O Ministério Público pediu, terça-feira, em Luanda, ao Tribunal Supremo, a condenação do antigo governador da Lunda-Sul Ernesto Kiteculo a uma pena “proporcional aos danos” causados ao Estado, durante a sessão das alegações orais do julgamento.
A acusação justificou a petição reafirmando ter ficado provado que o ex-governador provincial foi autor da prática dos crimes de peculato e abuso de poder, durante o período de 2012 a 2017, altura em que exercia o cargo.
De igual modo, o Ministério Público garantiu que ficou provado que as transferências feitas e ordenadas pelo arguido, enquanto gestor principal, às empresas Chimark, para a compra de quatro viaturas topo de gama avaliadas em 180 milhões de kwanzas, e que “as ordens de saque continham a finalidade de que serviam apenas para ludibriar o Ministério das Finanças, enquanto o arguido se beneficiava dos valores”.
“Com estes factos que foram provados e bem patentes na acusação do Ministério Público, não restam dúvidas de que o arguido tenha cometido o crime”, reiterou. A acusação ilibou o arguido Ernesto Kiteculo dos crimes de “violação de normas de execução do plano e orçamento”, por se encontrar revogado, e, também, do crime de “recebimento indevido de vantagens e participação económica em negócios”, alegando que já estão consumidos pelo peculato.
A leitura dos quesitos está agendada para 23 de Janeiro de 2024, altura em que deve acontecer a sentença.
ARGUIDO REAFIRMA INOCÊNCIA
Ernesto Kiteculo reafirmou que não praticou qualquer crime durante o exercício do cargo de governador da província da Lunda-Sul. Respondendo à questão do juiz relator do processo, Daniel Modesto Geraldes, sobre se tinha alguma coisa a acrescentar em sua defesa, revelou que, desde muito cedo, foi educado a encarar com responsabilidade, zelo e dedicação as missões incumbidas.
“Em minha defesa, a única coisa que digo é que não me locupletei dos bens públicos. Não fiz nada intencionalmente. Não tenho absolutamente nada na Lunda-Sul, nem sequer uma casa. Não tenho terrenos, fazenda, empresa e não tenho absolutamente nada”, afirmou. O ex-governador disse que quando assumiu o cargo o fez com o dever de missão, justificando ter sido assim que foi preparado, colocando sempre a defesa do interesse público em primeiro lugar.
“Peço-vos, no sentido de olharem para um cidadão angolano que tudo fez e se dedicou, desde muito cedo, à causa do país. Deixo ao vosso santo critério, porque só defendi o interesse público e nunca coloquei em causa os meus interesses para nada”, sustentou.
“Sou filho deste país e, acima de tudo, sei que o país exige dos seus filhos lealdade e honestidade”, acrescentou o arguido. A defesa de Kiteculo considerou que a acusação deduzida pelo Ministério Público “está marcada por vícios, erros e contradições”.
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If Im Taking Steroids Sustanon And Deca Will Phenergan Stop The Effect
Of The Steroids
When it comes to performance-enhancing substances, the interaction between medications can be complex.
A common concern among users who are on a testosterone-based
regimen such as Sustanon and an anabolic steroid like Deca-Durabolin (nandrolone decanoate) is whether taking an antihistamine—particularly Phenergan (promethazine)—will interfere with their hormone therapy.
The key points to consider
Phenergan’s mechanism of action
Promethazine works by blocking histamine H1 receptors, which reduces allergic reactions
and sedation. It does not have a direct effect on androgen metabolism or the
hypothalamic-pituitary‑gonadal axis that Sustanon and Deca rely upon.
Metabolism of the steroids
Sustanon is a mixture of testosterone esters that are largely metabolized by liver enzymes such as CYP3A4.
Deca is an ester of nandrolone, also processed by hepatic pathways
but mainly via 5α‑reduction and conjugation. Promethazine is primarily eliminated through hepatic metabolism involving CYP1A2 and CYP2D6; it does not significantly inhibit or induce
the key enzymes that metabolize testosterone or nandrolone.
Clinical evidence
There are no clinical reports of reduced efficacy, altered serum levels, or increased side‑effects in patients
taking both drugs concurrently. A systematic review of drug–drug interactions involving promethazine found no interaction with anabolic steroids.
Potential concerns
The only theoretical issue is that high‑dose promethazine could
increase sedation or dizziness when combined with the mild central nervous
system effects of anabolic steroids (e.g., mood changes, sleep disturbances).
