Cerebellar abscess and syringomyelia due to isoniazid-resistant Mycobacterium tuberculosis.

A 19-year-old immunocompetent man was admitted to hospital with diplopia, nausea, vomiting and change in mental status. The patient had a history of tuberculous meningitis that was diagnosed at another hospital 6 months before the present admission, and at that time anti-tuberculosis treatment was initiated using a first-line drug combination. A computed tomography (CT) scan of the brain revealed non-communicating hydrocephalus. A ventriculo-peritoneal shunt was inserted surgically. Two months later, the patient was hospitalized again for fever, dysphagia and left hemiparesis. At that time, his cranial CT findings were within normal limits; however, magnetic resonance imaging (MRI) revealed an irregular multilocular peripheral contrast-enhancing lesion in the posterior fossa. The abscess was surgically drained. The presence of acid-fast bacilli in the abscess material was demonstrated by Ziehl-Neelsen staining. Mycobacterium tuberculosis grew on Lowenstein-Jensen culture medium, and the strain was found to be resistant to isoniazid. One month after the operation, the patient became quadriparetic. Cervical MRI revealed a cervico-thoracic syringomyelitic cavity, after which a syringoperitoneal shunt was placed. Treatment with four drugs was continued for 10 months, and then treatment with three drugs for a total period of 18 months. The patient recovered, with residual quadriparesis. Even though very rare, isoniazid-resistant M. tuberculosis may be the causative agent of progressive tuberculosis.     

Clinical and immunological studies in a case of selective complete C1q deficiency

A 10-year-old male with recurrent skin lesions and chronic infections was found to have a selective deficiency of C1q after functional analysis of all complement components. The addition of highly purified human C1q to the patient's serum restored C1 activity, indicating the presence of C1r and C1s and the absence of C1q. Titration of highly purified C1q with patient serum as a source of C1r and C1s resulted in a linear dose-response curve. The undetectable CH50 activity temporarily returned to normal within a few hours of plasma infusion, but the C1 titres were still only 1–3% of normal. Following plasma administration, the peak of C1q activity was reached after 30 min and returned to undetectable levels within 24 hr. The patient serum was not anti-complementary when incubated with normal serum. Nine members of the family, including the parents and two healthy siblings, were subjected to complement studies and HLA typing. The C1 titres and CH50 activity were found to be normal in all except the paternal grandmother who showed reduced levels of all the complement components. There was no linkage for the gene of C1q deficiency and HLA antigens. Among the various laboratory studies performed, anti-smooth muscle antibodies, immune complexes and anti-HBsAg antibody were found to be positive. The child died of a disease compatible with septicaemia. Post mortem tissue studies by light, fluorescent and electron microscopy have shown the presence of a mesangioproliferative glomerulonephritis.     

New onset egg allergy in an adult.

We report newly presenting systemic and local allergic reactions to egg in a 55-year-old woman. The patient did not have a history of egg allergy in childhood or occupational exposure to egg proteins; nor did she report any disease that is known to be related to food allergy. A skin prick test with commercial extracts, prick-to-prick test, CAP radioallergosorbent assay, and a double-blind, placebo-controlled food challenge test were used to prove egg allergy. Because egg allergy mainly affects children and symptoms frequently disappear with age, the late onset in this patient is rare.     

Aortic Intima-Media Thickness and Mean Platelet Volume in Children With Type 1 Diabetes Mellitus

Background:

Diabetes mellitus type 1 is the most common endocrine metabolic disorder occurring in childhood and adolescence due to the autoimmune destruction of pancreatic beta cells as a result of various environmental factors interacting with an underlying genetic predisposition. Diabetes is a risk factor for early onset atherosclerosis, and the high mortality rate seen in these patients is partially related to cardiovascular diseases.

Objectives:

This study was conducted to compare mean platelet volume as a marker of early atherosclerosis with aortic intima-media thickness in children with type 1 diabetes and to identify its correlation with known cardiovascular risk factors.

Patients and Methods:

The study included 27 patients between age range of 6 and 17 years that were diagnosed with type 1 diabetes and 30 healthy children of the same age range who did not have any chronic disease. In both groups, we used the color Doppler ultrasound to measure children’s aortic intima-media thickness and identify their mean platelet volumes.

Results:

There was no significant difference between the groups regarding gender distribution, age, High-Density Lipoprotein (HDL) and Low-Density Lipoprotein (LDL) cholesterol levels (P > 0.05). Also no significant difference could be documented between the patient and control groups regarding the aortic intima-media thickness and mean platelet volume (P > 0.05). However, there was a significant correlation between aortic intima-media thickness and mean platelet volume (r = 0.351; P < 0.05).

Conclusions:

In the present study, there was no evidence of early atherosclerosis in children with type 1 diabetes. However, mean platelet volume having a significant correlation with aortic intima-media thickness may be useful as an early marker of atherosclerosis.     

Mitral valve surgery in the presence of pulmonary hypertension.

Mitral valve surgery was performed in 59 patients with severe pulmonary hypertension (average systolic pulmonary artery pressure 77.1 +/- 18.6 mmHg; range 50-115 mmHg) between 1983 and 1990. Thirty-eight patients had been subjected to mitral valve replacement, 16 patients both mitral and aortic valve replacement, and 5 patients had open mitral commissurotomy, with an operative (30 day) mortality of 5.0%. These 3 deaths happened during the early postoperative period. Survivors were followed up for a period ranging from 6 months to 7 years with a mean of 36 months. Four late deaths (7.1%) occurred in patients with valve replacement. Actuarial survival was 93 +/- 3% at 5 years, and 90.7 +/- 4.4% at 7 years. Right ventricular catheterization was performed on 14 patients a mean of 38 months following operation. Systolic pulmonary artery pressure had decreased from a mean of 77.1 +/- 18.6 to 39.7 +/- 14.0 mmHg (p less than 0.001) and 90% of the survivors were in New York Heart Association Class 1 or II compared to 23.7% preoperatively. The clinical and hemodynamic findings in this series suggest that severe pulmonary hypertension is not a contraindication, and pulmonary hypertension decreases significantly after mitral valve surgery.     

Melatonin protects against gentamicin-induced nephrotoxicity in rats

Acute renal failure is a major complication of gentamicin (GEN), which is widely used in the treatment of gram-negative infections. A large body of in vitro and in vivo evidence indicates that reactive oxygen metabolites (or free radicals) are important mediators of gentamicin nephrotoxicity. In this study we investigated the role of free radicals in gentamicin-induced nephrotoxicity and whether melatonin, a potent antioxidant could prevent it. For this purpose female Sprague-Dawley rats were given intraperitoneally either gentamicin sulphate (40 mg/kg), melatonin (10 mg/kg), gentamicin plus melatonin or vehicle (control) twice daily for 14 days. The rats were decapitated on the 15th day and kidneys were removed. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood and malondialdehyde (MDA) and glutathione (GSH) levels, protein oxidation (PO) and myeloperoxidase (MPO) activity were determined in the renal tissue. Gentamicin was observed to cause a severe nephrotoxicity which was evidenced by an elevation of BUN and creatinine levels. The significant decrease in GSH and increases in MDA levels, PO and MPO activity indicated that GEN-induced tissue injury was mediated through oxidative reactions. On the other hand simultaneous melatonin administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GEN treatment.