Ustekinumab therapy for Crohn's disease during pregnancy: a case report and review of the literature.

WHAT IS KNOWN AND OBJECTIVES: The safety of continued ustekinumab (UST) therapy during pregnancy remains unclear in patients with Crohn's disease (CD). There are no meta-analysis reports of exposure to UST during pregnancy. The objective was to describe a case of a pregnant patient with CD who was successfully treated with UST maintenance therapy throughout the pregnancy and delivered a baby boy without any congenital malformations, neurological abnormalities or birth defects. CASE SUMMARY: A 37-year-old patient with CD treated with UST became pregnant. She had been receiving UST for 8 months at the time. After discussion with the patient and the obstetric team, the UST therapy was continued. The result of treatment was an uneventful pregnancy with delivery, at term, of a healthy boy and the maintenance of clinical, biological and endoscopic remission of CD during and after pregnancy. WHAT IS NEW AND CONCLUSION: To our knowledge, this is the first reported use of continued UST therapy for CD throughout a pregnancy. The result of treatment was an uncomplicated pregnancy with the mother giving birth to a healthy boy at term and the maintenance of clinical biological and endoscopic remission of CD during and after pregnancy.

Foot ischaemia and toe skin necrosis associated with interleukin-2 infusion in an HIV-infected patient.

A 39-year-old white man developed a severe left toe foot ischaemia and toe skin necrosis following his 12 courses of interleukin (IL)-2 (4.5 MIU twice a day, subcutaneously) for five days every two months. He had no known general risk factors for thrombosis other than HIV infection. An arterial Doppler ultrasound examination of the leg confirmed the permeability of the posterior tibial artery and its digital pulse. A diagnosis of foot ischaemia and toe skin necrosis was made. The suspected causative agent was IL-2 since this was the only drug that the patient was taking before the symptoms appeared. The patient was empirically treated with an aspirin and pentoxifylline in order to improve local microcirculation. We observed a satisfactory response with a quick resolve of skin lesions. The most possible cause of foot ischaemia and toe skin necrosis was considered to be IL-2 because of the temporal relationship between the exposure to the drug and onset of symptoms. Based on the Naranjo probability scale, IL-2 could be considered the probable cause of the foot ischaemia and toe skin necrosis. If clinical evaluation leads to the suspicion of ischaemic process, therapy with IL-2 should be discontinued immediately.

Adverse cutaneous reactions associated with the newest antiretroviral drugs in patients with human immunodeficiency virus infection.

HIV-infected patients have a higher risk of developing cutaneous reactions than the general population, which has a significant impact on patients' current and future care options. The severity of cutaneous adverse reactions varies greatly, and some may be difficult to manage. HIV-infected patients just at the beginning of antiretroviral treatment can frequently show a wide variety of adverse drug effects such as drug rashes, hyperpigmentation, hair loss, hypersensitivity reactions, injection site reaction, urticarial reaction, erythema multiforme, toxic epidermal necrolysis or Stevens-Johnson syndrome. The early detection and treatment of cutaneous adverse drug reactions, plus identification of the causative agent, are essential to prevent the progression of the reaction, preventing additional exposures and ensuring the appropriate use of medications for the current condition and keeping in mind others, such as patient age. This article emphasizes the most common features of an antiretroviral drug-induced cutaneous reaction from protease inhibitors, non-nucleoside analogue reverse transcriptase inhibitors, fusion inhibitors, nucleoside reverse transcriptase inhibitors, integrase inhibitors and inhibitors of the CCR5 chemokine receptor, paying special attention to the newest drugs approved for the treatment of HIV infection, such as tipranavir, darunavir, etravirine, enfuvirtide, raltegravir and maraviroc.

Septic shock and community-acquired pneumonia associated with etanercept therapy.

