Hypertension, its treatment, hyperuricaemia and gout.

PURPOSE OF REVIEW: Gout is increasing worldwide. An appreciation that hyperuricaemia and gout are associated with hypertension and chronic kidney disease is well established, but the cause and effect relationships are controversial. Studies which address this conundrum have been reviewed. RECENT FINDINGS: Epidemiological surveys have confirmed the strong relationship of gout and hyperuricaemia with hypertension and diuretic treatment. There are multiple confounders such as obesity and alcohol consumption which despite adjustments make interpretation of the epidemiology difficult. There are data to suggest that hyperuricaemia itself causes hypertension and renovascular disease, and that lowering of serum urate may assist in control of hypertension. The mechanism for diuretic-induced hyperuricaemia may operate through volume depletion and reduced secretion of uric acid. The latter effect may be genetically influenced. SUMMARY: Recent population surveys have strongly supported the association of gout and hyperuricaemia with hypertension. The prevailing explanation that renal dysfunction causes both phenomena or that they are caused by shared factors is challenged by the evidence that hyperuricaemia drives hypertension. A confounder of epidemiology studies is the use of diuretics for treating hypertension. A closer understanding of the mechanisms of diuretic-induced hyperuricaemia may lead to the creation of uricosuric diuretics. Losartan is exceptional amongst antihypertensive drugs in possessing mild uricosuric properties and therefore has a role in treating hypertensive patients with gout. Overcoming diuretic-induced hyperuricaemia is difficult and there is need for a uricosuric diuretic.

Interstitial keratitis and sensorineural hearing loss as a manifestation of rheumatoid arthritis: clinical lessons from a rare complication.

Cogan's syndrome or non-syphilitic interstitial keratitis with vestibule-auditory dysfunction is a serious and under-recognised complication of rheumatoid arthritis. It is an autoimmune condition characterised by inflammatory infiltrates on the cornea and extensive vestibulocochlear damage. If left untreated, patients progress to develop profound hearing loss. We present a case that was incorrectly diagnosed and treated as conjunctivitis by several emergency departments prior to being correctly recognised as Cogan's syndrome.

Hyperuricemia, gout and the kidney.

PURPOSE OF REVIEW: (a) To examine the latest information about renal tubular handling of uric acid, its genetic background and contribution to the causation of hyperuricemia. (b) To review the association of hyperuricemia, gout and chronic kidney damage and whether hyperuricemia is cause or effect of renal dysfunction. RECENT FINDINGS: The gene SLC2A9 encodes for GLUT9, an important proximal tubule transporter of uric acid. Polymorphisms of the gene have been linked to gout susceptibility and to hereditary hypouricemia. Familial childhood gout with progressive renal impairment attributable to mutations of the uromodulin (UMOD) gene is associated with reduced uromodulin in the proximal tubule cilia. Familial juvenile hyperuricemic nephropathy (FJHN) is one of three similar clinical disorders associated with uromodulin gene mutations. Genetic studies of urate transportation and of uromodulin-related nephropathy emphasize the pivotal importance of the proximal tubule in uric acid homeostasis. Studies of allopurinol and febuxostat lowering of serum urate have once again raised the tantalizing possibility that hyperuricemia is harmful to the kidneys by showing better preservation of glomerular filtration rate (GFR) in treated patients. SUMMARY: Renal tubular handling of uric acid is dependent on tubular transporters, one of which is GLUT9. Mutations of its gene SLC2A9 are associated with aberrations of uric acid disposal. Familial hyperuricemia due to uromodulin deficiency precedes but does not cause kidney failure. Nevertheless, both allopurinol and febuxostat treatment has sustained the hypothesis that hyperuricemia itself can have an adverse impact on kidney function.

Septic arthritis: an extensive variety of pathology.

Septic arthritis typically presents as a hot, swollen joint. Rapid recognition and treatment of this condition is essential to prevent permanent joint damage. However, septic arthritis does not always present in a textbook manner. The case presented here concerns septic arthritis affecting the right sternoclavicular joint. The patient did not have any risk factors for septic arthritis and presented with a swollen tender joint that was not hot. He was treated with penicillin and then amoxicillin for a total of 12 weeks and made a full recovery. The organism isolated from his right sternoclavicular joint was Neisseria elongata, which is the first ever documented case of this organism causing septic arthritis. This case emphasises that the suspicion of septic arthritis should remain high when unexplained monoarthritis occurs and there should be a low threshold in treating monoarthritis as septic arthritis even in the absence of risk factors.

Low back pain, sacroiliitis, and the relationship with HLA-B27 in Crohn's disease.

OBJECTIVE: To determine the prevalence of sacroiliitis in patients who have back pain in Crohn's disease (CD) using computed tomography (CT); and to reassess the association of sacroiliitis in CD with HLA-B27. METHODS: A total of 134 consecutive patients with CD completed a questionnaire about musculoskeletal symptoms. Those reporting low back pain were assessed, including plain radiographs and CT of the sacroiliac joints. HLA-B27 status was determined in patients with and without back pain. RESULTS: There were 70 (52%) patients with low back pain, of whom 31 (45%) had CT evidence of sacroiliitis. These were characterized by more frequent morning spinal stiffness and positive sacroiliac compression tests even when sacroiliitis was not suspected. Nine had previously recognized radiological and clinical ankylosing spondylitis (AS), and of these 78% were HLA-B27 positive. Of those with newly identified sacroiliitis, 14% were HLA-B27 positive. This frequency was not statistically dissimilar to the 9% HLA-B27 positivity of those without back pain. CONCLUSION: Sacroiliitis defined by CT is a common cause of low back pain in CD. A relationship of sacroiliitis and HLA-B27 could be confirmed only for those with classical AS. Our results accord with the possibility that sacroiliitis in CD is an isolated phenomenon, which is unrelated to HLA-B27 and which may evolve into classical spinal ankylosis in genetically susceptible subjects.