Abuse of neuroleptic drug by psychiatric patients

Due to the depaminergic neurotrasmission in the mesocortical and mesolimbic reward systems, the neuroleptic drugs have been considered free from the risk of abuse or dependence because of their antidopaminergic properties. Here, two cases of neuroleptic abuse have been described and a possibility of reward circuits other than mesocortical and mesolimbic systems operational behind this phenomenon has been postulated. There is a need to clinically recognise the abuse potential of neuroleptic drugs.     

Basaloid squamous carcinoma metastatic to renal-cell carcinoma: Fine-needle aspiration cytology of tumor-to-tumor metastasis

We describe an unusual case of a basaloid squamous-cell carcinoma (BSCC) of the tonsil in a 56-yr-old man that metastasized to a primary renal-cell carcinoma (RCC) and the lung. The diagnosis of the second primary, the RCC, was based on fine-needle aspiration (FNA) cytology. A subsequent nephrectomy specimen revealed BSCC metastatic to RCC, clear-cell type. Retrospective analysis of the FNA of the renal mass revealed classic RCC morphology and, in addition, another cytologically distinctive pattern characterized by occasional sheets of cohesive neoplastic cells with hyperchromatic nuclei and nuclear molding representative of BSCC. The cytologic features of a subsequent FNA of the lung were characteristic of metastatic BSCC. Our retrospective analysis of cytologic material from the renal mass underscores the importance of raising the possibility of tumor-to-tumor metastasis when distinctly different morphologic features are seen in an otherwise typical cytology of a neoplasm in patients with an already known or suspected second primary. To our knowledge, this case report is the first one documenting metastasis of BSCC to RCC. Diagn. Cytopathol. 1997;17:379–382. © 1997 Wiley-Liss, Inc.     

Diisocyanate asthma and gene-environment interactions with IL4RA, CD-14, and IL-13 genes.

BACKGROUND: Diisocyanate asthma (DA) affects 2% to 10% of exposed workers, yet the pathogenetic mechanisms underlying this disorder remain ill defined. OBJECTIVE: To determine if specific single nucleotide polymorphisms (SNPs) of interleukin 4 receptor alpha (IL4RA), IL-13, and CD14 promoter genes are associated with DA. METHODS: Sixty-two workers with DA confirmed by specific inhalation challenge (SIC) and 75 diisocyanate-exposed, SIC-negative workers were analyzed for SNPs associated with IL4RA, IL-13, and CD14 promoter genes. RESULTS: No associations were found with individual SNPs and DA. When stratified according to specific diisocyanate exposure, a significant association was found between IL4RA (I50V) II and DA among individuals exposed to hexamethylene diisocyanate (HDI) (odds ratio [OR], 3.29; 95% confidence interval [CI], 1.33-8.14; P = .01) only. Similarly, the IL4RA (I50V) II and IL-13 (R110Q) RR combination was significantly associated with DA in HDI-exposed workers (OR, 4.13; 95% CI, 1.35-12.68; P = .01), as was the IL4RA (I50V) II and CD14 (C159T) CT genotype combination (OR, 5.2; 95% CI, 1.82-14.88; P = .002) and the triple genotype combination IL4RA (I50V) II, IL-13 (R110Q) RR, and CD14 (C159T) CT (OR, 6.4; 95% CI, 1.57-26.12; P = .01). CONCLUSIONS: Gene-environmental interactions may contribute to the pathogenesis of DA, and gene-gene interactions may modulate this relationship.     

Myostatin blockade improves function but not histopathology in a murine model of limb-girdle muscular dystrophy 2C

Myostatin is a negative regulator of skeletal muscle growth. Myostatin mutations and pharmacological strategies increase muscle mass in vivo, suggesting that myostatin blockade may prove useful in diseases characterized by muscle wasting, such as the muscular dystrophies. We subjected the gamma-sarcoglycan-deficient (Sgcg(-/-)) mouse model of limb-girdle muscular dystrophy (LGMD) 2C to antibody-mediated myostatin blockade in vivo. Myostatin inhibition led to increased fiber size, muscle mass, and absolute force. However, no clear improvement in muscle histopathology was evident, demonstrating discordance between physiological and histological improvement. These results and previous studies on the dyw/dyw mouse model of congenital muscular dystrophy and in the late-stage delta-sarcoglycan-deficient (Sgcd(-/-)) mouse model of LGMD2F document disease-specific limitations to therapeutic strategies based on myostatin blockade in the more severe mouse models of different muscular dystrophies.     

CT patterns of nodal disease in pediatric chest tuberculosis

AIM:To highlight various patterns of nodal involvement and post treatment changes in pediatric chest tuberculosis based on contrast enhanced computed tomography(CECT) scans of chest.METHODS:This was a retrospective study consisting of 91 patients aged less than 17 years,who attended Paediatrics OPD of All India Institute of Medical Sciences with clinically diagnosed tuberculosis or with chest radiographs suggestive of chest tuberculosis.These patients had an initial chest radiograph as well as CECT of the chest and follow up imaging after 6 mo,and in some cases 9 mo,of completion of anti-tubercular treatment(ATT).CECT of these patients was reviewed for the location and extent of nodal involvement along with determination of site,size,enhancement pattern and calcification.RESULTS:Enlargement of mediastinal or hilar lymph nodes was found in 88/91 patients(96.7%),with the most common locations being paratracheal(84.1%),and subcarinal(76.1%).The most common pattern of enhancement was found to be inhomogenous.The nodes were conglomerate in 56.8% and discrete in 43.2%.In addition,perinodal fat was obscured in 84.1% of patients.In the post-treatment scan,there was 87.4% reduction in the size of the nodes.All nodes post-treatment were discrete and homogenous with perinodal fat present.Calcification was found both pre-and post-treatment,but there was an increase in incidence after treatment(41.7%).There was hence a reduction in size,change in enhancement pattern,and appearance of perinodal fat with treatment.CONCLUSION:Tubercular nodes have varied appearance and enhancement pattern.Conglomeration and obscuration of perinodal fat suggest activity.In residual nodes decision to continue ATT requires clinical correlation.     

Osteomyelitis of the lower extremity: pathophysiology,imaging, and classification,with an emphasis on diabetic foot infection

Osteomyelitis is inflammation of the bone caused by an infectious organism, and is a difficult clinical problem. The pathophysiology, imaging, and classification of osteomyelitis are challenging, varying with the age of the patient (child versus adult), the chronicity of the infection (acute versus chronic), and the route of spread (hematogenous versus contiguous focus), as well as the immune and vascular status of the patient and affected region. The two most common classification schemes are those of Lew and Waldvogel, and Cierny and Mader. Brodie’s abscess is seen in subacute osteomyelitis, while sequestrum, involucrum, and cloaca are inter-related entities of chronic osteomyelitis. Imaging workup of suspected osteomyelitis should begin with radiographs, although MRI is the most accurate imaging test. Three patterns of T1 signal change have been described in the setting of suspected osteomyelitis including confluent intramedullary, hazy reticular, and subcortical. The confluent intramedullary pattern is most associated with osteomyelitis, while hazy reticular is rarely associated with hematogenous osteomyelitis, and subcortical is not associated with osteomyelitis. It can be challenging to differentiate neuropathic arthropathy from osteomyelitis. Osteomyelitis tends to involve a single bone subjacent to an ulcer or sinus tract. In contrast, neuropathic arthropathy tends to involve multiple bones of the midfoot. Subchondral cystic change, thin rim enhancement of a joint effusion, and the presence of intra-articular bodies are more indicative of a neuropathic joint without infection. Biopsy can play an important role in diagnosis and treatment of osteomyelitis.