OBJECTIVE: To report a case of septic shock and community-acquired pneumonia in a patient with psoriatic arthritis receiving treatment with etanercept. PATIENT DETAILS: A 65-year-old woman diagnosed as having psoriatic arthritis had received treatment with etanercept. Chest X-ray studies were normal and the tuberculin skin test was negative. Two months after etanercept therapy, the patient presented to our emergency department with fever, cough, chest pain and generalized weakness. Chest radiography revealed a right pulmonary infiltrate. Her condition rapidly deteriorated and she went into shock with a further drop in her blood pressure, tachycardia and tachypnea. She was intubated, mechanically ventilated and was treated with fluids, cardioversion and amiodarone. Empiric therapy with levofloxacin, amikacin and cefepime were initiated. In the urinalysis, the result of a rapid test for Streptococcus pneumoniae was positive. Etanercept treatment was suspended due to a possible adverse reaction associated with this drug. At the start of therapy her clinical condition improved slowly. On Day 28, the patient was afebrile and she was discharged from the intensive care unit. DISCUSSION: Most of the infections associated with etanercept therapy have been reported in patients with rheumatoid arthritis. Based on our observations, etanercept was the possible offender in the development of septic shock and respiratory failure in community-acquired pneumonia. There was a temporal relationship between exposure to the drug and onset of symptoms. Etanercept was the only drug administered before the septic shock developed. Based on the Naranjo algorithm, the adverse reaction could be considered possible. CONCLUSION: Patients initiated on etanercept should be counseled and receive appropriate screening before drug initiation. All febrile and newly occurring concomitant illnesses should be promptly evaluated. General practitioners should discontinue etanercept treatment and institute prompt and aggressive intervention if infection develops.

Exacerbation of psoriatic skin lesions in a patient with psoriatic arthritis receiving adalimumab.

OBJECTIVE: To report a case of a patient with psoriatic arthritis (PsA) receiving adalimumab, who developed an exacerbation of palmoplantaris pustulosa psoriasis. CASE SUMMARY: A 38-year-old woman diagnosed with PsA had received treatment with non-steroidal antiinflammatory drugs. Two months prior to admission, the patient had a Disease Activity Score of 3.8; diclofenac therapy was suspended and physicians considered treatment with adalimumab. Chest X-rays were normal and the tuberculin skin test was negative. Treatment with adalimumab was started. After the third dose of adalimumab, the patient developed an exacerbation of psoriatic skin lesions on palms and soles. The clinical course was consistent with an exacerbation of palmoplantaris pustulosa psoriasis. Adalimumab treatment was suspended. The patient was treated with oral methotrexate 2.5 mg once weekly. One month after methrotexate was started, the patient developed a severe alopecia. Methrotexate therapy was suspended. Three months later, the patient continued with psoriatic skin lesions on palms and soles. Treatment with Psoralen and ultraviolet A therapy was initiated and the patient condition improved without occurrence of psoriatic skin lesions in the next 4 months. DISCUSSION: Cases of worsening or exacerbation of psoriatic skin lesions induced by anti-tumour necrosis factor (TNF) agents in patients diagnosed PsA are infrequently described in the literature. The most likely cause of the exacerbation of palmoplantaris pustulosa psoriasis in this case was considered to be adalimumab because of the close temporal relationship between exposure to the drug and onset of symptoms. Adalimumab was the only identifiable precipitant that the patient encountered before the exacerbation of psoriasis developed. In accordance with the data obtained and based on the Naranjo algorithm, the adverse reaction could be considered probable. CONCLUSIONS: Patients initiated on adalimumab therapy should be closely monitored for the development of exacerbation of psoriasis. Clinicians should be aware of this rare adverse effect of this anti-TNF drug.

Successful desensitization protocol for hypersensitivity reactions caused by oxaliplatin.

