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C Choonhakarn

Publications and source records attributed to C Choonhakarn.

12 recordsLinked to original sources

Major histocompatibility complex class I chain-related gene A in Thai psoriasis patients: MICA association as a part of human leukocyte antigen-B-Cw haplotypes.

Psoriasis is a chronic inflammatory skin disorder. Although the aetiology and pathogenesis of psoriasis are unproven, it is hypothesised that the major histocompatibility complex (MHC) gene/haplotype contributes to the susceptibility of psoriasis in many populations. MHC class I chain-related gene A (MICA), located 46-kb centromeric of HLA-B, is expressed on keratinocytes and fibroblasts. MICA is in linkage disequilibrium with HLA-B and is involved in natural killer-cell functions. To investigate the relative contribution of the MICA gene in the pathogenesis of psoriasis, extracellular polymorphisms of MICA were studied by polymerase chain reaction-sequence specific primers in 128 Thai psoriasis patients (87 and 41 were Types I and II, respectively) from Srinagarind Hospital, Faculty of Medicine, Khon Kaen University. The control group included 255 healthy, unrelated Northeast Thais. We observed 11 MICA alleles (or groups of alleles) in the patients. A comparison of the psoriasis patients and the control group revealed that MICA*010 and MICA*017 were associated with Type I psoriasis whereas only MICA*010 was associated with Type II. The haplotype analysis revealed that MICA*008-HLA-B*13-Cw*0602 and MICA*010-HLA-B*4601-Cw*01 were significantly increased in both Types I and II, whereas MICA*002-HLA-B*38-Cw*07 (01-03) and MICA*017-HLA-B*57-Cw*0602 were elevated only in Type I. MICA*010 was in strong linkage with Cw*01. Analysis of independent association of MICA*010 in individuals lacking Cw*01 failed to maintain an association. Our results suggest that a significant increase of the MICA alleles in the patient group is a part of HLA-B-Cw haplotypes. It is conceivable that an unknown susceptibility gene, on certain HLA-B-Cw haplotypes, is responsible for the development of psoriasis.

Alleles↗

Concurrent subcutaneous and visceral basidiobolomycosis in a renal transplant patient.

Basidiobolomycosis is a chronic inflammatory disease that occurs exclusively in healthy individuals. Clinically, the infection is generally restricted to subcutaneous tissue; however, the disease has been documented to emerge in visceral organs but seldom spreads to cause disseminated infection. We describe the first culture-confirmed case of systemic Basidiobolus ranarum infection in an immunosuppressed patient. A 55-year-old female renal transplant recipient developed chronic hard nonpitting oedema of the right lower extremity and abdominal wall concurrent with the infection from the same organism involving the uterus, urinary bladder and intra-abdominal lymph nodes. The patient responded successfully, both clinically and radiographically, to medical therapy without surgical resection. The treatment regimen consisted of potassium iodide and trimethoprim/sulfamethoxazole for 3 months, and the patient remains clear of symptoms after 10 months' follow-up.

Edema↗

Corneodesmosin gene: no evidence for PSORS 1 gene in North-eastern Thai psoriasis patients.

Psoriasis vulgaris, a common inflammatory skin disorder, is known to be associated with the HLA-Cw*06 allele. It has been recently suggested by microsatellite mapping that a real susceptible gene for psoriasis resides in the approximately 100-kb genomic region telomeric of the HLA-C gene. In this respect, the corneodesmosin (CDSN) gene 160-kb telomeric of HLA-C is a strong candidate because of its location and its functional role in corneocyte cohesion and desquamation. In fact, a significant association between CDSN polymorphism and psoriasis was recently recognized in Caucasian populations. However, this association has not been replicated in other studies, being still controversial. In this study, we investigated the genetic polymorphism of the CDSN gene in 139 psoriasis patients and 144 healthy controls in the North-eastern Thai population. By direct sequencing technique, a total of 28 polymorphic sites were found, consisting of 26 single nucleotide polymorphisms (SNPs) and two indels (insertion/deletion). Among them, six SNPs have not been previously reported. Through this analysis, as many as 28 different SNP/indel haplotypes within the CDSN gene were identified. Seven SNPs and one indel, namely 9C, 614 A, 722T, 971T, 1215G, 1243C, 1331G and 1606AAG (deletion), revealed significant deviation in the allelic frequencies of the patients from those of the healthy controls. However, none of them are likely to be responsible for controlling the susceptibility of psoriasis, but these associations can be explained by a linkage disequilibrium to a real pathogenic allele of a nearby gene. Further, the large variations between the CDSN SNP/indel haplotypes and the psoriatic major histocompatibility complex (MHC) haplotypes also make it unlikely that CDSN is a major psoriasis-susceptible gene.

