poor/ Fair Months/years always >20% Severe Polyarteritis Nodosa Poor Months/years Always >20% Severe Hypereosinophilic syndrome Fair Years None >20% Moderate/ Severe Tropical Pulmonary Eosinophilia Fair Years None 5-20% Moderate/ Severe Asthmatic Bronchopulmonary Eosinophilia Good >1/12 None >20% Mild/ Moderate Prolonged Pulmonary Eosinophilia Good <1/12 None 10% Mild Simple Pulmonary Eosinophilia Outcome Duration Multi-system involve-ment Blood Eosino-phils% Symptoms Disease
  10. 10. Simple versus Prolonged Pulmonary Eosinophilia <ul><li>Simple Pulmonary Eosinophilia </li></ul><ul><li>Mild illness </li></ul><ul><li>Fever & cough lasting less than 2 weeks </li></ul><ul><li>Probably due to a transient allergic reaction in the alveolus </li></ul><ul><li>Self limiting </li></ul><ul><li>Prolonged Pulmonary Eosinophilia </li></ul><ul><li>Similar to simple but lasting more than a month </li></ul><ul><li>High fever </li></ul><ul><li>Peripheral eosinophilia </li></ul><ul><li>Localised or diffuse CXR opacities </li></ul><ul><li>Resolves with steroids. </li></ul>
  11. 11. Asthmatic Bronchopulmonary Eosinophilia <ul><ul><li>Characterised by asthma, transient CXR shadows and blood or sputum eosinophilia. </li></ul></ul><ul><ul><li>Most common cause is allergy to aspergillus fumigatus. </li></ul></ul><ul><ul><li>Aspergillus actually grows in the wall of the bronchi and eventually produces proximal bronchiectasis. </li></ul></ul><ul><ul><li>Episodes of wheeze,cough,fever and malaise. </li></ul></ul><ul><ul><li>Association with expectoration of sputum plugs leading to clearing of CXR appearances. </li></ul></ul><ul><ul><li>Extremely high IgE & +ve aspergillus precipitans </li></ul></ul><ul><ul><li>Treatment with 30mg prednisolone ~ may need 15mg for maintenance </li></ul></ul><ul><ul><li>Untreated can result in progressive fibrosis that may mimic TB on CXR. </li></ul></ul>
  12. 12. <ul><li>Polyarteritis Nodosa </li></ul><ul><li>Characterised by foci of necrotizing arteritis </li></ul><ul><li>Affects most organs. </li></ul><ul><li>Lung involvement unusual except in Churg-Strauss syndrome. </li></ul><ul><li>CXR may show ill-defined shadows that disappear & reappear over weeks. </li></ul><ul><li>5 yr survival is 80% with steroid and immunosuppression </li></ul><ul><li>Churg-Strauss Syndrome . </li></ul><ul><li>Occurs in the fourth decade </li></ul><ul><li>Eosinophilic infiltration in individuals with previous history of rhinitis and asthma. </li></ul><ul><li>High eosinophils, vasculitis of small vessels and extra vascular granulomas. </li></ul><ul><li>Renal failure less likely than in PAN. </li></ul><ul><li>pANCA can be positive. </li></ul><ul><li>Responds to steroids. </li></ul>
  13. 13. Drug induced Eosinophilia <ul><li>Eosinophilia has been reported as a side effect of many drugs including: </li></ul><ul><li>NSAID’s </li></ul><ul><li>ACEI’s </li></ul><ul><li>Statins (peripheral) </li></ul><ul><li>Penicillins, Tetracyclines, Sulphonamides </li></ul><ul><li>Phenytoin, Carbamazepine </li></ul><ul><li>Chlorpropamide. </li></ul><ul><li>Potential drug SE’s are under reported since there is often little hard evidence </li></ul><ul><li>? Not much known about a mechanism of eosinophilia. May precipitate a reaction in a susceptible individual. </li></ul>
  14. 14. Conclusion…. <ul><li>Mrs H’s symptoms resolved when all meds were stopped. </li></ul><ul><li>At follow up she was well. </li></ul><ul><li>Na 2+ was 135, but eosinophils remained elevated at 3.1 </li></ul><ul><li>After much excitement about possible drug causes, she was treated with steroids and made a good recovery! </li></ul><ul><li>NB: aspergillus precipitans were never measured </li></ul>
  15. 15. Hyponatraemia & SIADH <ul><li>ADH causes water retention </li></ul><ul><li>In hypovolaemia the action of aldosterone causes sodium retention & therefore urine Na is low </li></ul><ul><li>In SIADH only water is retained so urine Na remains inapproriately high </li></ul><ul><li>No diuretics </li></ul><ul><li>Normal adrenal & thyroid function </li></ul><ul><li>No hypotension (or low K+) </li></ul><ul><li>Low plasma osmolality with inappropriately high urine osmolality & sodium </li></ul>
  16. 16. Hyponatraemia & SIADH <ul><li>In this case the patient had lost salt and water in vomit and via diuretics </li></ul><ul><li>She would have tried to replace volume with water, but continued to take bendrofluazide hence ongoing salt & water loss </li></ul><ul><li>Her ACEI would interfere with the action of angiotensin 2 on the adrenals, further reducing her ability to salt conserve </li></ul><ul><li>At this sodium level treatment is simply replacing volume with saline & stopping diuretics </li></ul><ul><li>ACEI should be stopped in the short term when a patient is hypovolaemic </li></ul><ul><li>Bendrofluazide has been implicated in a few more dramatic recent cases of hyponatraemia which Dr Jones would love to tell you all about! </li></ul>