Amlodipine-induced Gingival Hyperplasia - A Case Report and Review.

Anticonvulsants, antihypertensive calcium channel blockers and immunosuppressants are the three main classes of drugs known to cause drug-induced gingival hypertrophy or hyperplasia. Among the calcium channel blockers, nifedipine administration has most frequently been associated with medication-related gingival hyperplasia. The incidence with amlodipine, which has a mode of action pharmacodynamically comparable to nifedipine, has rarely been reported. Here, we present a rare case of amlodipine-induced gingival hyperplasia in a hypertensive patient.

Resuscitation after modified Fontan procedure.

As the survival rate after modified Fontan procedure is increasing, cardiopulmonary resuscitation may be needed in such patients for other causes not related to their cardiac status. The state-of-the-art cardiopulmonary resuscitation with external chest compression may not be sufficient to revive such patients, and the addition of external abdominal compressions may help in the final outcome, as is reported here.

Deformities of the uvula in the oral cavity- a case series.

BACKGROUND: Disorders of the palatal uvula is one of the least highlighted areas of medical literature, inspite the fact that uvula is a key organ in functions like speech, deglutition and mastication. The aim of this paper is to present a series of cases of wide range of uvular deformities ranging from bifid uvula to absence of uvula.

Screening of C-kit gene Mutation in Acute Myeloid Leukaemia in Northern India.

BACKGROUND: Acute Myeloid Leukaemia (AML) is a cancer of blood-forming cells in bone marrow. C-kit gene is a Receptor Tyrosine Kinase class III (RTK) that is expressed by early hematopoietic progenitor cells and plays an important role in hematopoietic stem cell proliferation, differentiation and survival. It is known that c-kit is a proto-oncogene and the activating c-kit mutations are likely to contribute in the development of leukaemia in humans. Exon 11 of c-Kit gene is the frequent site for mutations in different kinds of tumours. METHODS: In order to determine the frequency and prevalence of exon 11 mutations in 51 AML cases, we have done polymerase chain reaction-single-strand conformational polymorphism followed by direct DNA sequencing. RESULTS: The c-kit mutations in exon 11 were detected in 15.68% (8/51) in AML cases. We have detected totally ten missense mutations in eight AML cases those include Lys550Asn, Tyr568Ser, Ile571Leu, Tyr578Pro, Trp582Ser and Arg588Met and novel missense mutations at codons Ile563Lys and Val569Leu. Mutations at codons Ile571Leu and Trp582Ser was found in two independent cases. CONCLUSION: The presence of c-kit mutations in our study adds to investigative spectrum of AML cases. Since the c-kit mutations are seen in other malignancies, mutations in exon 11 of the c-kit gene might be involve in pathogenesis and represent useful predictive genetic marker in AML. Further studies in larger group of cases possibly will be required to determine the prognostic implications and to investigate how these mutations are co-related to the progression and pathogenesis of AML.