Gene Frequency↗

Papular elastorrhexis: a distinct variant of connective tissue nevi or an incomplete form of Buschke-Ollendorff syndrome?

Papular elastorrhexis is a rare entity, possibly a form of multiple elastic tissue naevi. The cutaneous lesions in this disorder are characterized by multiple white papules usually occurring on the trunk. These tend to be nonfollicular and scattered evenly over the affected area. Histopathologically, there is a decrease of elastic fibres, that may also appear thin and fragmented. Most reported cases are sporadic but familial occurrence has been described and some authors believe that papular elastorrhexis may represent a mild form of Buschke-Ollendorff syndrome. We report an 18-year-old woman whose clinical and histopathological features were compatible with papular elastorrhexis. There was no evidence of skeletal changes or relevant family history.

Adolescent↗

Disseminated infection due to rapidly growing mycobacteria in immunocompetent hosts presenting with chronic lymphadenopathy: a previously unrecognized clinical entity.

Disseminated infection due to rapidly growing mycobacteria is uncommon and occurs mostly in immunocompromised patients. We report 16 cases of such infection with an unusual presentation seen at Srinagarind Hospital, a university hospital in northeastern Thailand. The clinical features were different from those in previous reports. All of the patients presented with chronic bilateral cervical lymphadenopathy. Twelve had mycobacterial involvement of other organs (sinuses, 6 patients; lungs, 4; liver, 4; spleen, 3; skin, 3; bone and joint, 2; and tonsils, 2). An interesting occurrence in 11 patients was 14 episodes of reactive skin manifestations (Sweet's syndrome, 9; generalized pustulosis and erythema nodosum, 2 each; and pustular psoriasis, 1). No identifiable predisposing factors, including human immunodeficiency disease, were found in these patients. However, 8 patients had 11 episodes of prior infection or coinfection with other opportunistic pathogens (salmonellosis, 4; penicilliosis, 3; pulmonary tuberculosis, 2; and melioidosis and cryptococcosis, 1 each). These findings suggest that cell-mediated immunity is defective in these patients.

Adult↗

Sweet's syndrome associated with non-tuberculous mycobacterial infection: a report of five cases.

We report the rare association of Sweet's syndrome with non-tuberculous mycobacteria in five patients (three women, two men, aged 25-41 years). Clinical and histological evidence supported the diagnosis of Sweet's syndrome in all patients. The skin lesions responded well to systemic corticosteroid but recurred in two cases. All of our patients had chronic disseminated non-tuberculous mycobacterial infection. They initially presented with lymphadenopathy and developed involvement in other organs later. All of them were treated as having tuberculous lymphadenitis based on pathological findings before definite diagnosis was made by culture. The organisms isolated were Mycobacterium chelonae in three cases, M. scrofulaceum in one case and M. avium intracellulare complex in one case. All the patients gradually improved with treatment but one had multiple recurrences. The search for an infectious agent, especially non-tuberculous mycobacteria, should be performed in cases of Sweet's syndrome that appear in association with chronic granulomatous lymphadenitis which is recalcitrant to antituberculous drugs.

Adult↗

Drug eruptions in Bangkok: a 1-year study at Ramathibodi Hospital.

BACKGROUND: As new drugs are introduced onto the market, it is important to determine those that can cause cutaneous reactions and with what frequency. In addition, drugs that have been used for a long period of time may cause new types of eruption that have not been observed previously. The purpose of this study was to evaluate the types of drug eruption and the causative agents in a hospital-based population for a period of 1 year. METHODS: All in- and outpatients consulting for drug eruptions at the Dermatology Clinic, Ramathibodi Hospital from June 1995 to May 1996 were included in the study. The history and physical examination were performed by one of the authors. In suspected cases, a skin biopsy was carried out to confirm the diagnosis. Rechallenge tests with suspected drugs were performed with informed consent. RESULTS: One hundred and thirty-two patients were enrolled in the study. The most common types of drug eruption were maculopapular eruption, fixed drug eruption, and urticaria. Antimicrobial agents were found to be the most common causative drugs, followed by antipyretic/anti-inflammatory agents and drugs acting on the central nervous system. CONCLUSIONS: Although the most common type of drug eruption and the most common causative agents were not different from those found in previous studies, the new generation of antibiotics and antifungal agents were found to be a frequent cause of drug eruptions. New types of drug eruption, such as generalized exanthematous pustulosis and acral erythema, were observed in this study.

Adolescent↗