OBJECTIVE: To report the successful desensitization of a patient with a hypersensitivity reaction to oxaliplatin. CASE SUMMARY: A 57-year-old woman with metastatic colon cancer was receiving oxaliplatin, fluorouracil and leucovorin every 2 weeks and showed a partial response to therapy. During the fourth cycle, an anaphylactic reaction with palpitations and rash occurred. The patient was hypotensive with mild pulmonary wheezing. Since oxaliplatin was the probable cause of the hypersensitivity reaction, therapy with this drug was discontinued. Therapy in the patient was continued using cetuximab and irinotecan but this resulted in progression of the cancer. In view of the initial satisfactory response to the oxaliplatin-based regimen, it was decided to attempt desensitization to oxaliplatin using a protocol adapted from carboplatin regimens. The desensitization procedure was successful and the patient subsequently tolerated an additional three cycles using this regimen without further symptoms of hypersensitivity. DISCUSSION: In cases with moderate-to-severe reactions to oxaliplatin, reexposure is not usually considered. However, a need to use first-line therapy when there is recurrence of the cancer has encouraged the development of rapid desensitization procedures which allow patients to be treated with medications to which they have previously shown hypersensitivity reactions. A combination of premedication using intravenous dexamethasone and a desensitization regimen was designed which was used successfully to increase concentrations and flow rates of oxaliplatin. CONCLUSIONS: Hypersensitivity reactions to oxaliplatin are not rare and physicians need to be aware of these. When substitution of another antineoplastic drug is not feasible, oxaliplatin desensitization should be considered even when hypersensitivity reactions to oxaliplatin are severe.

Possible macular exanthema associated with linezolid therapy.

OBJECTIVE: To report a case of macular exanthema associated with linezolid therapy. CASE SUMMARY: A 54-year-old white man diagnosed as having laryngeal epidermoid carcinoma attended our emergency department because of fatigue, fever, neck pain and a fistulized fixed mass in the right side of the neck with purulent exudation. Treatment with amoxicillin/clavulanic acid 875 mg/125 mg p.o. every 8 hours as empirical therapy was started. Cultures of the exudates from the fistula confirmed the presence of methicillin-resistant Staphylococcus aureus (MRSA). Amoxicillin/clavulanic acid was discontinued and therapy was started with linezolid 600 mg p.o. every 12 hours but 5 days after commencing linezolid the patient came to our emergency room because of generalized erythematous macular eruptions. A diagnosis of severe and generalized macular exanthema induced by linezolid was made. Administration of linezolid was suspended and there was an improvement in the skin lesions and general state of health. The patient was discharged without further symptoms. DISCUSSION: In this case, there was a close temporal correlation between drug exposure and the onset of symptoms. When linezolid was discontinued, the skin lesions resolved quickly and the general condition of the patient improved. Furthermore, linezolid was the only drug added before the cutaneous lesions appeared. It is possible that the adverse reaction was associated with administration of amoxicillin/clavulanic acid. However, the patient had been treated with this antibiotic previously without appearance of any cutaneous reaction. An objective causality assessment revealed that an adverse effect was possible. CONCLUSION: Based on our observations, we conclude that linezolid was the most likely cause of the adverse reaction. Clinicians should be aware of this infrequent but severe reaction.

[Assessment of quality as perceived by users of an outpatient pharmaceutical care unit]. / Evaluación de la calidad percibida por los usuarios de una unidad de atención farmacéutica a pacientes externos.

OBJECTIVE: To assess quality of care by an Outpatient Pharmaceutical Care Unit (OPCU) from patient satisfaction regarding the unit s premises and activities. METHOD: A transversal study performed at the OPCU using a patient survey. Patient opinions were obtained regarding structural aspects, pharmaceutical care, patient information, overall satisfaction, and preference for care in the OPCU or pharmacy office. The response variable was the presumed choice for the OPCU or traditional pharmacy office. A multivariate analysis using logistic regression was used to evaluate the independent effect of variables. RESULTS: In all, 256 surveys were administered, of which 195 were assessable. Response rate was 76%. Responses with highest scores included communication and interaction with professionals (4.8 points on average) and care received (4.5 points). Worst assessments included OPCU s timetable (3.8 points) and location (3.9 points); 98.4% of patients were satisfied or very satisfied with care received, and only 18.4% would switch to the pharmacy office if allowed to. The multivariate analysis suggested that variables associated with the pharmacy office choice included a negative rating of OPCU s location (OR 9.8, CI 1.3-76.8) and a negative rating of information delivered (OR 4.1, CI 1.7-9.8); p < 0.05. CONCLUSIONS: Information received and OPCU s location had the greatest impact on patient satisfaction. Patient remarks and suggestions were very useful to identify areas of improvement, and to introduce modification suiting their views.

