HIV diagnosis: why and how do we miss important clues?
Research has found that a significant proportion of patients diagnosed late with HIV infection had been in contact with healthcare professionals in the preceding year with symptoms attributable to HIV. We report a unique case of late HIV diagnosis missed when seen by a number of specialists and discuss whether with better communication the diagnosis could have been alerted earlier.
A significant proportion of patients diagnosed late with HIV infection reportedly had been in contact with healthcare professionals in the preceding year with symptoms attributable to HIV.1
A recent letter from the Chief Medical Officer to all clinicians highlights this and emphasises the importance of early recognition of HIV infection to stem the HIV epidemic.2 Cases of specialists in other fields missing HIV diagnosis repeatedly have been reported, unfamiliarity being the presumed excuse,3 but even specialists in the field of HIV need to be more alert.
In 2005, a 41-year-old gay man was referred to the genitourinary medicine (GUM) clinic by his general practitioner (GP) following a positive HIV test. A Kaposi’s sarcoma lesion on the tip of his nose showed he had AIDS. Disturbingly, the patient had previously attended the same clinic and several other clinics for apparently separate problems without the possibility of HIV being raised.
He first attended the GUM clinic in 2001 on four occasions without ever having an HIV test, despite this being one of the clinics that had pioneered “HIV testing for all”.4 At presentation the patient had transferred his care for perianal warts, diagnosed elsewhere, emphasising that he had been fully investigated, but, had this been checked, it would have been found not to have included HIV testing.
The patient registered with his present GP in 2001 with a complex medical history. The predominant clinical problem was severe chronic fatigue syndrome (CFS/ME) following glandular fever in his teens. He was referred to a CFS/ME clinic for advice on pain control. Sexual orientation was not recorded. CFS/ME is commonly triggered by infection; glandular fever due to Epstein-Barr virus (EBV) is a common precursor. But HIV is a definite but very uncommon trigger for CFS/ME, and HIV can cause a glandular fever-like illness at seroconversion. The CFS/ME referral was for clinical management of someone already diagnosed. The clinical features of the patient’s CFS/ME were characteristic and none raised any especial concern about another diagnosis; the focus over the next 2 years was on practical management. Although identifying the trigger for CFS/ME usually has no utility, HIV would be an exception. Failure to consider HIV infection, though explicable, could have been avoided: by a lower threshold of suspicion; a weighted assessment of relevant probabilities; less fragmentation of care; better communication between specialists and looking beyond one’s narrow domain of responsibility.
In 2003 the patient was referred to a gastroenterologist for rapid weight loss and change in bowel habit. All investigations proved negative and weight returned to normal. His sexuality was recorded. When referred for weight loss, abdominal discomfort and intermittent non-bloody semi-solid diarrhoea, the patient remained well-nourished; the gastroenterologist might have underestimated the significance of weight loss in his setting of low HIV incidence. Examination and investigations, including procto-sigmoidoscopy, were unremarkable and irritable bowel syndrome considered likely (commonly seen in CFS/ME).
In 2004 he was referred for open access endoscopy for dysphagia. The endoscopist found oesophageal candidiasis, attributed it to use of a steroid inhaler, and fluconazole treatment was successful. No sexual history was taken. Presented with dysphagia, a brief routine sexual history and a higher index of suspicion for HIV could have provided an additional clue.
When symptoms recurred the GP suggested HIV testing. The patient, being in a long term monogamous relationship and never sexually promiscuous, agreed reluctantly and was shocked when the results returned positive. The GP was unaware of the patient’s previous GUM clinic attendances. Could better communication have alerted the GP earlier?
The patient accepted the outcome stoically and was glad when the Kaposi’s sarcoma lesions resolved and HIV RNA became undetectable after highly active anti retroviral treatment (HAART). He is pleased that his case has contributed to the learning curve among clinicians and also led to his partner’s HIV diagnosis. He feels that patients too should be more proactive, forthright and find out more about their care, especially when it is fragmented.
Competing interests: None.
Patient consent: Mark is the patient and wanted to be named as the last author.
1. Sullivan AK, Curtis H, Sabin CA, et al. Newly diagnosed HIV infections: review in UK and Ireland. BMJ 2005; 330: 1301–2.
2. Donaldson L, Beasley C. Improving the detection and diagnosis of HIV in non-HIV specialties including primary care. DOH letter 13 September 2007. Gateway Ref no: 8519.
3. Winceslaus S J, Schofield J. A sore anus for 6 months. Lancet 1999; 353: 1672.
4. Read J, Winceslaus SJ. New strategies for increasing the detection of HIV: analysis of routine data. BMJ 2003; 326: 1066–7.
Updated information and services can be found at: http:// sti.bmj.com/cgi/content/full/84/2/101
S J Winceslaus, A J Pinching, A Harris, V Ankrett, Mark
Maidstone and Tunbridge Wells NHS Trust, UK;
Peninsula Medical School, Royal Cornwall Hospital, UK;
Kent & Sussex Hospital, Tunbridge Wells, Kent, UK;
The Beacon Surgery, Crowborough, UK;
Correspondence to: Dr S J Winceslaus, Consultant GUM physician, Department of GU Medicine, Culverden Suite, Kent & Sussex Hospital, Mount Ephraim, Tunbridge Wells, Kent TN4 8AT, UK;