1/5. Coincidental supraorbital neuralgia and sinusitis.headache interpreted as treatment failure may be encountered after FESS or pharmacological treatment for chronic sinusitis. This persistent symptom may lead, even in the presence of minimal sinus disease, to frequent office visits, medical treatment, primary surgery, and revision procedures. A prospective study of patients with a documented history and imaging-verified sinus disease with persistent atypical refractory headache were evaluated. Diagnostic measures included injection of local anesthetic and response to carbamazepine. Severe neuralgia of the supraorbital nerve was identified in 11 patients with chronic sinusitis, treated either medically or surgically before inclusion in the study. Eight of the patients underwent surgery for sinus disease, and five of them had revision surgery because of persisting complaints. All patients responded favorably to the local injection, and eight were treated with carbamazepine. In certain cases, headache in sinusitis patients may be caused or aggravated by supraorbital neuralgia. Sinus disease is possibly a causative factor but conceivably plays the role of a "red herring." This readily diagnosed and treated coexistence may be more prevalent than recognized formerly.- - - - - - - - - - ranking = 1keywords = treatment failure (Clic here for more details about this article) |
2/5. Case report: Nitazoxanide treatment failure in chronic isosporiasis.We report a 60-year-old immunocompetent patient with chronic biliary isosporiasis who failed to respond to orally administered cotrimoxazole prophylaxis and orally administered treatment with nitazoxanide, a 5-nitrothiazole benzamide compound. Severe malabsorption was regarded as responsible for the subtherapeutic levels of nitazoxanide in plasma and bile, resulting in treatment failure. Intravenously administered cotrimoxazole stopped the shedding of isospora belli oocysts in bile within 5 days, excluding initially suspected resistance to cotrimoxazole. patients with malabsorption and cholangitis due to coccidia such as isospora belli and cryptosporidium spp. or due to protozoa that cause microsporidiasis seem to be predisposed to fail to respond to otherwise effective treatment.- - - - - - - - - - ranking = 5keywords = treatment failure (Clic here for more details about this article) |
3/5. tissue plasminogen activator for treatment of livedoid vasculitis.Livedoid vasculitis, a hyalinizing vasculopathy, is characterized by extensive formation of microthrombi and deposition of fibrin in the middermal vessels, which result in epidermal infarction, ulceration, and formation of stellate scars. In a prospective study of nonhealing ulcers in patients with livedoid vasculitis, we found a high incidence of anticardiolipin antibodies, lupus anticoagulants, increased levels of plasminogen activator inhibitor, and low levels of endogenous tissue plasminogen activator (t-PA) activity. This procoagulant tendency and decreased fibrinolysis may provide an explanation for the occlusive vasculopathy often noted in biopsy specimens from these patients. On the basis of these findings, we proposed that fibrinolysis with recombinant t-PA would lyse microvascular thrombi, restore circulation, and promote wound healing. In six patients who had nonhealing ulcers caused by livedoid vasculitis and in whom numerous conventional therapies had failed, low-dose t-PA (10 mg) was administered intravenously during a 4-hour period daily for 14 days. Five of the six patients had dramatic improvement; almost complete healing of the ulcers occurred during hospitalization, and tissue oxygenation, as measured by transcutaneous oximetry, increased. The one treatment failure was due to rethrombosis of the microvasculature; this patient was subsequently re-treated but with concurrent anticoagulation, and her leg ulcers healed. We conclude that daily administration of a low dose of t-PA is safe and effective treatment for nonhealing ulcers due to occlusive vasculopathy.- - - - - - - - - - ranking = 1keywords = treatment failure (Clic here for more details about this article) |
4/5. exocrine pancreatic insufficiency in celiac sprue: a cause of treatment failure.The coexistence of nontropical sprue and advanced pancreatic insufficiency is uncommon. The purposes of this report are to: (a) describe 3 patients with non-tropical spruc and severe pancreatic insufficiency, (b) determine the frequency, magnitude, and clinical importance of diminished pancreatic secretion in nontropical sprue, and (c) assess whether patients with pancreatic insufficency secondary to chronic pancreatitis or pancreatic cancer have jejunal mucosal histologic abnormalities. In each of 3 patients with nontropical sprue and associated severe exocrine pancreatic insufficiency, an optimal clinical response required the appropriate treatment of both causes of malabsorption. Of 31 subjects with proved nontropical sprue, cholecystokinin-stimulated duodenal tryptic activity or lipolytic activity (or both) was reduced in 13 (42%) but severely reduced in only the three case reports (10%). The morphologic structure of the small bowel was normal in 21 patients with primary pancreatic insufficiency secondary to chronic pancreatitis or pancreatic cancer. Mild-to-moderate exocrine pancreatic insufficiency is a frequent finding in untreated nontropical sprue, is presumably reversible, and rarely contributes to the development of steatorrhea. However, if patients with nontropical sprue fail to respond to a gluten-free diet, coexistent severe pancreatic insufficiency is a possible cause for treatment failure.- - - - - - - - - - ranking = 5keywords = treatment failure (Clic here for more details about this article) |
5/5. Clinical and cytogenetic remission induced by interferon-alpha in a patient with chronic eosinophilic leukemia associated with a unique t(3;9;5) translocation.A patient with chronic eosinophilic leukemia and a unique complex chromosomal translocation 46,XY,t(3;9;5)(q25;q34;q33) who had elevated blood interleukin-5 is reported. Complete cytogenetic remission was induced by interferon-alpha after treatment failure with corticosteroids and cytotoxic drugs. Severe cardiopulmonary symptoms due to hypereosinophilia and thromboembolic complication improved dramatically in the first 6 months of interferon therapy. Since it is known that the gene encoding for interleukin-5 resides on the long arm of chromosome 5, it may be possible that the chromosomal translocation in our patient resulted in overproduction of this cytokine, and our findings may be helpful for understanding the pathogenesis of this disorder.- - - - - - - - - - ranking = 1keywords = treatment failure (Clic here for more details about this article) |