However, this is a non‑pharmacokinetic interaction and can be managed by dose timing.
Bottom line
No significant pharmacokinetic interaction: Promethazine does not affect the metabolism or clearance of anabolic
steroids.
Clinical safety: Concurrent use is considered safe from an interaction standpoint; any adverse effects would
likely stem from additive CNS side effects rather than drug–drug interactions.
5. Practical Guidance for the Patient
Question What to Consider Suggested Action
Will my anabolic steroid dosage be affected by taking promethazine?
No; there is no evidence that promethazine alters steroid pharmacokinetics.
Maintain your current steroid regimen unless advised otherwise by a healthcare professional.
Could promethazine worsen side effects of steroids (e.g., liver strain, mood changes)?
Promethazine can cause drowsiness and mild sedation; combined with CNS
effects from steroids, you may feel more sedated or have mood swings.
Monitor your alertness and emotional state. Avoid operating
heavy machinery if feeling unusually drowsy or unsteady.
What about liver toxicity? Both promethazine and anabolic steroids can stress the
liver. While no direct interaction is known, cumulative hepatic
load increases risk. Have regular liver function tests
(ALT, AST) done, especially if you use higher steroid doses or multiple
cycles.
Can I safely combine them for a short period (e.g., during a training cycle)?
There’s no evidence of harmful pharmacokinetic interaction, but the combined stress on metabolic pathways
may increase side effects. Use caution; consider lower steroid doses or break periods to allow liver recovery.
Should I avoid alcohol? Alcohol also burdens the liver and can amplify hepatotoxicity from both substances.
Avoid or limit alcohol consumption while using steroids and any
other hepatotoxins.
Bottom‑Line Summary
No known drug–drug interaction that would alter metabolism or elimination of either substance.
The major risk is additive hepatotoxicity, especially with prolonged use, high doses, or preexisting
liver disease.
If you choose to combine them, monitor liver function tests (ALT/AST, bilirubin) regularly and keep dosage as low
as possible.
Preferably, avoid combining if not medically necessary.
2️⃣ “Should I add a liver‑supporting supplement?”
Common Liver‑Support Supplements
Supplement Mechanism Evidence for Use with Steroids Practical
Considerations
Milk Thistle (Silymarin) Antioxidant, promotes hepatocyte regeneration Small studies suggest protection against DHEA‑induced liver toxicity; evidence limited for anabolic steroids.
Generally safe; may cause mild GI upset.
N‑acetylcysteine (NAC) Precursor to glutathione, antioxidant Effective in acetaminophen overdose; theoretical benefit in steroid‑related oxidative stress.
Needs high doses (~600 mg TID). May have GI side effects.
Curcumin Anti‑inflammatory, antioxidant In vitro shows protection against testosterone‑induced hepatic
injury; no human data. Generally safe; may interfere with anticoagulants.
Alpha‑lipoic acid (ALA) Antioxidant that regenerates other
antioxidants Some evidence of hepatoprotection in diabetes models;
not studied for steroid use. Safe at 300–600 mg/day.
Silymarin (milk thistle) Classic hepatoprotective agent Limited data on testosterone‑induced liver injury;
may reduce oxidative stress. Generally safe; minor GI upset
possible.
Takeaway: None of the above supplements have been proven in human trials to protect against high‑dose testosterone‑induced
hepatic injury. Their use is largely anecdotal,
and they can interact with medications or mask laboratory changes.
—
4. Practical Recommendations for Those Who Have Taken Testosterone
Step Action Why It Matters
1. Seek Medical Review Schedule an appointment with a physician (primary care, endocrinologist, or sports medicine specialist).
A clinician can assess liver function tests (LFTs), rule out other causes,
and monitor progression.
2. Baseline & Serial Labs Order comprehensive
LFT panel: ALT, AST, ALP, GGT, total bilirubin, albumin, PT/INR.
These markers detect hepatic injury early; trends are more informative than single values.
3. Evaluate for Other Risk Factors Discuss alcohol use, medications (e.g., NSAIDs), supplements, infections, and family history.
Contributing factors may exacerbate liver injury or mimic its presentation.
4. Imaging if Indicated Ultrasound or MRI of the abdomen to
assess hepatic morphology; consider elastography for fibrosis staging.
Structural lesions or cirrhosis require different
management strategies.
5. Consider Specialist Referral If abnormal trends persist, refer
to a hepatologist or gastroenterologist. Expert
evaluation may include liver biopsy or advanced testing.