Acute renal failure associated with an accidental overdose of colchicine.

CASE SUMMARY: A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. Leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis A, B, C and HIV viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l. DISCUSSION: The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.

Unsuspected rhabdomyolysis associated with phenytoin.

CASE SUMMARY: A case of rhabdomyolysis, in which the etiology could be associated with phenytoin administration is presented and guidelines are described which may assist the early recognition, treatment and prevention of renal failure when such patients are treated in intensive care units. A 46-year-old white man experienced a generalized tonic-clonic seizure at home lasting approximately two minutes. The patient presented with similar crises when seen by the emergency services and had a neurological status of seven points on the Glasgow scale. He was intubated orotracheally and mechanically ventilated. Administration of a 1,250 mg loading dose of phenytoin in 250 ml 0.9% sodium chloride injection were administered intravenously according to guidelines approved by the hospital. These require administration of the loading dose over 30 - 60 minutes followed by phenytoin 150 mg/8 h i.v. administered as a drip diluted in 0.9% NaCl 50 ml over 30 - 60 minutes. Obtained plasma levels were within the therapeutic range but on Day 3 the level of creatine kinase (CK) increased. We initiated treatment to prevent renal failure but the level doubled daily reaching a peak of 54,000 U/I on the fifth day. It was suspected that the increase in CK was due to the treatment with phenytoin which was stopped and replaced by valproic acid 500 mg/8 h orally. The cumulative total dose of phenytoin was 3,050 mg. The subsequent serial determinations of CK showed a decrease beginning on the day phenytoin was stopped and levels falling to 14,229 U/l on the day the patient left the ICU. The patient had no recurrence of the convulsive episodes after the day of admission. In the neurology ward, the patient recovered satisfactorily and the CK value gradually returned to normal. The patient was asymptomatic when released on the ninth day. DISCUSSION: The most likely cause of the rhabdomyolysis was phenytoin treatment because of the close temporal relationship between exposure to the drug and onset of symptoms and the rapid resolution of the symptoms and signs after phenytoin was discontinued. An objective causality assessment concluded that a possible adverse drug reaction had occurred.

[Acute intoxication with sustained-release lithium carbonate tablets. A propos of a case]. / Intoxicación aguda por comprimidos de liberación sostenida de carbonato de litio. A propósito de un caso clínico.

OBJECTIVE: To describe the case of a patient who ingested 50 sustained release lithium carbonate 400 mg tablets, and reached a late peak concentration above 3 mEq/L. CASE REPORT: A 32-year-old male with bipolar mood disorder ingested 50 sustained-release lithium carbonate tablets. Upon admission to the emergency room, a gastric wash was performed,from which several tablet remnants were obtained, as well as an intestinal lavage using activated carbon. PHYSICAL EXAMINATION: good general status, no fever, blood pressure 160/90 mm Hg, no edemas. Neurologic, pulmonary, and cardiac examinations were normal. CBC and the chemistry panel were normal. The patient's psychopathological examination suggested a stable status with no apparent manifestations arising from a decompensated mood disorder. Five hours after his massive lithium ingestion the drug's plasma levels were 0.75 mEq/L. At 22 hours post-ingestion a chemistry panel was obtained, which showed serum creatinin at 1.38 mg/dL and a lithium plasma concentration of 3.15 mEq/L. A hemodyalisis trial was attempted for 4 hours. At 73 hours post-ingestion, lithium plasma levels were 0.6 mEq/L, that is, within therapeutic range. The patient was hemodynamically stable and serial blood tests were normal; he was discharged. COMMENT: Acute lithium intoxication with plasma levels above 3 mEq/l can be fatal or result in irreversible neurologicsequelae in almost one third of cases, with persistent cerebellar dysfunction in association with dementia of variable degree, andrenal, blood, and liver disturbances. Sustained-release tablets may prolong absorption and delay peak plasma concentrations. In such cases, therefore, it is recommended that drug plasma concentrations be monitored during 48-72 hours post-ingestion.

