A Case of Gastric and Duodenal Strongyloidiasis

Strongyloides stercoralis is a nematode parasite which causes a protracted asymptomatic intestinal infection. It is considered a life threatening condition in immunocompromised patients when hyperinfection is associated with disseminated disease. The diagnosis by routine stool examination is very limited since the larval output in stools is very low. We present the case of a 52 year-old Omani man from Salalah, in the southern region of Oman, with a 15-year history of type 2 diabetes mellitus and recently discovered to have hairy cell leukaemia, who complained of nausea, abdominal pain, loss of appetite and loss of weight. An oesophagogastroduodoscopic biopsy was obtained and histopathologic examination revealed gastrointestinal strongyloidiasis.

Interstitial Cells of Cajal : Pathology, injury and repair

Interstitial cells of cajal (ICC) are specialised cells located within the musculature of the gastrointestinal tract (GIT). Although they form only 5% of the cells in the musculature of the GIT, they play a critical role in regulating smooth muscle function and GIT motility in coordination with the enteric nervous system. C-kit is a transmembrane glycoprotein that plays a critical role in ICC development and maturation. Physiological conditions such as ageing, as well as pathological conditions that have different disease processes, negatively affect ICC networks and function. Absent or disordered ICC networks can be associated with disorders in GIT motility. This review highlights the mechanism of ICC recovery from various types of injury which entails understanding the development of ICC and the factors affecting it. ICC transformation into malignant tumours (gastrointestinal stromal tumours) and their potential as contributors to therapeutic resistance is also discussed

Adrenal Oncocytic Neoplasm with Uncertain Malignant Potential

Adrenal oncocytic neoplasms (AONs) are a rare group of tumours with a somewhat uncertain natural history and clinical behaviour. Out of 46 cases of AON reported to date, 6 cases were histologically classified as neoplasms with uncertain malignant potential. We report the case of a 35-year-old male with an incidentally detected large AON with mostly benign morphology and some characteristics which would make its behaviouruncertain

Scapular Bronchogenic Cyst: A Case Report and Literature Review

Bronchogenic cysts originate from abnormal budding of the tracheal diverticula during the embryological period. Inaccuracy in the process of growing of the ventral foregut will give rise to bronchogenic cyst. Scapular bronchogenic cyst is an extremely rare form of this anomaly. A three years old boy suffered for 2 years with left sided suprascapular cystic lesion which was gradually increasing in size. The swelling was 4 × 3 cm in size and non tender. The cyst was evaluated by CT scan that showed complex cystic lesion over the left scapular spine. Total excision of the cyst was done and histopathology showed cutaneous bronchogenic cyst. The proposed mechanism for such cutaneous lesion is that the accessory buds from the tracheobronchial tree/primitive foregut migrated from the thorax in an aberrant manner to lie in periscapular positions. The definitive treatment of scapular lesions is total surgical excision. The final diagnosis is based on the histopathological findings in the majority of cases

Adult Sickle Cell Disease: A Five-year Experience of Intensive Care Management in a University Hospital in Oman

Objectives: Sickle cell disease (SCD) is an inherited disease caused by an abnormal type of haemoglobin. It is one of the most common genetic blood disorders in the Gulf area, including Oman. It may be associated with complications requiring intensive care unit (ICU) admission. This study investigated the causes of ICU admission for SCD patients. Methods: This was a retrospective analysis of all adult patients ≥12 years old with SCD admitted to Sultan Qaboos University Hospital (SQUH) ICU between 1st January 2005 and 31st December 2009. Results: A total number of 49 sickle cell patients were admitted 56 times to ICU. The reasons for admission were acute chest syndrome (69.6%), painful crises (16.1%), multi-organ failure (7.1%) and others (7.2%). The mortality for SCD patients in our ICU was 16.1%. The haemoglobin (Hb) and Hb S levels at time of ICU admission were studied as predictors of mortality and neither showed statistical significance by Student’s t-test. The odds ratio, with 95% confidence intervals, was used to study other six organ supportive measures as predictors of mortality. The need for inotropic support and mechanical ventilation was a good predictor of mortality. While the need for noninvasive ventilation, haemofiltration, blood transfusions and exchange transfusions were not significant predictors of mortality. Conclusion: Acute chest syndrome is the main cause of ICU admission in SCD patient. Unlike other supportive measures, the use of inotropic support and/or mechanical ventilation is an indicator of high mortality rate SCD patient

Impaired Macrophage and Satellite Cell Infiltration Occurs in a Muscle-Specific Fashion Following Injury in Diabetic Skeletal Muscle