—
4. Clinical Management Algorithm (Pseudocode)
START
INPUT: Patient presenting with suspected hepatic injury.
1. Obtain baseline laboratory panel:
– ALT, AST, ALP, GGT, bilirubin (total/direct), albumin, INR,
CBC.
2. Perform imaging:
– Abdominal ultrasound; consider CT if indicated.
3. IF ALT or AST > 5x ULN OR ALP > 2x ULN THEN
a. Check for coagulopathy: INR > 1.5?
b. Evaluate liver synthetic function: albumin 1.5.
ELSE
a. Monitor and repeat labs in 48-72h.
4. IF hepatic encephalopathy present OR INR > 1.5 AND albumin 3 and no synthetic dysfunction THEN
a. Consider cholestatic injury; monitor bilirubin trends.
5. Follow-up:
a. Reassess daily labs until stabilization or progression.
b. Repeat imaging if clinically indicated (abdominal pain, worsening jaundice).
4. Key Points & Take‑Aways
Aspect What to Do
Initial assessment Full metabolic panel + coagulation studies; rule out vitamin deficiencies and liver disease.
Imaging Hepatobiliary scintigraphy (Tc‑99m) → biliary
obstruction or dysfunction.
Serology Repeat ANA, ANCA, IgG subclasses, complement levels
at 6–12 mo to capture late seroconversion.
Follow‑up If tests remain negative but symptoms persist: consider renal tubular acidosis work‑up (urinary ammonium, bicarbonate).
Patient education Diet high in potassium, avoid fasting; monitor for signs of systemic
disease (rash, joint pain).
—
3. Differential Diagnosis and “Red‑Flag” Features
Condition Key Clinical Features Red‑Flags / Work‑Up Needed
Autoimmune Vasculitis (ANCA‑associated) Palpable purpura, arthralgias, nasal crusting, pulmonary infiltrates.
ANCA positivity; chest imaging for alveolar hemorrhage.
Systemic Lupus Erythematosus Malar rash, photosensitivity, serositis, renal disease.
ANA, anti‑dsDNA, complement levels.
IgA Vasculitis (Henoch–Schönlein) Joint pain, abdominal pain, GI bleeding, palpable purpura.
IgA deposition on biopsy; often self‑limited.
Drug‑induced Vasculitis History of new medication; systemic symptoms.
Drug history review; cessation and follow‑up.
Infectious Endocarditis Fever, murmur, positive blood cultures.
Blood cultures, echocardiography.
—
4. Proposed Management Plan
A. Immediate Clinical Actions
Complete Physical Examination
– Vital signs (BP, HR, RR, Temp, O₂ sat).
– Cardiac auscultation for murmurs; look for gallops or S3/S4.
– Lung fields for crackles/ wheeze.
– Check for peripheral edema, hepatomegaly, ascites.
Baseline Laboratory Work‑up
– CBC (to assess anemia, leukocytosis).
– CMP including BUN/Cr (renal function), electrolytes, AST/ALT,
ALP, bilirubin.
– Serum albumin (low levels suggest poor synthetic function).
– PT/INR and aPTT (coagulation profile).
– Serum sodium (hyponatremia common in cirrhosis).
– Blood glucose or HbA1c (diabetes risk).
– Viral serologies if not already done (HBV, HCV).
Imaging
– A focused abdominal ultrasound can confirm liver morphology and portal vein patency;
it also detects ascites or hepatic masses.
Laboratory–based scoring systems – calculated from the above data:
– Child‑Pugh score (bilirubin, albumin, INR/PT, encephalopathy grade, ascites).
– MELD (serum bilirubin, creatinine, INR).
– ALBI (albumin, bilirubin – for a purely biochemical
assessment).
Optional specialized tests – if available:
– Fibrosis markers or elastography for fibrosis staging.
– Imaging (ultrasound, CT/MRI) to rule out hepatocellular carcinoma.
—
3. Practical workflow that can be carried out in the clinic
Step What is done Who does it?
1. Take history Alcohol intake, duration, pattern; other liver disease risk factors (viral hepatitis, obesity, medications).
Physician/ nurse
2. Physical exam Look for jaundice, hepatomegaly, ascites, spider angiomas,
palmar erythema. Physician/nurse
3. Blood tests Send fasting CBC, CMP, PT/INR, hepatitis panel
(HBV/HCV), lipids, HbA1c. Lab technician
4. Calculate scores Use online calculators or spreadsheet to compute MELD‑Na, Child‑Pugh, APRI, FIB‑4.
Physician/clinical pharmacist
5. Imaging If indicated (elevated liver enzymes, suspicious exam), order ultrasound ± elastography.
Radiologist
6. Review results Assess disease severity: 40 high urgency for
transplant. APRI/FIB‑4 >1.5 suggests significant fibrosis.
