Pseudogout attack associated with chronic thyroiditis and Sjogren's syndrome.
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A 66-year-old woman, diagnosed with chronic thyroiditis at age 63, presented with anorexia and fatigue. Therapy for the chronic thyroiditis consisted of levothyroxine sodium (100 microg/day). Her symptoms were attributed to the insufficient supply of levothyroxine sodium. Following a dosage increase to 150 microg/day, she suffered from an acute attack of pseudogout. Clinical features were complicated by Sjogren's syndrome, which appeared after treatment onset. Pseudogout was effectively treated by colchicine after administration of diclofenac sodium failed to alleviate the symptoms. Pseudogout is a recognized complication of thyroid replacement therapy, but association with Sjogren's syndrome has not been previously reported. (+info)
Diagnosis and management of gout.
(2/202)
Gout is a disease resulting from the deposition of urate crystals caused by the overproduction or underexcretion of uric acid. The disease is often, but not always, associated with elevated serum uric acid levels. Clinical manifestations include acute and chronic arthritis, tophi, interstitial renal disease and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues or body fluids. Treatment goals include termination of the acute attack, prevention of recurrent attacks and prevention of complications associated with the deposition of urate crystals in tissues. Pharmacologic management remains the mainstay of treatment. Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids. Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks. Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia. These potentially exacerbating factors should be identified and modified. (+info)
MEFV-Gene analysis in armenian patients with Familial Mediterranean fever: diagnostic value and unfavorable renal prognosis of the M694V homozygous genotype-genetic and therapeutic implications.
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Familial Mediterranean fever (FMF) is a recessively inherited disorder that is common in patients of Armenian ancestry. To date, its diagnosis, which can be made only retrospectively, is one of exclusion, based entirely on nonspecific clinical signs that result from serosal inflammation and that may lead to unnecessary surgery. Renal amyloidosis, prevented by colchicine, is the most severe complication of FMF, a disorder associated with mutations in the MEFV gene. To evaluate the diagnostic and prognostic value of MEFV-gene analysis, we investigated 90 Armenian FMF patients from 77 unrelated families that were not selected through genetic-linkage analysis. Eight mutations, one of which (R408Q) is new, were found to account for 93% of the 163 independent FMF alleles, with both FMF alleles identified in 89% of the patients. In several instances, family studies provided molecular evidence for pseudodominant transmission and incomplete penetrance of the disease phenotype. The M694V homozygous genotype was found to be associated with a higher prevalence of renal amyloidosis and arthritis, compared with other genotypes (P=.0002 and P=.006, respectively). The demonstration of both the diagnostic and prognostic value of MEFV analysis and particular modes of inheritance should lead to new ways for management of FMF-including genetic counseling and therapeutic decisions in affected families. (+info)
Superimposed primary chancre in a patient with Adamantiades-Behcet's disease.
(4/202)
Adamantiades-Behcet's disease was diagnosed in a 42 year old Turkish patient with recurrent oral aphthae, genital ulcerations, papules, and sterile pustules, histologically presenting as cutaneous vasculitis, and intermittent arthritis with joint effusion particularly of the knees. Six months after initial improvement under treatment with colchicine 2 mg/day, a solitary genital ulcer with enlarged inguinal lymph nodes appeared and persisted for 7 weeks despite the continuation of colchicine treatment and the introduction of clindamycin 2 mg/day intravenously. The unusual persistence of the ulcer and the failure of clindamycin therapy led to further differential diagnostic considerations and the identification of primary syphilis. The genital lesion healed 4 weeks after initiation of treatment with tetracycline 2 mg/day by mouth for 15 days. (+info)
Colchicine protects mice from the lethal effect of an agonistic anti-Fas antibody.
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The aim of this study was to determine whether colchicine, which has been reported to protect against various hepatotoxic insults, influences the susceptibility of mice to the agonistic anti-Fas antibody, Jo2. All mice that were pretreated with colchicine (2 mg/kg) survived the lethal challenge of intraperitoneal administration of 10 microg of Jo2, whereas all control mice pretreated with gamma-lumicolchicine succumbed to the challenge. Twelve micrograms of Jo2 killed less than half of colchicine-pretreated mice and its lethal effects were delayed relative to control mice, which all died within 8 hours. Other microtubule-disrupting agents such as Taxol, vinblastine, and nocodazole also improved the survival of mice treated with the lethal dose of Jo2. Histologic examination showed that colchicine protected against Jo2-induced fulminant liver injury, and TUNEL assay demonstrated that colchicine protected against massive apoptosis of hepatocytes. Hepatocytes isolated from colchicine-pretreated mice exhibited decreased susceptibility to Jo2-induced apoptosis. In addition, colchicine pretreatment reduced surface expression of Fas and decreased Jo2- and TNF-alpha-induced apoptosis of cultured hepatocytes in the presence of actinomycin D, but did not affect the susceptibility of cultured sinusoidal endothelial cells to Jo2-induced apoptosis. Remarkably, Fas and TNF receptor-1 mRNA and intracellular protein levels increased after colchicine treatment, indicating that colchicine protects against death ligand-induced apoptosis in the liver by decreasing death-receptor targeting to the cell surface. (+info)
Actin filament disruption inhibits L-type Ca(2+) channel current in cultured vascular smooth muscle cells.
(6/202)
To clarify interactions between the cytoskeleton and activity of L-type Ca(2+) (Ca(L)) channels in vascular smooth muscle (VSM) cells, we investigated the effect of disruption of actin filaments and microtubules on the L-type Ca(2+) current [I(Ba(L))] of cultured VSM cells (A7r5 cell line) using whole cell voltage clamp. The cells were exposed to each disrupter for 1 h and then examined electrophysiologically and morphologically. Results of immunostaining using anti-alpha-actin and anti-alpha-tubulin antibodies showed that colchicine disrupted both actin filaments and microtubules, cytochalasin D disrupted only actin filaments, and nocodazole disrupted only microtubules. I(Ba(L)) was greatly reduced in cells that were exposed to colchicine or cytochalasin D but not to nocodazole. Colchicine even inhibited I(Ba(L)) by about 40% when the actin filaments were stabilized by phalloidin or when the cells were treated with phalloidin plus taxol to stabilize both cytoskeletal components. These results suggest that colchicine must also cause some inhibition of I(Ba(L)) due to another unknown mechanism, e.g., a direct block of Ca(L) channels. In summary, actin filament disruption of VSM cells inhibits Ca(L) channel activity, whereas disrupting the microtubules does not. (+info)
Familial Mediterranean fever and systemic amyloidosis in untreated Turkish patients.
(7/202)
We compared the frequencies of seven MEFV mutations (M694V, M680I, V726A, M694I, K695R, R761H, E148Q) and the clinical findings in 20 Turkish FMF patients who had not developed amyloidosis by the age of 40 years in the absence of colchicine therapy, with those in 27 Turkish amyloidosis patients. No mutation frequency, including that of M694V, was different between the two groups. Family history of amyloidosis and parental consanguinity were noted to be higher in the amyloidosis group. The seven mutations do not appear to be sufficient to explain the development of amyloidosis in Turkish FMF patients. Other genetic factors may be important for this association. (+info)
Indomethacin induced psychosis.
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Indomethacin is a commonly prescribed non-steroidal anti-inflammatory drug. While its adverse effects on gastrointestinal and renal systems are well described, its central nervous system effects are less well known. This case report describes an elderly man, prescribed indomethacin for gout, who presented with psychosis. (+info)