<div><p>Background</p><p>Systemic elevations in PAI-1 suppress the fibrinolytic pathway leading to poor collagen remodelling and delayed regeneration of tibialis anterior (TA) muscles in type-1 diabetic Akita mice. However, how impaired collagen remodelling was specifically attenuating regeneration in Akita mice remained unknown. Furthermore, given intrinsic differences between muscle groups, it was unclear if the reparative responses between muscle groups were different.</p><p>Principal Findings</p><p>Here we reveal that diabetic Akita muscles display differential regenerative responses with the TA and gastrocnemius muscles exhibiting reduced regenerating myofiber area compared to wild-type mice, while soleus muscles displayed no difference between animal groups following injury. Collagen levels in TA and gastrocnemius, but not soleus, were significantly increased post-injury versus controls. At 5 days post-injury, when degenerating/necrotic regions were present in both animal groups, Akita TA and gastrocnemius muscles displayed reduced macrophage and satellite cell infiltration and poor myofiber formation. By 10 days post-injury, necrotic regions were absent in wild-type TA but persisted in Akita TA. In contrast, Akita soleus exhibited no impairment in any of these measures compared to wild-type soleus. In an effort to define how impaired collagen turnover was attenuating regeneration in Akita TA, a PAI-1 inhibitor (PAI-039) was orally administered to Akita mice following cardiotoxin injury. PAI-039 administration promoted macrophage and satellite cell infiltration into necrotic areas of the TA and gastrocnemius. Importantly, soleus muscles exhibit the highest inducible expression of MMP-9 following injury, providing a mechanism for normative collagen degradation and injury recovery in this muscle despite systemically elevated PAI-1.</p><p>Conclusions</p><p>Our findings suggest the mechanism underlying how impaired collagen remodelling in type-1 diabetes results in delayed regeneration is an impairment in macrophage infiltration and satellite cell recruitment to degenerating areas; a phenomena that occurs differentially between muscle groups.</p></div

Macrophage and satellite cell infiltration into necrotic muscle is impaired in Akita diabetic mice at 5 days post injury.

<p>(A) The necrotic area of the TA demonstrates a reduced number of macrophages as evidenced by less F4/80 positive cells. * denotes significant difference by t-test (p<0.05). (B) A similar, though non-significant, trend of attenuated F4/80 positive cells was observed in necrotic gastrocnemius (GAS) (P = 0.09). (C) Representative images of necrotic regions of TA and GAS immunofluorescently stained for F4/80 (red), costained for type I collagen (green) and nuclei with DAPI (blue). Satellite cells (Pax7+ cells) were also reduced in number within necrotic areas of (D) Akita TA and (E) GAS (P = 0.06). (F) Representative images of Pax7 positive cells within necrotic regions of WT and Akita TA. Scale bar represents 50 um.</p

Necrosis of muscle fibers persists throughout muscle regeneration in Akita tibialis anterior muscle.

<p>(A) Uninjured (left), necrotic (center), and actively regenerating (right) regions of skeletal muscle are easily identified in collagen type I immunostain (green) with DAPI (blue) counterstain. Note the presence of centrally located nuclei in muscle fibers in regenerating muscle, indicative of new myofiber formation. (B) TA of diabetic mice have clearly defined areas of necrosis remaining at 10 days post-injury (significant interaction [P<0.05]; * denotes post-hoc difference). Similarly, gastrocnemius (GAS) (C) follows this pattern although not statistically significant (P = 0.21). In contrast, both WT and Akita soleus (SOL) display no areas of necrosis at 5 or 10 days post-injury (not shown). (D) Representative image of TA muscle undergoing regeneration at 10 days post-injury in WT and Akita TA. Note the distinct area of necrosis in the Akita TA. Scale bar represents 500 um.</p

Macrophage and satellite cell infiltration into necrotic Akita diabetic muscle is restored with PAI-039 treatment.

<p>(A) Representative images of the necrotic area of the TA muscles of WT, Akita and Akita+PAI-039. Sections were stained with F4/80 (macrophage marker; red), collagen type 1 (green) and DAPI (nuclear dye; blue). A visible decrease in the number of F4/80 positive cells is seen in Akita muscle sections with a detectable increase in F4/80 cells in Akita TA muscles of mice treated with a PAI-1 inhibitor (PAI-039). (B) The number of F4/80 positive cells within the necrotic area of injured Akita TA muscles was returned to WT levels when these mice were treated with PAI-039. The number of F4/80 positive cells was greater in Akita+PAI-039 TA (panel B; P = 0.06) and gastrocnemius (panel C; P = 0.07) muscles compared to untreated Akita animals. A similar trend was observed for Pax7 positive cells which were also found to be improved in necrotic TA (D) and gastrocnemius (E) with PAI-039 treatment (P<0.05).</p