[Pharmaceutical care of patients with rheumatoid and psoriatic arthritis receiving etanercept]. / Atención farmacéutica a pacientes con artritis reumatoide y psoriásica en tratamiento con etanercept.

OBJECTIVE: To evaluate a pharmaceutical care protocol for patients with rheumatoid arthritis (RA) or psoriatic arthritis who begin treatment with etanercept with the objective of identifying potential medication-related problems and implementing therapeutic measures to improve the way this drug is used. METHOD: An observational, prospective, 3-month study of patients with RA receiving etanercept therapy from March to December 2003 was conducted and a pharmaceutical care protocol was set up. During the first visit, a pharmacotherapeutic record was initiated for each patient, including socio-demographic data, personal history, diagnosis, DMARDs (disease-modifying anti-rheumatic drugs) previously received, and concomitant therapies for other underlying conditions. Patients were briefed on dosage, administration route, and potential adverse events both orally and in writing. Correct drug administration and preservation were verified during the second visit, where potential adverse effects were identified, treatment adherence was confirmed, and, if needed, potential drug interactions with other ongoing medications were disclosed. During the third visit, adherence was assessed, adverse events were recorded, and patients evaluated their response to treatment. RESULTS: Fifty patients were included, 40 with a diagnosis of rheumatoid arthritis (80%) and 10 diagnosed with psoriatic arthritis (20%). In all, 72% had received previous treatment with methotrexate (MTX), 40% with leflunomide, 20% with infliximab, 56% with corticoids, 2% with analgesics, 56% with NSAIDs, and 30% with other DMARDs. CONCLUSIONS: No significant drug interactions were found. Regarding adherence to treatment, 7.7% of patients skipped one or more doses, with travelling being the most common reason. Adverse events reported included: injection site reaction (27%), headache (7.7%) and nausea (7.7%). At 3 months after treatment onset, a reduction of MTX doses was seen in 18% of patients, of leflunomide dosage in 8%, of corticoids in 18%, of analgesic usage in 6%, and of NSAIDs in 8% of patients. In agreement with these results, 92% of patients reported having experienced improvment.

[Drug therapy for corneo-conjunctival neoplasm]. / Tratamiento farmacológico de la neoplasia corneal y conjuntival.

BACKGROUND: The goal of therapy for corneo-conjunctival neoplasm is lesion removal, with the most widespread procedure being complete tumor resection with or without associated chemotherapy lines. As this sort of procedure entails a high relapse rate (9-52%) the use of adjuvant therapies to reduce the occurence of relapse becomes a need. The administration of a number of topically administered drugs has been used for adjuvant therapy, including mitomycin C, 5-fluorouracil and interferon a 2b. OBJECTIVE: To determine the clinical experience published regarding the effectiveness of the various drug therapies for cor-neo-conjunctival neoplasm. SEARCH STRATEGY: Information reported on this topic in the Medline database (1966-2004) was searched using corneo-conjunctival neoplasm, 5-fluorouracil, mitomycin C, and interferon ca2b as key words. SELECTION CRITERIA: All papers quoting dosage for drugs used,treatment length, adverse effect development, and clinical response obtained were included. PRIMARY RESULTS: Papers reporting the use of 5-fluorouracil re few when compared to those quoting other drugs, with a response rate of 88% and a relapse rate of 20%. The use of mitomycin C is widely described in the medical literature with a response rate of 90% and a relapse rate of 13%, but in association with the development of adverse effects in a high percentage of patients. Interferon ca 2b is the last drug to be incorporated in the treatment of these ocular lesions, with a response rate of 100% and a low incidence of adverse effects, with a relapse rate of 4%. CONCLUSIONS: Mitomycin C is an effective drug, but its use is associated with a high number of adverse events, some of which may lead to therapy discontinuation. Interferon ct 2b has efficacy outcomes comparable to mitomycin C and a lower incidence of adverse effects, which are mostly mild in nature. The use of 5-fluorouracil is relegated to a second-tier status.

Erythrodermia induced by omeprazole.

