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Feline asthma syndrome (FAS) is a clinical condition characterised by recurrent bouts of coughing, wheezing and, or, dyspnoea. While the aetiology is unproven, the condition is believed to involve a type I immediate hypersensitivity reaction to inhaled allergens. In this paper the clinical data from 29 cats, where a diagnosis of FAS was made, are assessed retrospectively. The most common clinical presentation was recurrent bouts of coughing (n = 26) and dyspnoea (n = 21). Radiographic changes were noted in 24 cats, which included increased bronchial (n = 5), interstitial (n = 7) and mixed (n = 12) (bronchial and interstitial) patterns. Right middle lung lobe collapse was noted in two cats. Abnormal bronchial cytology was present in 16 cats. A predominant eosinophilic sample was collected in only three cats. There were minimal changes in differential white cell counts, and mild eosinophilia was found in only five cats. Prednisolone alone was the most effective therapy, although avoidance of putative aeroallergens and antibacterial therapy was effective in some. On the basis of the data from these cases it would appear that the diagnosis of FAS depends largely on the clinical presentation and radiographic findings. The value of ancillary tests in the diagnosis of FAS appears to be limited.
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PMID:Feline asthma syndrome: a retrospective study of the clinical presentation in 29 cats. 858 22

A 45-year-old woman had pyrexia, headaches, collapse and hyponatraemia. Intracerebral abscess, bacterial meningitis and subarachnoid haemorrhage were excluded. She was given intravenous antibiotics and gradually recovered. One month later she was readmitted with diplopia, headache and vomiting. Serum sodium was low (107 mmol/l) and a diagnosis of inappropriate ADH secretion was made. MRI scan showed a suprasellar tumour arising from the posterior pituitary gland. A skin rash gradually faded. Serum cortisol, prolactin, gonadotrophins and thyroid hormone levels were low. A pituitary tumour was removed trans-sphenoidally, she had external pituitary radiotherapy, and replacement hydrocortisone and thyroxine. She was well for 12 months when she developed progressive weakness and numbness of both legs. Examination suggested spinal cord compression at the level of T2 where MRI scanning showed an intradural enhancing mass. This spinal tumour was removed and her neurological symptoms disappeared. Nine months after this she developed facial pain and nasal obstruction. CT scan showed tumour growth into the sphenoid sinus and nasal cavities. A right Cauldwell-Luc operation was done and residual tumour in the nasal passages was treated by fractionated external radiotherapy and Prednisolone. Histological examination of the specimens from pituitary, spinal mass, and nasal sinuses showed Rosai-Dorfman disease, a rare entity characterized by histiocytic proliferation, emperipolesis (lymphophagocytosis) and lymphadenopathy. Aged 48 she developed cranial diabetes insipidus. Although Rosai-Dorfman syndrome is rare, it is being reported with increasing frequency, and should be borne in mind as a possible cause of a pituitary tumour.
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PMID:Rosai-Dorfman disease presenting as a pituitary tumour. 1034 67