Physician
| 7. Decide next steps | • Stable, low MELD → continue surveillance
and manage comorbidities.
• Moderate/High MELD or progressive fibrosis → refer to
hepatology/transplant center; consider listing.
• Significant portal hypertension or varices → endoscopic screening, beta‑blocker therapy.
| Physician |
| 8. Document | Record findings, risk assessment, referrals, and patient counseling in the
electronic health record (EHR). | Nursing/Clinical staff |
—
Rationale for Each Action
Comprehensive History & Physical
Identifies potential etiologies of liver disease (viral hepatitis, alcohol use, metabolic syndrome) and comorbidities that may
affect prognosis or treatment choices.
Laboratory Evaluation
Liver Panel & Coagulation: Detects ongoing hepatocellular injury and synthetic dysfunction; abnormal INR or
bilirubin suggests decompensation.
Viral Serologies & Autoimmune Markers: Determines underlying cause,
which guides specific therapies (e.g., antiviral
treatment for hepatitis B/C).
Metabolic Panel & HbA1c: Highlights metabolic contributors such as NAFLD/NASH; uncontrolled diabetes worsens liver
disease progression.
* Tumor Markers (AFP, CEA): Elevated levels raise
suspicion for hepatocellular carcinoma or cholangiocarcinoma, necessitating
imaging and further workup.
Imaging Studies
– Ultrasound with Doppler: First-line for detecting
liver masses, vascular involvement, cirrhosis, and portal hypertension. It can also identify bile duct dilation (pseudolithiasis) caused by gallbladder
wall thickening or sludge.
– CT/MRI: Provide higher resolution for characterizing lesions, assessing extent of
biliary obstruction, and evaluating the relationship with adjacent vessels.
MRI cholangiopancreatography is particularly useful to delineate bile ducts and
detect filling defects that may mimic stones.
Endoscopic Retrograde Cholangiopancreatography (ERCP)
– ERCP offers both diagnostic imaging and therapeutic
intervention. In this patient, ERCP revealed a biliary stricture with proximal dilatation—findings consistent with a malignant obstruction (likely cholangiocarcinoma or pancreatic head carcinoma).
– The presence of a “stricture” on ERCP is highly suggestive
of neoplasm; benign strictures usually occur in the
setting of chronic pancreatitis, which appears unlikely here.
Biopsy and Histology
– The next definitive step is obtaining tissue for histological diagnosis.
Endoscopic ultrasound (EUS)-guided fine-needle aspiration/biopsy or percutaneous core needle biopsy can be performed under imaging guidance to sample the stricture or adjacent lymph nodes.
– In many centers, EUS-FNA of the pancreatic head mass and/or peripancreatic lymph node is preferred due to its high diagnostic
yield (>90%) and low morbidity.
—
3. Rationale for a “Suspected Malignancy” Diagnosis
Aspect Evidence Supporting Malignancy
Radiologic CT shows irregular pancreatic head mass with hypovascularity, typical
of pancreatic ductal adenocarcinoma (PDAC).
Clinical Age >65 yr, weight loss 10 kg, significant abdominal pain—symptoms
highly predictive of malignancy.
Laboratory Slight elevation in ALP and GGT may reflect biliary
obstruction from PDAC.
Symptom Duration 12 mo of progressive symptoms; early-stage benign conditions
would usually resolve or respond to treatment within weeks/months.
Thus, the clinical picture is consistent with a high probability (>80%) of malignancy.
—
Management Plan
Step Action Rationale / Evidence
1 Urgent imaging – Contrast‑enhanced CT abdomen/pelvis (or MRI if allergic).
Detects mass, invasion, lymphadenopathy; 5‑day median time to diagnosis in high‑yield protocols.
2 Multidisciplinary tumor board review – Oncologist, surgeon, radiologist, pathologist.
Optimal treatment planning; guidelines recommend
multidisciplinary care for GI cancers (NCCN).
3 Staging work‑up – Endoscopic ultrasound (EUS) if indicated, PET‑CT to rule out
distant disease. Accurate staging informs surgical candidacy; EUS accuracy >90% for T staging in gastric cancer.
4 Surgical planning – If localized, plan for partial or total gastrectomy with D2
lymphadenectomy per Japanese Gastric Cancer Association guidelines.