OBJECTIVE: To report a case of erythrodermia that appears to be related to the intake of omeprazole (OMP) for treatment of gastroesophageal reflux disease. CASE SUMMARY: We describe a case of erythrodermia associated with OMP therapy in a 58-year-old white woman with no predisposing factors. In 1995, at the Rheumatology Outpatients' Clinic, she was diagnosed as having scleroderma (CREST subgroup) and Sjögren's syndrome associated with corticoid osteoporosis and multiple crushed vertebrae, Raynaud's disease and joint pain. In March 1998, treatment with OMP 20 mg/d p.o. was started for treatment of gastroesophageal reflux disease. She came to our hospital emergency room in October 1999 because of a severe cutaneous reaction and poor general health. The dermatology service diagnosed the erythrodermia as a skin reaction to medication. We suspected that the causative agent was OMP. Examination of a skin biopsy specimen demonstrated that it was compatible with a toxicodermic reaction to medication. Administration of OMP was suspended and the skin lesions and the patient's general state of health improved. She was discharged without symptoms. CONCLUSIONS: Our case reports, and others from the literature, suggest the importance of recognizing of the possibility of cutaneous adverse drug reactions even with medications, such as OMP, which has a good safety profile. Caution is recommended with the use of OMP, especially in elderly patients, in patients with renal insufficiency or decompensating liver disease and in patients who receive drugs that affect OMP metabolism.

Kinetic alteration of theophylline at therapeutic doses.

OBJECTIVE: To report a case of a patient diagnosed as having bronchial asthma treated with intravenous infusion of theophylline, who presented an episode of altered theophylline metabolism with a disproportionately increase in serum concentrations together with tachycardia and symptoms of intoxication. CASE SUMMARY: A 51-year-old white woman with a history of bronchial asthma was treated with intravenous infusion of theophylline in an Intensive Care Unit. Bayesian pharmacokinetic approach for dose individualization was done and linear kinetics of theophylline were observed. At therapeutic dose, an alteration of theophylline metabolism had happened, that induced a decrease on the theophylline clearance coinciding with an increase of dose. The serum concentration at this dose was 23.9 microg/ml and this was associated with symptoms compatible with intoxication by theophylline. All factors that could change theophylline elimination were analyzed. A possible drug interaction, hypothyroidism and cardiac failure were ruled out. Clinical hepatic insufficiency was not determined, but an increase of hepatic enzymes was observed. Theophylline infusion was suspended during 5 hours, the serum levels returned to therapeutic values and hepatic enzymes returned to their initial values. DISCUSSION: Episodes of anormal theophylline kinetics may occur, even with doses and serum concentrations considered to be therapeutic, especially in critically ill patients or those whose physical condition has deteriorated. This makes it necessary to carry out therapeutic drug monitoring of theophylline in this group of the population.

Henoch-Schönlein purpura associated with clarithromycin. Case report and review of literature.

OBJECTIVE: To report a case of Henoch-Schönlein purpura that appears to be related to the intake of clarithromycin for pharyngitis/tonsillitis. CASE SUMMARY: We describe a case of Henoch-Schönlein associated with clarithromycin therapy in a 48-year-old white man with no history of allergic drug reactions. Four days after starting therapy, he came to our hospital emergency room because of a non-pruritic palpable purpuric rash on the trunk and extremities and arthralgias involving elbows and knees. Administration of clarithromycin was suspended, in a few days, arthralgias and skin lesions quickly resolved. Three weeks later, the patient presented again with abdominal pain, dark-red urine and swelling of the legs. Urinalysis revealed proteinuria of 11 g/24 h and hematuria. A percutaneous renal biopsy showed a diffuse endocapillary proliferative glomerulonephritis with segmental areas of fibrinoid necrosis within glomeruli, on immunofluorescence study granular deposits of IgA and C3 were present in the mesangium and capillary walls. A diagnosis of HSP was made. We suspected that the causative agent might be clarithromycin since this was the only drug added before the cutaneous and renal condition appeared. CONCLUSIONS: Our case and the previous case suggest that HSP may represent a potential adverse effect of clarithromycin, clinicians should be alerted to this potentially severe side effect of such a widely used drug. In accordance with the data obtained and based on the Naranjo algorithm, the adverse reaction could be considered possible.