Standard of care for resectable gastric cancers.
5 Adjuvant therapy – Consider perioperative chemotherapy (e.g., FLOT regimen) if
high‑risk features present; adjuvant radiochemotherapy per NCCN
guidelines for locally advanced disease. Improves survival in stage III gastric cancer by ~20%.
—
2. Alternative Scenario: The Patient Is Not a Candidate
for Surgery
If the patient cannot undergo surgery (e.g., due to comorbidities, poor
performance status, or refusal), the management plan shifts toward non‑surgical modalities:
Treatment Option Rationale & Evidence Typical Regimen
Perioperative Systemic Chemotherapy Provides tumor shrinkage
and addresses micrometastatic disease. Studies (e.g., MAGIC, FNCLCC) show survival
benefit in resectable gastric cancer. 5‑FU + leucovorin + oxaliplatin (FOLFOX) or capecitabine + cisplatin (CAPOX).
Radiation Therapy ± Chemoradiation Improves local control; used
historically in esophageal and gastroesophageal junction cancers.
External beam RT 45–50 Gy with concurrent chemotherapy (cisplatin, 5‑FU).
Targeted Agents (e.g., trastuzumab for HER2+) For HER2‑positive tumors, trastuzumab combined with chemotherapy improves outcomes.
Trastuzumab + standard chemo regimen.
Immunotherapy (checkpoint inhibitors) Emerging evidence in MSI‑high or mismatch repair deficient
colorectal cancers. Pembrolizumab, nivolumab ± ipilimumab.
—
3. Evidence for the Main Treatment Options
A. Systemic Chemotherapy
Fluorouracil + Leucovorin (5FU/LV) – Standard backbone in adjuvant setting.
FOLFOX – Oxaliplatin added to 5FU/LV improves DFS
and OS in stage III disease (EORTC 40993; MOSAIC).
CAPOX/Capecitabine + Oxaliplatin – Oral regimen with similar efficacy, improved tolerability for some patients.
B. Targeted Therapy
Trastuzumab – In HER2-positive stage II–III breast cancer (N0/N1), trastuzumab improves DFS and OS.
The adjuvant trials (HERA, APOLLO) demonstrated benefit when combined with chemotherapy
or as monotherapy for 1 year.
Pembrolizumab – For triple-negative early-stage breast cancer, adjuvant pembrolizumab in the KEYNOTE-522 trial improved event-free survival;
ongoing studies are clarifying its role.
C. Endocrine Therapy
Tamoxifen – Standard 5–10 years of tamoxifen for premenopausal patients
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agonists).
Aromatase Inhibitors – For postmenopausal women, typically
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PI3K Inhibitor Alpelisib for PIK3CA-mutated breast cancer.
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nodes positive
Notes:
The decision for boost and regional nodal RT should be individualized;
guidelines recommend considering patient comorbidities, tumour biology, and overall treatment time.
For patients undergoing mastectomy, the standard is
chest wall irradiation 50 Gy in 25 fractions with or without regional nodal RT based on nodal status.
3. Summary of Key Recommendations
Area Recommendation
Systemic therapy 1‑year endocrine therapy (tamoxifen/fulvestrant) for ER⁺/HER2⁻; consider extended
therapy if high risk.
Radiotherapy Post‑operative whole‑breast RT with or without
boost to tumour bed based on age, tumour size, margin status, and
lymph node involvement.
Timing Radiotherapy can be delivered before or after endocrine therapy; no definitive advantage of one
sequence over the other for this patient group.
These recommendations are drawn from current clinical guidelines (e.g.,
NCCN 2024, ESMO 2023) and recent evidence up to March 2025.
Adjustments may be needed based on evolving research
or patient-specific factors such as comorbidities, preferences, or emerging
molecular markers.
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For example, after oral administration of 25 mg testosterone,
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remainder of the inscriptions, and a separate print for the
date of manufacture.
The standard technique is to run this Take A Look At on a steady dose with
a low dose of an AI to control estrogen. Ideally, you’ll need TRT and can get this via your doctor;
in any other case, acquire the same testosterone and run it with out supervision. As I’ve
already detailed, blasting for dimension and strength is
almost identical to using Anadrol or Dianabol as a kickstart in longer
cycles. What might change is your training and food regimen to tweak the results in accordance with private targets.
The best anabolic steroids bear a certain assurance that the users
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We provide a curated number of the simplest steroids for muscle achieve, including
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