[Riluzole as a treatment for amyotrophic lateral sclerosis]. / Riluzol como tratamiento de la esclerosis lateral amiotrófica.

INTRODUCTION: The Amyotrophic Lateral Sclerosis (ALS) is a disease characterized by the selective degeneracy of the superior motoneurons of the cortex motor and of the inferior motoneurons at level of the encephalic trunk and spinal marrow. Exist sporadic and familiar forms, being estimated an incidence of 1-2 cases by 100,000 inhabitants. The cause of the neuronal degeneracy is yet unknown, being implied, between other mechanisms, the glutamic exotoxicity is the responsible for the death neuronal. The riluzol is a benzothiazole derivative whose neuroprotector mechanism still it has not been totally clarified, though seems that reduces the neuroexcitatory action of the glutamic acid blocking his transmission. DEVELOPMENT: Two clinical trials have been accomplished with similar characteristics: multicentre, randomized, double blind, and placebo-controlled. Between both studies have been included more than 1,100 patient, obtained significant statistic results in the prolongation of the survival time, however this effect was not going accompanied of an improvement in the muscular force neither of the pulmonary capacity, what is translated in which the riluzol does not modify the quality of life of the patient. The drug presents good tolerance and mild adverse effects and as consequence of this in 1996, the FDA approved his marketing and utilization in the treatment of the ALS. The approval of the riluzol as first agent for the treatment of the ALS has raised an important number of problems about the efficiency and cost of the treatment. CONCLUSION: Though its benefits are modest, it is considered a starting point in the pharmacotherapy of the ALS.

[Treatment of persistent epithelial defects using autologous serum application]. / Tratamiento de defectos epiteliales persistentes mediante suero autólogo.

PURPOSE: To study the impact of topical treatment with autologous serum on the clinical evolution of persistent corneal epithelial defects (PED) and to observe its effect on squamous metaplasia in 7 cases of dry eye. PATIENTS AND METHODS: In this prospective, clinical, non-comparative case series study we evaluated a total of 17 eyes (14 patients). We analized the clinical evolution (fluorescein staining, Schirmer's I and II tests and photographic control) of PED in these patients, to whom 20% autologous serum eyedrops were applied for 28 days. Using impression cytology technique (Tseng's method) we evaluated the involution of squamous metaplasia in 7 eyes of 4 patients with ocular cicatricial pemphigoid and dry eye who were treated with autologous serum. The Wilconxon test was used for the statistical treatment of the data. RESULTS: The epithelial defect healed within 2 weeks in 6 eyes (35.2%). Eight eyes (47%) healed within 2-4 weeks and 3 eyes (17.6%) did not heal after week 4. The duration of PED, before serum therapy was 36 days. Six of seven eyes treated with autologous serum presented an involution of squamous metaplasia 28 days after initiation of the serum drops. CONCLUSIONS: Autologous serum treatment accelerates PED healing. Autologous serum application causes an involution of squamous metaplasia.

[Headache associated with cyclosporin ina patient with membranous glomerulonephritis]. / Cefalea asociada a ciclosporina en una paciente con glomerulonefritis membranosa.

OBJECTIVE: To report the case of a patient diagnosed with membranous glomerulonephritis and autoimmune non-central neutropenia under treatment with cyclosporin who developed severe, disabling headache. CASE REPORT: A 66-year-old female patient with no history of headache or adverse drug reactions was diagnosed with membranous glomerulonephritis and autoimmune non-central neutropenia. Neoral (cyclosporin A) was initiated at a dose of 2.5 mg/kg/24 h (100 mg/12 h), with whole blood cyclosporin levels within the therapeutic range. After 5 days the patient reported holocranial severe, disabling headache. A cranial CT scan was normal and other headache causes were also ruled out; her headache subsided only upon cyclosporin discontinuation. COMMENT: Severe headache is an uncommon adverse effect of cyclosporin whose recognition is relevant, since it may compromise therapy compliance and require the drug to be discontinued. The attribution of cyclosporin with this neurotoxic effect was analyzed using Naranjo's probability estimation method for adverse drug reactions, which resulted in causality being considered probable.